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Gene Information
Gene symbol: GIP
Gene name: gastric inhibitory polypeptide
HGNC ID: 4270
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 111943 | Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance. |
| 2 | 111943 | To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. |
| 3 | 111943 | Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. |
| 4 | 111943 | Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance. |
| 5 | 111943 | To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. |
| 6 | 111943 | Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. |
| 7 | 111943 | Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance. |
| 8 | 111943 | To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. |
| 9 | 111943 | Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. |
| 10 | 323091 | Effect of synthetic gastric inhibitory polypeptide (GIP) on insulin and glucagon secretion was stuied in vivo and in vitro in the rat. |
| 11 | 323091 | In in-vitro experiments with isolated pancreatic islets, GIP significantly augmented insulin release induced by either 8.3 mM or 16.7 mM glucose, whereas the augmentation of glucagon release was observed at 3.3 mM, 8.3 MM, and 16.7 mM glucose concentrations. |
| 12 | 323091 | Three peptides, consisting of 1-28, 22-43, and 15-43 amino acids of GIP, failed to potentiate insulin and glucagon secretion. |
| 13 | 323091 | These results suggest that synthetic GIP has a stimulating effect on insulin and glucagon secretion. |
| 14 | 323091 | Effect of synthetic gastric inhibitory polypeptide (GIP) on insulin and glucagon secretion was stuied in vivo and in vitro in the rat. |
| 15 | 323091 | In in-vitro experiments with isolated pancreatic islets, GIP significantly augmented insulin release induced by either 8.3 mM or 16.7 mM glucose, whereas the augmentation of glucagon release was observed at 3.3 mM, 8.3 MM, and 16.7 mM glucose concentrations. |
| 16 | 323091 | Three peptides, consisting of 1-28, 22-43, and 15-43 amino acids of GIP, failed to potentiate insulin and glucagon secretion. |
| 17 | 323091 | These results suggest that synthetic GIP has a stimulating effect on insulin and glucagon secretion. |
| 18 | 323091 | Effect of synthetic gastric inhibitory polypeptide (GIP) on insulin and glucagon secretion was stuied in vivo and in vitro in the rat. |
| 19 | 323091 | In in-vitro experiments with isolated pancreatic islets, GIP significantly augmented insulin release induced by either 8.3 mM or 16.7 mM glucose, whereas the augmentation of glucagon release was observed at 3.3 mM, 8.3 MM, and 16.7 mM glucose concentrations. |
| 20 | 323091 | Three peptides, consisting of 1-28, 22-43, and 15-43 amino acids of GIP, failed to potentiate insulin and glucagon secretion. |
| 21 | 323091 | These results suggest that synthetic GIP has a stimulating effect on insulin and glucagon secretion. |
| 22 | 323091 | Effect of synthetic gastric inhibitory polypeptide (GIP) on insulin and glucagon secretion was stuied in vivo and in vitro in the rat. |
| 23 | 323091 | In in-vitro experiments with isolated pancreatic islets, GIP significantly augmented insulin release induced by either 8.3 mM or 16.7 mM glucose, whereas the augmentation of glucagon release was observed at 3.3 mM, 8.3 MM, and 16.7 mM glucose concentrations. |
| 24 | 323091 | Three peptides, consisting of 1-28, 22-43, and 15-43 amino acids of GIP, failed to potentiate insulin and glucagon secretion. |
| 25 | 323091 | These results suggest that synthetic GIP has a stimulating effect on insulin and glucagon secretion. |
| 26 | 324834 | The diabetics were nonobese and treated by diet alone; they exhibited exaggerated increments of plasma IRGIP in association with delayed and diminished peak increases in plasma immunoreactive insulin, suggesting relative failure of the beta-cell response to GIP. |
| 27 | 324834 | It is suggested that the defective beta-cell response may lead to diminished feedback inhibition of GIP secretion by insulin in diabetes mellitus and that the glucagonotropic action of GIP may be expressed under these conditions. |
| 28 | 324834 | The diabetics were nonobese and treated by diet alone; they exhibited exaggerated increments of plasma IRGIP in association with delayed and diminished peak increases in plasma immunoreactive insulin, suggesting relative failure of the beta-cell response to GIP. |
| 29 | 324834 | It is suggested that the defective beta-cell response may lead to diminished feedback inhibition of GIP secretion by insulin in diabetes mellitus and that the glucagonotropic action of GIP may be expressed under these conditions. |
| 30 | 393872 | [Negative feedback effect of insulin on the secretion of gastric inhibitory polypeptide (GIP) (author's transl)]. |
| 31 | 400725 | Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. |
| 32 | 400725 | Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. |
| 33 | 400725 | Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. |
| 34 | 400725 | Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. |
| 35 | 400725 | Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. |
| 36 | 400725 | Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. |
| 37 | 400725 | Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. |
| 38 | 400725 | Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. |
| 39 | 400725 | Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. |
| 40 | 400725 | Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. |
| 41 | 400725 | Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. |
| 42 | 400725 | Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. |
| 43 | 400725 | Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. |
| 44 | 400725 | Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. |
| 45 | 400725 | Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. |
| 46 | 400725 | Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. |
| 47 | 457845 | Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. |
| 48 | 457845 | The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. |
| 49 | 457845 | An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. |
| 50 | 457845 | Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. |
| 51 | 457845 | These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects. |
| 52 | 457845 | Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. |
| 53 | 457845 | The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. |
| 54 | 457845 | An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. |
| 55 | 457845 | Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. |
| 56 | 457845 | These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects. |
| 57 | 457845 | Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. |
| 58 | 457845 | The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. |
| 59 | 457845 | An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. |
| 60 | 457845 | Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. |
| 61 | 457845 | These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects. |
| 62 | 457845 | Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. |
| 63 | 457845 | The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. |
| 64 | 457845 | An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. |
| 65 | 457845 | Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. |
| 66 | 457845 | These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects. |
| 67 | 457845 | Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. |
| 68 | 457845 | The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. |
| 69 | 457845 | An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. |
| 70 | 457845 | Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. |
| 71 | 457845 | These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects. |
| 72 | 488570 | The reduction of GIP or GLI secretion may, therefore, be partly responsible for the smaller rise in plasma insulin observed in normal volunteers when guar is added to meals. |
| 73 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 74 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 75 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 76 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 77 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 78 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 79 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 80 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 81 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 82 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 83 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 84 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 85 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 86 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 87 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 88 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 89 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 90 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 91 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 92 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 93 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 94 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 95 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 96 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 97 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 98 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 99 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 100 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 101 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 102 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 103 | 510813 | Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. |
| 104 | 510813 | Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. |
| 105 | 510813 | Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. |
| 106 | 510813 | After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. |
| 107 | 510813 | GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. |
| 108 | 510813 | The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. |
| 109 | 516774 | Intravenous infusion of porcine GIP in man induces insulin release when a degree of hyperglycemia is present. |
| 110 | 640238 | Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. |
| 111 | 640238 | The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide. |
| 112 | 640238 | Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. |
| 113 | 640238 | The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide. |
| 114 | 680412 | The effect of endogenous gastric inhibitory polypeptide on glucose-induced insulin secretion in mild diabetes. |
| 115 | 976601 | Serum GIP, insulin, and glucose concentrations were determined during a standard oral glucose tolerance test in 80 individuals, 45 of whom were normal and 35 of whom had adult-onset diabetes mellitus according to USPHS criteria. |
| 116 | 976601 | However, since our current understanding suggests the GIP may be an important enteric signal for the release of insulin in man, and because GIP has been shown to stimulate the release of immunoreactive glucagon, GIP may play a role in the pathogenesis of diabetes mellitus. |
| 117 | 976601 | Serum GIP, insulin, and glucose concentrations were determined during a standard oral glucose tolerance test in 80 individuals, 45 of whom were normal and 35 of whom had adult-onset diabetes mellitus according to USPHS criteria. |
| 118 | 976601 | However, since our current understanding suggests the GIP may be an important enteric signal for the release of insulin in man, and because GIP has been shown to stimulate the release of immunoreactive glucagon, GIP may play a role in the pathogenesis of diabetes mellitus. |
| 119 | 1357529 | After a 48-hour culture period, insulin release in response to glucose (17.8 mmol/L) either alone, with glucose-dependent insulinotropic polypeptide (GIP) +/- somatostatin (SS), or with Arg +/- SS was measured. |
| 120 | 1357529 | The addition of GIP (1 nmol/L) enhanced glucose-stimulated insulin secretion from BBN rat islets (2.9% +/- 0.42% TCC), but had no effect on BBD islets (2.04% +/- 0.57% TCC). |
| 121 | 1357529 | Somatostatin (1 mumol/L) completely reversed the glucose- and/or GIP-stimulated insulin secretion from both BBN and BBD rat islets to basal levels (0.42% +/- 0.043%, 0.42% +/- 0.09% TCC, respectively). |
| 122 | 1357529 | After a 48-hour culture period, insulin release in response to glucose (17.8 mmol/L) either alone, with glucose-dependent insulinotropic polypeptide (GIP) +/- somatostatin (SS), or with Arg +/- SS was measured. |
| 123 | 1357529 | The addition of GIP (1 nmol/L) enhanced glucose-stimulated insulin secretion from BBN rat islets (2.9% +/- 0.42% TCC), but had no effect on BBD islets (2.04% +/- 0.57% TCC). |
| 124 | 1357529 | Somatostatin (1 mumol/L) completely reversed the glucose- and/or GIP-stimulated insulin secretion from both BBN and BBD rat islets to basal levels (0.42% +/- 0.043%, 0.42% +/- 0.09% TCC, respectively). |
| 125 | 1357529 | After a 48-hour culture period, insulin release in response to glucose (17.8 mmol/L) either alone, with glucose-dependent insulinotropic polypeptide (GIP) +/- somatostatin (SS), or with Arg +/- SS was measured. |
| 126 | 1357529 | The addition of GIP (1 nmol/L) enhanced glucose-stimulated insulin secretion from BBN rat islets (2.9% +/- 0.42% TCC), but had no effect on BBD islets (2.04% +/- 0.57% TCC). |
| 127 | 1357529 | Somatostatin (1 mumol/L) completely reversed the glucose- and/or GIP-stimulated insulin secretion from both BBN and BBD rat islets to basal levels (0.42% +/- 0.043%, 0.42% +/- 0.09% TCC, respectively). |
| 128 | 1553183 | Glucose, insulin, gastric inhibitory polypeptide, and pancreatic polypeptide responses to polycose during pregnancy. |
| 129 | 1553183 | In the pregnant subjects, even though the plasma insulin response to carbohydrate challenge was higher than in the nonpregnant subjects, gastric inhibitory polypeptide levels were significantly lower. |
| 130 | 1553183 | Glucose, insulin, gastric inhibitory polypeptide, and pancreatic polypeptide responses to polycose during pregnancy. |
| 131 | 1553183 | In the pregnant subjects, even though the plasma insulin response to carbohydrate challenge was higher than in the nonpregnant subjects, gastric inhibitory polypeptide levels were significantly lower. |
| 132 | 1576919 | Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. |
| 133 | 1576919 | To investigate the mechanism of oral carbohydrate-stimulated secretion of the two most potent incretin candidates, gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1), we studied the changes in the plasma levels of these peptides in five healthy men after sucrose ingestion with or without pretreatment with an alpha-D-glucosidase inhibitor (AO-128). |
| 134 | 1576919 | After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. |
| 135 | 1576919 | Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. |
| 136 | 1576919 | To investigate the mechanism of oral carbohydrate-stimulated secretion of the two most potent incretin candidates, gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1), we studied the changes in the plasma levels of these peptides in five healthy men after sucrose ingestion with or without pretreatment with an alpha-D-glucosidase inhibitor (AO-128). |
| 137 | 1576919 | After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. |
| 138 | 1576919 | Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. |
| 139 | 1576919 | To investigate the mechanism of oral carbohydrate-stimulated secretion of the two most potent incretin candidates, gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1), we studied the changes in the plasma levels of these peptides in five healthy men after sucrose ingestion with or without pretreatment with an alpha-D-glucosidase inhibitor (AO-128). |
| 140 | 1576919 | After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. |
| 141 | 1600330 | There were significant inverse correlations of plasma C-peptide, GIP, and gastrin immunoreactivity to endogenous creatinine clearance (kidney function). |
| 142 | 1600330 | In conclusion, the overall pattern of pancreatic and gastrointestinal hormone release is normal in patients after combined pancreas-kidney-transplantation, but there are some peculiarities due to (a) systemic venous drainage of the pancreas graft (elevated fasting IR insulin) and (b) impaired kidney function (negative correlation of fasting plasma values to endogenous creatinine clearance for C-peptide, GIP, and gastrin). |
| 143 | 1600330 | There were significant inverse correlations of plasma C-peptide, GIP, and gastrin immunoreactivity to endogenous creatinine clearance (kidney function). |
| 144 | 1600330 | In conclusion, the overall pattern of pancreatic and gastrointestinal hormone release is normal in patients after combined pancreas-kidney-transplantation, but there are some peculiarities due to (a) systemic venous drainage of the pancreas graft (elevated fasting IR insulin) and (b) impaired kidney function (negative correlation of fasting plasma values to endogenous creatinine clearance for C-peptide, GIP, and gastrin). |
| 145 | 1645253 | Preperifusion of HIT-T15 cells with 100 nmol/liter glucagon (10 min) or 100 nmol/liter gastric inhibitory peptide (GIP) (10 min) had no effect on the insulin secretory response to 10 nmol/liter GLP-(7-37). |
| 146 | 1645253 | Prior exposure of cells to 100 nmol/liter GLP-(7-37) (10 min) did not alter the GIP-induced (10 nmol/liter) insulin release, but 100 nmol/liter GIP (10 min) reduced the insulin secretion during stimulation with 10 nmol/liter GIP by 56%. |
| 147 | 1645253 | Preperifusion of HIT-T15 cells with 100 nmol/liter glucagon (10 min) or 100 nmol/liter gastric inhibitory peptide (GIP) (10 min) had no effect on the insulin secretory response to 10 nmol/liter GLP-(7-37). |
| 148 | 1645253 | Prior exposure of cells to 100 nmol/liter GLP-(7-37) (10 min) did not alter the GIP-induced (10 nmol/liter) insulin release, but 100 nmol/liter GIP (10 min) reduced the insulin secretion during stimulation with 10 nmol/liter GIP by 56%. |
| 149 | 1675542 | Additionally, the distribution of gastric inhibitory polypeptide, somatostatin, glucagon, and insulin immunoreactive cells was also quantitated. |
| 150 | 1675542 | The glucagon, gastric inhibitory polypeptide, and somatostatin containing cells were intermingled with the beta-cells. |
| 151 | 1675542 | Additionally, the distribution of gastric inhibitory polypeptide, somatostatin, glucagon, and insulin immunoreactive cells was also quantitated. |
| 152 | 1675542 | The glucagon, gastric inhibitory polypeptide, and somatostatin containing cells were intermingled with the beta-cells. |
| 153 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 154 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 155 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 156 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 157 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 158 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 159 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 160 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 161 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 162 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 163 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 164 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 165 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 166 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 167 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 168 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 169 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 170 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 171 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 172 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 173 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 174 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 175 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 176 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 177 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 178 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 179 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 180 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 181 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 182 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 183 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 184 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 185 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 186 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 187 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 188 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 189 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 190 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 191 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 192 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 193 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 194 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 195 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 196 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 197 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 198 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 199 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 200 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 201 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 202 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 203 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 204 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 205 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 206 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 207 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 208 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 209 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 210 | 1683622 | Gastrointestinal hormones with insulinotropic effects, like cholecystokinin (CCK) and gastric inhibitory polypeptide (GIP) might tentatively be used in the treatment of non-insulin-dependent diabetes mellitus. |
| 211 | 1683622 | We therefore examined the effects of intravenous injection of pharmacological dose levels of CCK-8 (100 and 300 pmol/kg), CCK-33 (100 pmol/kg), GIP (100 pmol/kg), and CCK-8 plus GIP (100 pmol/kg of each) on plasma levels of glucose, insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) in healthy human volunteers. |
| 212 | 1683622 | CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. |
| 213 | 1683622 | CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. |
| 214 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 215 | 1683622 | CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. |
| 216 | 1683622 | We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. |
| 217 | 1782606 | The insulin response from the isolated perfused pancreas to glucose and the glucose-dependent insulinotropic hormone, gastric inhibitory polypeptide (GIP), was reduced by 95%. |
| 218 | 1782606 | Islet content of other endocrine peptides, glucagon, somatostatin, and pancreatic polypeptide, was normal at onset and at 2 weeks post onset. |
| 219 | 1984341 | Influence of breakfasts with different nutrient contents on glucose, C peptide, insulin, glucagon, triglycerides, and GIP in non-insulin-dependent diabetics. |
| 220 | 1984341 | Thus, in NIDDM subjects, glucose and insulin responses to different mixed meals do not appear to be exclusively mediated by GIP. |
| 221 | 1984341 | Influence of breakfasts with different nutrient contents on glucose, C peptide, insulin, glucagon, triglycerides, and GIP in non-insulin-dependent diabetics. |
| 222 | 1984341 | Thus, in NIDDM subjects, glucose and insulin responses to different mixed meals do not appear to be exclusively mediated by GIP. |
| 223 | 2097092 | With the exception of insulin sensitivity which was enhanced with safflowerseed oil, plasma concentrations of glucose and gastric inhibitory polypeptide (GIP), glucose tolerance, intestinal GIP content and the GIP response to oral fat were similar. |
| 224 | 2097092 | Since the hyperinsulinaemic action of sucrose cannot be attributed to elevated GIP or glucose concentrations, the involvement of other insulin-releasing hormones released from the intestine by sucrose is suggested. |
| 225 | 2097092 | With the exception of insulin sensitivity which was enhanced with safflowerseed oil, plasma concentrations of glucose and gastric inhibitory polypeptide (GIP), glucose tolerance, intestinal GIP content and the GIP response to oral fat were similar. |
| 226 | 2097092 | Since the hyperinsulinaemic action of sucrose cannot be attributed to elevated GIP or glucose concentrations, the involvement of other insulin-releasing hormones released from the intestine by sucrose is suggested. |
| 227 | 2146178 | We therefore examined the effects of glucagonlike peptide I-(7-36)-amide (truncated GLP-I) and gastric inhibitory polypeptide (GIP) on insulin and glucagon release from isolated perfused pancreases of diabetic rats (12-14 wk of age, mean +/- SE fasting plasma glucose 8.9 +/- 0.6 mM, n = 25) after an injection of 90 mg/kg streptozocin on the 2nd day after birth and compared the results with those of nondiabetic control rats. |
| 228 | 2146178 | In diabetic rats, the infusion of 1 nM GLP-I or GIP in perfusates with varying glucose concentrations (2.8, 5.6, 8.3, 11.1, or 22.2 mM) caused a nearly equal degree of insulin stimulation from a similar basal insulin level. |
| 229 | 2146178 | Meanwhile, basal and GLP-I- or GIP-stimulated insulin release increased in correlation with the ambient glucose concentration in nondiabetic rats. |
| 230 | 2146178 | We therefore examined the effects of glucagonlike peptide I-(7-36)-amide (truncated GLP-I) and gastric inhibitory polypeptide (GIP) on insulin and glucagon release from isolated perfused pancreases of diabetic rats (12-14 wk of age, mean +/- SE fasting plasma glucose 8.9 +/- 0.6 mM, n = 25) after an injection of 90 mg/kg streptozocin on the 2nd day after birth and compared the results with those of nondiabetic control rats. |
| 231 | 2146178 | In diabetic rats, the infusion of 1 nM GLP-I or GIP in perfusates with varying glucose concentrations (2.8, 5.6, 8.3, 11.1, or 22.2 mM) caused a nearly equal degree of insulin stimulation from a similar basal insulin level. |
| 232 | 2146178 | Meanwhile, basal and GLP-I- or GIP-stimulated insulin release increased in correlation with the ambient glucose concentration in nondiabetic rats. |
| 233 | 2146178 | We therefore examined the effects of glucagonlike peptide I-(7-36)-amide (truncated GLP-I) and gastric inhibitory polypeptide (GIP) on insulin and glucagon release from isolated perfused pancreases of diabetic rats (12-14 wk of age, mean +/- SE fasting plasma glucose 8.9 +/- 0.6 mM, n = 25) after an injection of 90 mg/kg streptozocin on the 2nd day after birth and compared the results with those of nondiabetic control rats. |
| 234 | 2146178 | In diabetic rats, the infusion of 1 nM GLP-I or GIP in perfusates with varying glucose concentrations (2.8, 5.6, 8.3, 11.1, or 22.2 mM) caused a nearly equal degree of insulin stimulation from a similar basal insulin level. |
| 235 | 2146178 | Meanwhile, basal and GLP-I- or GIP-stimulated insulin release increased in correlation with the ambient glucose concentration in nondiabetic rats. |
| 236 | 2163805 | BAY m1099 reduced the test breakfast plasma responses of glucose (p less than 0.001) and gastric inhibitory polypeptide (GIP, p less than 0.01) and increased those of peptide tyrosine-tyrosine (p less than 0.05) and motilin (p less than 0.01). |
| 237 | 2191884 | Despite similar 4-h blood glucose areas, large reductions were seen in serum insulin (54 +/- 10%, P less than 0.001) and C-peptide (47 +/- 12%, P less than 0.01) areas after sipping, together with lower gastric inhibitory polypeptide and enteroglucagon levels and urinary catecholamine output. |
| 238 | 2192849 | Cholecystokinin (CCK) and acetylcholine activate the hydrolysis of polyphosphoinositides, and gastric inhibitory polypeptide (GIP) and glucagonlike peptide 1 activate adenylate cyclase. |
| 239 | 2436870 | The levels of insulin, C-peptide, gastric inhibitory polypeptide (GIP), glucagon, somatostatin, triglyceride and glycerol were followed after the breakfast meals. |
| 240 | 2446948 | The inhibitor significantly (p less than 0.05) reduced postprandial plasma glucose, C-peptide, insulin, and gastric inhibitory polypeptide concentrations, significantly increased (p less than 0.05) breath hydrogen excretion, and caused carbohydrate malabsorption. |
| 241 | 2465985 | Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). |
| 242 | 2647605 | Glucose dependent insulinotropic polypeptide (GIP) infused intravenously is insulinotropic in the fasting state in type 2 (non-insulin dependent) diabetes mellitus. |
| 243 | 2647605 | Frequent plasma glucose, insulin, C-peptide and GIP measurements were made throughout and the study was continued until 200 min. |
| 244 | 2647605 | During the GIP infusion there was an early significant rise in insulin concentration from 0.058 +/- 0.006 nmol/l to 0.106 +/- 0.007 nmol/l (P less than 0.01) within 6 min of commencing the GIP infusion and insulin levels reached a peak of 0.131 +/- 0.011 nmol/l at 10 min (P less than 0.01). |
| 245 | 2647605 | Insulin levels remained significantly elevated during the rest of the GIP infusion (P less than 0.01-0.001) and returned to basal values 20 min post infusion. |
| 246 | 2647605 | Glucose dependent insulinotropic polypeptide (GIP) infused intravenously is insulinotropic in the fasting state in type 2 (non-insulin dependent) diabetes mellitus. |
| 247 | 2647605 | Frequent plasma glucose, insulin, C-peptide and GIP measurements were made throughout and the study was continued until 200 min. |
| 248 | 2647605 | During the GIP infusion there was an early significant rise in insulin concentration from 0.058 +/- 0.006 nmol/l to 0.106 +/- 0.007 nmol/l (P less than 0.01) within 6 min of commencing the GIP infusion and insulin levels reached a peak of 0.131 +/- 0.011 nmol/l at 10 min (P less than 0.01). |
| 249 | 2647605 | Insulin levels remained significantly elevated during the rest of the GIP infusion (P less than 0.01-0.001) and returned to basal values 20 min post infusion. |
| 250 | 2647605 | Glucose dependent insulinotropic polypeptide (GIP) infused intravenously is insulinotropic in the fasting state in type 2 (non-insulin dependent) diabetes mellitus. |
| 251 | 2647605 | Frequent plasma glucose, insulin, C-peptide and GIP measurements were made throughout and the study was continued until 200 min. |
| 252 | 2647605 | During the GIP infusion there was an early significant rise in insulin concentration from 0.058 +/- 0.006 nmol/l to 0.106 +/- 0.007 nmol/l (P less than 0.01) within 6 min of commencing the GIP infusion and insulin levels reached a peak of 0.131 +/- 0.011 nmol/l at 10 min (P less than 0.01). |
| 253 | 2647605 | Insulin levels remained significantly elevated during the rest of the GIP infusion (P less than 0.01-0.001) and returned to basal values 20 min post infusion. |
| 254 | 2647605 | Glucose dependent insulinotropic polypeptide (GIP) infused intravenously is insulinotropic in the fasting state in type 2 (non-insulin dependent) diabetes mellitus. |
| 255 | 2647605 | Frequent plasma glucose, insulin, C-peptide and GIP measurements were made throughout and the study was continued until 200 min. |
| 256 | 2647605 | During the GIP infusion there was an early significant rise in insulin concentration from 0.058 +/- 0.006 nmol/l to 0.106 +/- 0.007 nmol/l (P less than 0.01) within 6 min of commencing the GIP infusion and insulin levels reached a peak of 0.131 +/- 0.011 nmol/l at 10 min (P less than 0.01). |
| 257 | 2647605 | Insulin levels remained significantly elevated during the rest of the GIP infusion (P less than 0.01-0.001) and returned to basal values 20 min post infusion. |
| 258 | 2662384 | The aim of the present study was to examine the association between insulin and gastric inhibitory polypetide (GIP) secretion in conditions characterized by insulin resistance, i.e. obesity, impaired glucose tolerance (IGT), non-insulin dependent diabetes mellitus (NIDDM) and aging. |
| 259 | 2662384 | In contrast, lean NIDDM subjects showed both a reduced insulin/C-peptide repsonse and a decreased GIP response to the test meal indicating that dysfunction of GIP secretion could be involved in the impaired beta-cell function in NIDDM. |
| 260 | 2662384 | The data, therefore, suggest that hypersecretion of GIP does not contribute to hyperinsulinaemia and hyper-C-peptidaemia in insulin-resistant states. |
| 261 | 2662384 | The aim of the present study was to examine the association between insulin and gastric inhibitory polypetide (GIP) secretion in conditions characterized by insulin resistance, i.e. obesity, impaired glucose tolerance (IGT), non-insulin dependent diabetes mellitus (NIDDM) and aging. |
| 262 | 2662384 | In contrast, lean NIDDM subjects showed both a reduced insulin/C-peptide repsonse and a decreased GIP response to the test meal indicating that dysfunction of GIP secretion could be involved in the impaired beta-cell function in NIDDM. |
| 263 | 2662384 | The data, therefore, suggest that hypersecretion of GIP does not contribute to hyperinsulinaemia and hyper-C-peptidaemia in insulin-resistant states. |
| 264 | 2662384 | The aim of the present study was to examine the association between insulin and gastric inhibitory polypetide (GIP) secretion in conditions characterized by insulin resistance, i.e. obesity, impaired glucose tolerance (IGT), non-insulin dependent diabetes mellitus (NIDDM) and aging. |
| 265 | 2662384 | In contrast, lean NIDDM subjects showed both a reduced insulin/C-peptide repsonse and a decreased GIP response to the test meal indicating that dysfunction of GIP secretion could be involved in the impaired beta-cell function in NIDDM. |
| 266 | 2662384 | The data, therefore, suggest that hypersecretion of GIP does not contribute to hyperinsulinaemia and hyper-C-peptidaemia in insulin-resistant states. |
| 267 | 2675469 | [The functional relation of gastric inhibitory polypeptide and insulin (a review of the literature)]. |
| 268 | 2676668 | The glucose dependent insulinotropic polypeptide response to oral glucose and mixed meals is increased in patients with type 2 (non-insulin-dependent) diabetes mellitus. |
| 269 | 2676668 | Considerable disagreement exists regarding the levels of immunoreactive glucose dependent insulinotropic polypeptide in patients with Type 2 (non-insulin-dependent) diabetes mellitus. |
| 270 | 2676668 | The glucose dependent insulinotropic polypeptide response to oral glucose and mixed meals is increased in patients with type 2 (non-insulin-dependent) diabetes mellitus. |
| 271 | 2676668 | Considerable disagreement exists regarding the levels of immunoreactive glucose dependent insulinotropic polypeptide in patients with Type 2 (non-insulin-dependent) diabetes mellitus. |
| 272 | 2693029 | Frequent measurements of plasma glucose, C-peptide, insulin and GIP concentrations were made. |
| 273 | 2822518 | Binding of synthetic human GIP 1-31 and activation of adenylate cyclase. |
| 274 | 2822518 | The GIP binding sites of human insulinoma were coupled to adenylate cyclase stimulation. |
| 275 | 2822518 | GIP 1-31 regulated the adenylate cyclase activity to the same extent as GIP 1-42. |
| 276 | 2822518 | Binding of synthetic human GIP 1-31 and activation of adenylate cyclase. |
| 277 | 2822518 | The GIP binding sites of human insulinoma were coupled to adenylate cyclase stimulation. |
| 278 | 2822518 | GIP 1-31 regulated the adenylate cyclase activity to the same extent as GIP 1-42. |
| 279 | 2822518 | Binding of synthetic human GIP 1-31 and activation of adenylate cyclase. |
| 280 | 2822518 | The GIP binding sites of human insulinoma were coupled to adenylate cyclase stimulation. |
| 281 | 2822518 | GIP 1-31 regulated the adenylate cyclase activity to the same extent as GIP 1-42. |
| 282 | 2866196 | Effects of insulin on fasting and meal-stimulated somatostatin-like immunoreactivity in noninsulin-dependent diabetes mellitus: evidence for more than one mechanism of action. |
| 283 | 2866196 | We assessed the effects of insulin and normalization of blood glucose on plasma levels of somatostatin-like immunoreactivity (SLI) in patients with noninsulin-dependent diabetes mellitus (NIDDM). |
| 284 | 2866196 | Furthermore feedback insulin infusion enhanced GIP and decreased C-peptide responses, but did not affect the glucagon response to the meal. |
| 285 | 2866196 | We conclude that in patients with NIDDM, insulin significantly lowers basal SLI levels if normoglycemia is concomitantly attained; this action of insulin was partially dissociated from its hypoglycemic action; hyperglycemia per se inhibits a meal-induced SLI response, and insulin effects on SLI are not secondary to changes in glucagon or GIP levels. |
| 286 | 2866196 | Effects of insulin on fasting and meal-stimulated somatostatin-like immunoreactivity in noninsulin-dependent diabetes mellitus: evidence for more than one mechanism of action. |
| 287 | 2866196 | We assessed the effects of insulin and normalization of blood glucose on plasma levels of somatostatin-like immunoreactivity (SLI) in patients with noninsulin-dependent diabetes mellitus (NIDDM). |
| 288 | 2866196 | Furthermore feedback insulin infusion enhanced GIP and decreased C-peptide responses, but did not affect the glucagon response to the meal. |
| 289 | 2866196 | We conclude that in patients with NIDDM, insulin significantly lowers basal SLI levels if normoglycemia is concomitantly attained; this action of insulin was partially dissociated from its hypoglycemic action; hyperglycemia per se inhibits a meal-induced SLI response, and insulin effects on SLI are not secondary to changes in glucagon or GIP levels. |
| 290 | 2889321 | Extruded bread, based on wholegrain wheat flour, with high availability of in vitro starch, elicited a greater glucose response than wholegrain wheat bread, associated with a modest increase of GIP and insulin and with a stimulated early glucagon secretion. |
| 291 | 2890501 | The subjects underwent normoglycemic clamp studies and meal tests with determination of insulin, C-peptide, glucagon, somatostatin, and gastric inhibitory polypeptide in plasma. |
| 292 | 2890501 | Glyburide increased basal and meal-but not glucagon-stimulated insulin and C-peptide levels, and also augmented the effect of meals on somatostatin release. |
| 293 | 2951158 | Seventeen non-insulin-dependent diabetics poorly controlled by diet and sulphonylurea drugs took part in a long-term (20-52 weeks) trial of the effect of an alpha-glucosidase inhibitor (acarbose 100 mg thrice daily) on postprandial glycaemic and gastro-entero-pancreatic hormone responses. |
| 294 | 2951158 | Acarbose administration reduced the integrated postprandial plasma responses of glucose to 58 +/- 10% (mean +/- SEM, p less than 0.001), insulin to 61 +/- 10% (p less than 0.01) and gastric inhibitory polypeptide to 45 +/- 8% (p less than 0.001) of control values, increased the enteroglucagon response to 152 +/- 26% (p less than 0.001) of control and slightly prolonged the postprandial release of motilin. |
| 295 | 2959439 | Guar ingestion reduced postprandial insulin and enteroglucagon responses, the latter significantly so, but had no apparent effect on gastric inhibitory polypeptide, pancreatic glucagon, gastrin, and pancreatic polypeptide. |
| 296 | 2991171 | The extruded whole-grain product gave significantly larger areas under the glucose and insulin curves than the corresponding baked bread, and resulted in higher C-peptide, gastric inhibitory polypeptide, and glucagon concentrations at certain time points. |
| 297 | 2994452 | Blending of cooked beans made no difference to plasma glucose, insulin, or GIP (gastric inhibitory polypeptide) responses in nondiabetics, NIDD (noninsulin-dependent diabetics), and IDD (insulin-dependent diabetics). |
| 298 | 2994452 | In NIDD and IDD, however, the reverse applied for plasma glucose. |
| 299 | 3009077 | The gastric inhibitory polypeptide response was greater during the first part of the curve, while the somatostatin response after the beet-fibre meal displayed a significantly larger total area below the curve. |
| 300 | 3046973 | L 364718, at levels 10- to 100-fold greater than those necessary to attenuate CCK-8S-induced insulin secretion, had no adverse effect on the insulin secretory response of freshly isolated islets to 10 mM glucose alone, 5 mM D-glyceraldehyde, 15 mM alpha-ketoisocaproate, or 50 ng/ml gastric inhibitory polypeptide. |
| 301 | 3057329 | Fasting and postprandial concentrations of glucose, insulin, glucagon, enteroglucagon, and gastrointestinal inhibitory peptide (GIP) were measured after the first and last dose of Bay 1099, and the fecal excretions of protein, fat, fiber, and total calories were measured on the last three days of each diet. |
| 302 | 3057329 | Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. |
| 303 | 3057329 | Fasting and postprandial concentrations of glucose, insulin, glucagon, enteroglucagon, and gastrointestinal inhibitory peptide (GIP) were measured after the first and last dose of Bay 1099, and the fecal excretions of protein, fat, fiber, and total calories were measured on the last three days of each diet. |
| 304 | 3057329 | Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. |
| 305 | 3283195 | Effect of source of dietary fats on serum glucose, insulin, and gastric inhibitory polypeptide responses to mixed test meals in subjects with non-insulin dependent diabetes mellitus. |
| 306 | 3283195 | To determine if a similar phenomenon occurs in subjects with non-insulin dependent diabetes mellitus (NIDDM), serum glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) responses to three mixed test meals of varying fatty acid composition were assessed in twelve subjects with NIDDM. |
| 307 | 3283195 | Effect of source of dietary fats on serum glucose, insulin, and gastric inhibitory polypeptide responses to mixed test meals in subjects with non-insulin dependent diabetes mellitus. |
| 308 | 3283195 | To determine if a similar phenomenon occurs in subjects with non-insulin dependent diabetes mellitus (NIDDM), serum glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) responses to three mixed test meals of varying fatty acid composition were assessed in twelve subjects with NIDDM. |
| 309 | 3287838 | Gastric inhibitory polypeptide in newly diagnosed ketotic type I (insulin-dependent) diabetics. |
| 310 | 3287838 | Plasma concentrations of 5,000 daltons (5 kDa) immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured before and up to 16 hours after the start of low-dose insulin treatment in newly diagnosed ketotic type I (insulin-dependent) diabetics. |
| 311 | 3287838 | Gastric inhibitory polypeptide in newly diagnosed ketotic type I (insulin-dependent) diabetics. |
| 312 | 3287838 | Plasma concentrations of 5,000 daltons (5 kDa) immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured before and up to 16 hours after the start of low-dose insulin treatment in newly diagnosed ketotic type I (insulin-dependent) diabetics. |
| 313 | 3292314 | Although basal and integrated plasma glucose did not differ between oral and intravenous glucose, integrated responses of insulin (3.3 +/- 0.5 vs. 1.8 +/- 0.4 mU ml-1.240 min-1, P less than .001), C-peptide (456.5 +/- 58.5 vs. 327.9 +/- 46.3 ng.ml-1.240 min-1, P = .002), gastric inhibitory polypeptide, (16.8 +/- 3.5 vs. -2.8 +/- 1.0 micrograms.ml-1.240 min-1, P less than .001), and insulin secretion (6.6 +/- 1.1 vs. 4.7 +/- 0.7 U.240 min-1, P = .003) were greater with oral than intravenous glucose. |
| 314 | 3298936 | The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects. |
| 315 | 3298936 | In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all). |
| 316 | 3298936 | In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients. |
| 317 | 3298936 | The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects. |
| 318 | 3298936 | In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all). |
| 319 | 3298936 | In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients. |
| 320 | 3298936 | The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects. |
| 321 | 3298936 | In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all). |
| 322 | 3298936 | In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients. |
| 323 | 3309010 | Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. |
| 324 | 3320156 | To test the hypothesis that dietary fats may influence carbohydrate metabolism, serum glucose, insulin, and gastric inhibitory polypeptide (GIP) responses to three mixed test meals of varying fatty acid composition were assessed in 12 normal subjects. |
| 325 | 3320156 | The mechanism for this increased insulin secretion is unknown but did not appear to be mediated through differences in serum glucose values or through the insulin-otrophic effects of GIP. |
| 326 | 3320156 | To test the hypothesis that dietary fats may influence carbohydrate metabolism, serum glucose, insulin, and gastric inhibitory polypeptide (GIP) responses to three mixed test meals of varying fatty acid composition were assessed in 12 normal subjects. |
| 327 | 3320156 | The mechanism for this increased insulin secretion is unknown but did not appear to be mediated through differences in serum glucose values or through the insulin-otrophic effects of GIP. |
| 328 | 3322911 | The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal subjects and type 2 (non-insulin-dependent) diabetic patients on glucose tolerance and B-cell secretion. |
| 329 | 3322911 | The effects of porcine glucose-dependent insulinotropic polypeptide given by continuous intravenous infusion in normal subjects (n = 6) and Type 2 (non-insulin-dependent) diabetic patients (n = 6) have been investigated. |
| 330 | 3322911 | In the normal subjects insulin concentrations were greater from 10-35 min (p less than 0.01) following glucose-dependent insulinotropic polypeptide infusion and peak values were increased by 123%. |
| 331 | 3322911 | In the Type 2 diabetic patients following glucose-dependent insulinotropic polypeptide infusion insulin levels were increased from 4-40 min (p less than 0.01) but peak values were only increased by 27%. |
| 332 | 3322911 | The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal subjects and type 2 (non-insulin-dependent) diabetic patients on glucose tolerance and B-cell secretion. |
| 333 | 3322911 | The effects of porcine glucose-dependent insulinotropic polypeptide given by continuous intravenous infusion in normal subjects (n = 6) and Type 2 (non-insulin-dependent) diabetic patients (n = 6) have been investigated. |
| 334 | 3322911 | In the normal subjects insulin concentrations were greater from 10-35 min (p less than 0.01) following glucose-dependent insulinotropic polypeptide infusion and peak values were increased by 123%. |
| 335 | 3322911 | In the Type 2 diabetic patients following glucose-dependent insulinotropic polypeptide infusion insulin levels were increased from 4-40 min (p less than 0.01) but peak values were only increased by 27%. |
| 336 | 3322911 | The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal subjects and type 2 (non-insulin-dependent) diabetic patients on glucose tolerance and B-cell secretion. |
| 337 | 3322911 | The effects of porcine glucose-dependent insulinotropic polypeptide given by continuous intravenous infusion in normal subjects (n = 6) and Type 2 (non-insulin-dependent) diabetic patients (n = 6) have been investigated. |
| 338 | 3322911 | In the normal subjects insulin concentrations were greater from 10-35 min (p less than 0.01) following glucose-dependent insulinotropic polypeptide infusion and peak values were increased by 123%. |
| 339 | 3322911 | In the Type 2 diabetic patients following glucose-dependent insulinotropic polypeptide infusion insulin levels were increased from 4-40 min (p less than 0.01) but peak values were only increased by 27%. |
| 340 | 3322911 | The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal subjects and type 2 (non-insulin-dependent) diabetic patients on glucose tolerance and B-cell secretion. |
| 341 | 3322911 | The effects of porcine glucose-dependent insulinotropic polypeptide given by continuous intravenous infusion in normal subjects (n = 6) and Type 2 (non-insulin-dependent) diabetic patients (n = 6) have been investigated. |
| 342 | 3322911 | In the normal subjects insulin concentrations were greater from 10-35 min (p less than 0.01) following glucose-dependent insulinotropic polypeptide infusion and peak values were increased by 123%. |
| 343 | 3322911 | In the Type 2 diabetic patients following glucose-dependent insulinotropic polypeptide infusion insulin levels were increased from 4-40 min (p less than 0.01) but peak values were only increased by 27%. |
| 344 | 3464150 | The enteral stimulation of insulin secretion (the incretin effect) is diminished in pregnancy--both when determined indirectly and when the gastric inhibitory polypeptide (GIP) response to glucose ingestion is considered. |
| 345 | 3510224 | We have studied the relationships between GIP and immunoreactive insulin (IRI) and glucose turnover rates (D3H-3 glucose technique) in five poorly controlled type II diabetic patients and five normal subjects before and after a breakfast containing 500 kcal including 42 g sucrose. |
| 346 | 3510224 | We hypothesize that GIP may play a compensatory role to improve both impaired beta-cell insulin release and peripheral glucose utilization which are the recognized pathogenetic mechanisms underlying type II diabetes mellitus. |
| 347 | 3510224 | We have studied the relationships between GIP and immunoreactive insulin (IRI) and glucose turnover rates (D3H-3 glucose technique) in five poorly controlled type II diabetic patients and five normal subjects before and after a breakfast containing 500 kcal including 42 g sucrose. |
| 348 | 3510224 | We hypothesize that GIP may play a compensatory role to improve both impaired beta-cell insulin release and peripheral glucose utilization which are the recognized pathogenetic mechanisms underlying type II diabetes mellitus. |
| 349 | 3512343 | When glucose was given intravenously, morphine had no effect on plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), or pancreatic glucagon. |
| 350 | 3512343 | Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. |
| 351 | 3512343 | During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. |
| 352 | 3512343 | When glucose was given intravenously, morphine had no effect on plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), or pancreatic glucagon. |
| 353 | 3512343 | Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. |
| 354 | 3512343 | During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. |
| 355 | 3512343 | When glucose was given intravenously, morphine had no effect on plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), or pancreatic glucagon. |
| 356 | 3512343 | Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. |
| 357 | 3512343 | During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. |
| 358 | 3514334 | Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. |
| 359 | 3514334 | Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). |
| 360 | 3514334 | An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. |
| 361 | 3514334 | This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. |
| 362 | 3514334 | The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. |
| 363 | 3514334 | Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. |
| 364 | 3514334 | Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). |
| 365 | 3514334 | An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. |
| 366 | 3514334 | This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. |
| 367 | 3514334 | The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. |
| 368 | 3514334 | Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. |
| 369 | 3514334 | Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). |
| 370 | 3514334 | An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. |
| 371 | 3514334 | This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. |
| 372 | 3514334 | The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. |
| 373 | 3514334 | Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. |
| 374 | 3514334 | Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). |
| 375 | 3514334 | An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. |
| 376 | 3514334 | This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. |
| 377 | 3514334 | The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. |
| 378 | 3514334 | Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. |
| 379 | 3514334 | Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). |
| 380 | 3514334 | An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. |
| 381 | 3514334 | This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. |
| 382 | 3514334 | The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. |
| 383 | 3514335 | Plasma gastric inhibitory polypeptide (GIP) and insulin concentrations were measured in seven healthy volunteers given oral glucose loads ranging from 25 to 200 g. |
| 384 | 3514335 | Both the magnitude and duration of the GIP and insulin responses after oral glucose ingestion were dose dependent. |
| 385 | 3514335 | Plasma gastric inhibitory polypeptide (GIP) and insulin concentrations were measured in seven healthy volunteers given oral glucose loads ranging from 25 to 200 g. |
| 386 | 3514335 | Both the magnitude and duration of the GIP and insulin responses after oral glucose ingestion were dose dependent. |
| 387 | 3516764 | To evaluate the role of both parameters after different carbohydrate-enriched meals, we measured the arterialized venous blood glucose, immunoreactive insulin and gastric inhibitory polypeptide concentrations in seven Type 2 diabetic patients after ingestion of isocaloric test meals. |
| 388 | 3544634 | Heterogeneity of immunoreactive gastric inhibitory polypeptide in the plasma of newly diagnosed type 1 (insulin-dependent) diabetics. |
| 389 | 3545933 | In spite of marked hyperglycaemia, fat-stimulated GIP release did not raise plasma insulin in streptozotocin diabetic mice. |
| 390 | 3545933 | The results indicate that streptozotocin diabetes in mice is associated with ineffectiveness of the entero-insular axis, despite elevated GIP concentrations, which are probably mediated through hyperphagia and defective feedback inhibition by insulin on intestinal K cells. |
| 391 | 3545933 | In spite of marked hyperglycaemia, fat-stimulated GIP release did not raise plasma insulin in streptozotocin diabetic mice. |
| 392 | 3545933 | The results indicate that streptozotocin diabetes in mice is associated with ineffectiveness of the entero-insular axis, despite elevated GIP concentrations, which are probably mediated through hyperphagia and defective feedback inhibition by insulin on intestinal K cells. |
| 393 | 3595434 | Blood samples were collected between 0 and 240 min post-prandially and assayed for glucose, insulin, C-peptide, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide (GIP), and gastrin. |
| 394 | 3880559 | Immunoreactive gastric inhibitory polypeptide response to a meal during the first eighteen months after diagnosis of type 1 (insulin dependent) diabetes mellitus. |
| 395 | 3880559 | The changes in plasma concentrations of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal were examined in 21 normal subjects and 15 Type 1 (insulin dependent) diabetic patients 7 days, 14 days, and 3, 6, 9, 12, and 18 months after time of diagnosis. |
| 396 | 3880559 | Immunoreactive gastric inhibitory polypeptide response to a meal during the first eighteen months after diagnosis of type 1 (insulin dependent) diabetes mellitus. |
| 397 | 3880559 | The changes in plasma concentrations of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal were examined in 21 normal subjects and 15 Type 1 (insulin dependent) diabetic patients 7 days, 14 days, and 3, 6, 9, 12, and 18 months after time of diagnosis. |
| 398 | 3883205 | The effect of a dialysate exchange with both 1.5 and 4.25% glucose solutions on plasma levels of glucose, insulin, gastric inhibitory polypeptide (GIP), and glucagon has been investigated in 5 continuous ambulatory peritoneal dialysis (CAPD) patients. |
| 399 | 3886310 | High-carbohydrate, low-fat diet: effect on lipid and carbohydrate metabolism, GIP and insulin secretion in diabetics. |
| 400 | 3890129 | Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls. |
| 401 | 3890129 | Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. |
| 402 | 3890129 | Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation. |
| 403 | 3890129 | Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls. |
| 404 | 3890129 | Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. |
| 405 | 3890129 | Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation. |
| 406 | 3890129 | Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls. |
| 407 | 3890129 | Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. |
| 408 | 3890129 | Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation. |
| 409 | 3890139 | Effects of intravenously infused porcine GIP on serum insulin, plasma C-peptide, and pancreatic polypeptide in non-insulin-dependent diabetes in the fasting state. |
| 410 | 3890139 | Eight fasting patients with non-insulin-dependent diabetes (NIDD) and six healthy controls were given an intravenous infusion of porcine gastric inhibitory polypeptide (GIP). |
| 411 | 3890139 | During the GIP infusion mean plasma pancreatic polypeptide level increased significantly in both groups, whereas the mean serum insulin level increased in the NIDD group only, indicating a more important role for GIP in these patients than in healthy subjects. |
| 412 | 3890139 | Effects of intravenously infused porcine GIP on serum insulin, plasma C-peptide, and pancreatic polypeptide in non-insulin-dependent diabetes in the fasting state. |
| 413 | 3890139 | Eight fasting patients with non-insulin-dependent diabetes (NIDD) and six healthy controls were given an intravenous infusion of porcine gastric inhibitory polypeptide (GIP). |
| 414 | 3890139 | During the GIP infusion mean plasma pancreatic polypeptide level increased significantly in both groups, whereas the mean serum insulin level increased in the NIDD group only, indicating a more important role for GIP in these patients than in healthy subjects. |
| 415 | 3890139 | Effects of intravenously infused porcine GIP on serum insulin, plasma C-peptide, and pancreatic polypeptide in non-insulin-dependent diabetes in the fasting state. |
| 416 | 3890139 | Eight fasting patients with non-insulin-dependent diabetes (NIDD) and six healthy controls were given an intravenous infusion of porcine gastric inhibitory polypeptide (GIP). |
| 417 | 3890139 | During the GIP infusion mean plasma pancreatic polypeptide level increased significantly in both groups, whereas the mean serum insulin level increased in the NIDD group only, indicating a more important role for GIP in these patients than in healthy subjects. |
| 418 | 3900134 | Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs. |
| 419 | 3900134 | This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. |
| 420 | 3900134 | Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. |
| 421 | 3900134 | The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide. |
| 422 | 3900134 | Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs. |
| 423 | 3900134 | This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. |
| 424 | 3900134 | Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. |
| 425 | 3900134 | The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide. |
| 426 | 3900134 | Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs. |
| 427 | 3900134 | This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. |
| 428 | 3900134 | Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. |
| 429 | 3900134 | The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide. |
| 430 | 3900134 | Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs. |
| 431 | 3900134 | This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. |
| 432 | 3900134 | Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. |
| 433 | 3900134 | The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide. |
| 434 | 3901250 | Alterations of GIP secretion are not necessarily followed by alterations of insulin secretion. |
| 435 | 3902421 | GIP stimulates insulin release in the presence of hyperglycemia and as such is considered a major enteroinsular hormone. |
| 436 | 3902421 | Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. |
| 437 | 3902421 | Seventy-five grams of oral glucose was ingested after overnight fasting and samples were obtained at 0, 30, 60, 90, 120, and 180 min for serum glucose and immunoreactive insulin (IRI) and GIP (IRGIP). |
| 438 | 3902421 | GIP stimulates insulin release in the presence of hyperglycemia and as such is considered a major enteroinsular hormone. |
| 439 | 3902421 | Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. |
| 440 | 3902421 | Seventy-five grams of oral glucose was ingested after overnight fasting and samples were obtained at 0, 30, 60, 90, 120, and 180 min for serum glucose and immunoreactive insulin (IRI) and GIP (IRGIP). |
| 441 | 3902421 | GIP stimulates insulin release in the presence of hyperglycemia and as such is considered a major enteroinsular hormone. |
| 442 | 3902421 | Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. |
| 443 | 3902421 | Seventy-five grams of oral glucose was ingested after overnight fasting and samples were obtained at 0, 30, 60, 90, 120, and 180 min for serum glucose and immunoreactive insulin (IRI) and GIP (IRGIP). |
| 444 | 3902545 | GIP (gastric inhibitory polypeptide; glucose dependent insulin releasing peptide) remains the strongest incretin factor. |
| 445 | 3902545 | GIP is unlikely to be the gut factor which regulates hepatic insulin extraction. |
| 446 | 3902545 | GIP (gastric inhibitory polypeptide; glucose dependent insulin releasing peptide) remains the strongest incretin factor. |
| 447 | 3902545 | GIP is unlikely to be the gut factor which regulates hepatic insulin extraction. |
| 448 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 449 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 450 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 451 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 452 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 453 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 454 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 455 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 456 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 457 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 458 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 459 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 460 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 461 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 462 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 463 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 464 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 465 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 466 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 467 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 468 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 469 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 470 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 471 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 472 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 473 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 474 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 475 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 476 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 477 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 478 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 479 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 480 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 481 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 482 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 483 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 484 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 485 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 486 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 487 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 488 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 489 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 490 | 3902866 | Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. |
| 491 | 3902866 | Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. |
| 492 | 3902866 | Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. |
| 493 | 3902866 | Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. |
| 494 | 3902866 | Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. |
| 495 | 3902866 | Insulin administration did not alter these elevated GIP levels. |
| 496 | 3902866 | These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion. |
| 497 | 3910488 | The effect of insulin deprivation on fasting levels of 5000 dalton gastric inhibitory polypeptide in type 1 (insulin-dependent) diabetics. |
| 498 | 3910488 | To investigate whether metabolic decompensation has an effect on gastric inhibitory polypeptide (GIP), 8 fasting male type 1 diabetics were deprived of insulin for 12 h. |
| 499 | 3910488 | The effect of insulin deprivation on fasting levels of 5000 dalton gastric inhibitory polypeptide in type 1 (insulin-dependent) diabetics. |
| 500 | 3910488 | To investigate whether metabolic decompensation has an effect on gastric inhibitory polypeptide (GIP), 8 fasting male type 1 diabetics were deprived of insulin for 12 h. |
| 501 | 3930323 | In the steady state, plasma immunoreactive insulin (IRI) was significantly lower with EA (mean, 153 +/- 5 microU/ml) than with PA (mean, 226 +/- 15 microU/ml), which in turn was lower than with PA plus GIP (mean, 375 +/- 23 microU/ml, P less than 0.001 by ANOVA). |
| 502 | 4008608 | Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. |
| 503 | 4008608 | In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. |
| 504 | 4008608 | Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. |
| 505 | 4008608 | The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. |
| 506 | 4008608 | Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. |
| 507 | 4008608 | In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. |
| 508 | 4008608 | Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. |
| 509 | 4008608 | The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. |
| 510 | 4008608 | Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. |
| 511 | 4008608 | In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. |
| 512 | 4008608 | Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. |
| 513 | 4008608 | The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. |
| 514 | 4008608 | Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. |
| 515 | 4008608 | In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. |
| 516 | 4008608 | Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. |
| 517 | 4008608 | The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. |
| 518 | 4050722 | Xanthan gum also tended to lower fasting and postload levels of gastrin and gastric inhibitory polypeptide (GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions. |
| 519 | 6257457 | We investigated the effects of fiber on responses of blood glucose, serum insulin, gastric inhibitory polypeptide (GIP), and immunoreactive pancreatic glucagon (IRG) to ingestion of mixed meal with and without added fiber (5 g guar and 5 g pectin) in 12 normal, healthy subjects and in 12 age-, sex-, and weight-matched non-insulin-dependent, maturity-onset diabetic subjects (NIDDM). |
| 520 | 6257457 | Fiber markedly enhanced glucose tolerance in the normal subjects without a change in insulin or GIP but with a significant reduction in glucagon responses. |
| 521 | 6257457 | Fiber also markedly improved glucose tolerance in the NIDDMs without changing insulin or GIP but with a significant reduction in the glucagon responses. |
| 522 | 6257457 | In NIDDMs without AN, glucose tolerance was improved by fiber without a change in insulin, IRG, or GIP. |
| 523 | 6257457 | In diabetic subjects with AN, glucose tolerance was not improved, although glucagon levels were lowered and insulin and GIP responses were unchanged. |
| 524 | 6257457 | We investigated the effects of fiber on responses of blood glucose, serum insulin, gastric inhibitory polypeptide (GIP), and immunoreactive pancreatic glucagon (IRG) to ingestion of mixed meal with and without added fiber (5 g guar and 5 g pectin) in 12 normal, healthy subjects and in 12 age-, sex-, and weight-matched non-insulin-dependent, maturity-onset diabetic subjects (NIDDM). |
| 525 | 6257457 | Fiber markedly enhanced glucose tolerance in the normal subjects without a change in insulin or GIP but with a significant reduction in glucagon responses. |
| 526 | 6257457 | Fiber also markedly improved glucose tolerance in the NIDDMs without changing insulin or GIP but with a significant reduction in the glucagon responses. |
| 527 | 6257457 | In NIDDMs without AN, glucose tolerance was improved by fiber without a change in insulin, IRG, or GIP. |
| 528 | 6257457 | In diabetic subjects with AN, glucose tolerance was not improved, although glucagon levels were lowered and insulin and GIP responses were unchanged. |
| 529 | 6257457 | We investigated the effects of fiber on responses of blood glucose, serum insulin, gastric inhibitory polypeptide (GIP), and immunoreactive pancreatic glucagon (IRG) to ingestion of mixed meal with and without added fiber (5 g guar and 5 g pectin) in 12 normal, healthy subjects and in 12 age-, sex-, and weight-matched non-insulin-dependent, maturity-onset diabetic subjects (NIDDM). |
| 530 | 6257457 | Fiber markedly enhanced glucose tolerance in the normal subjects without a change in insulin or GIP but with a significant reduction in glucagon responses. |
| 531 | 6257457 | Fiber also markedly improved glucose tolerance in the NIDDMs without changing insulin or GIP but with a significant reduction in the glucagon responses. |
| 532 | 6257457 | In NIDDMs without AN, glucose tolerance was improved by fiber without a change in insulin, IRG, or GIP. |
| 533 | 6257457 | In diabetic subjects with AN, glucose tolerance was not improved, although glucagon levels were lowered and insulin and GIP responses were unchanged. |
| 534 | 6257457 | We investigated the effects of fiber on responses of blood glucose, serum insulin, gastric inhibitory polypeptide (GIP), and immunoreactive pancreatic glucagon (IRG) to ingestion of mixed meal with and without added fiber (5 g guar and 5 g pectin) in 12 normal, healthy subjects and in 12 age-, sex-, and weight-matched non-insulin-dependent, maturity-onset diabetic subjects (NIDDM). |
| 535 | 6257457 | Fiber markedly enhanced glucose tolerance in the normal subjects without a change in insulin or GIP but with a significant reduction in glucagon responses. |
| 536 | 6257457 | Fiber also markedly improved glucose tolerance in the NIDDMs without changing insulin or GIP but with a significant reduction in the glucagon responses. |
| 537 | 6257457 | In NIDDMs without AN, glucose tolerance was improved by fiber without a change in insulin, IRG, or GIP. |
| 538 | 6257457 | In diabetic subjects with AN, glucose tolerance was not improved, although glucagon levels were lowered and insulin and GIP responses were unchanged. |
| 539 | 6257457 | We investigated the effects of fiber on responses of blood glucose, serum insulin, gastric inhibitory polypeptide (GIP), and immunoreactive pancreatic glucagon (IRG) to ingestion of mixed meal with and without added fiber (5 g guar and 5 g pectin) in 12 normal, healthy subjects and in 12 age-, sex-, and weight-matched non-insulin-dependent, maturity-onset diabetic subjects (NIDDM). |
| 540 | 6257457 | Fiber markedly enhanced glucose tolerance in the normal subjects without a change in insulin or GIP but with a significant reduction in glucagon responses. |
| 541 | 6257457 | Fiber also markedly improved glucose tolerance in the NIDDMs without changing insulin or GIP but with a significant reduction in the glucagon responses. |
| 542 | 6257457 | In NIDDMs without AN, glucose tolerance was improved by fiber without a change in insulin, IRG, or GIP. |
| 543 | 6257457 | In diabetic subjects with AN, glucose tolerance was not improved, although glucagon levels were lowered and insulin and GIP responses were unchanged. |
| 544 | 6259009 | Mean basal plasma glucose concentrations were similar after both fibre diets; however, both mean basal plasma insulin and gastric inhibitory polypeptide (GIP) were significantly lower after the high fibre diet. |
| 545 | 6259009 | After the high fibre test meal, significantly lower mean plasma glucose, insulin and GIP concentrations were measured. |
| 546 | 6259009 | Mean basal plasma glucose concentrations were similar after both fibre diets; however, both mean basal plasma insulin and gastric inhibitory polypeptide (GIP) were significantly lower after the high fibre diet. |
| 547 | 6259009 | After the high fibre test meal, significantly lower mean plasma glucose, insulin and GIP concentrations were measured. |
| 548 | 6280423 | The impaired absorption of the food-stuffs and the defective feed-back regulation of GIP secretion by insulin are the major causes of these variations. |
| 549 | 6328896 | Effect of dietary fibre on blood glucose, plasma immunoreactive insulin, C-peptide and GIP responses in non insulin dependent (type 2) diabetics and controls. |
| 550 | 6337892 | Serial insulin (IRI) and gastric inhibitory polypeptide (GIP) levels were measured as well as the level of glucose infusion necessary to maintain the stable hyperglycemic level. |
| 551 | 6341393 | Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics. |
| 552 | 6341393 | The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. |
| 553 | 6341393 | As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia. |
| 554 | 6341393 | Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics. |
| 555 | 6341393 | The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. |
| 556 | 6341393 | As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia. |
| 557 | 6341393 | Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics. |
| 558 | 6341393 | The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. |
| 559 | 6341393 | As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia. |
| 560 | 6344327 | Diabetics showed significantly higher levels of plasma GIP in association with delayed and diminished peak increases in plasma insulin levels. |
| 561 | 6344327 | This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics. |
| 562 | 6344327 | Diabetics showed significantly higher levels of plasma GIP in association with delayed and diminished peak increases in plasma insulin levels. |
| 563 | 6344327 | This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics. |
| 564 | 6352886 | To study the role of enteroinsular hormones in fetal macrosomia and neonatal hypoglycemia in infants of diabetic mothers, we measured plasma concentrations of free and total immunoreactive insulin, C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide at birth in 35 IDMs and 35 infants of normal mothers. |
| 565 | 6356316 | The post-prandial responses of insulin and GIP can be improved by substituting an elemental meal, suggesting that malabsorption and local intestinal factors could be causative in the deficient responses. |
| 566 | 6364671 | Relation of immunoreactive gastric inhibitory polypeptide to changes in glycaemic control and B cell function in type 1 (insulin-dependent) diabetes mellitus. |
| 567 | 6364671 | The effect of strict glycaemic control on plasma immunoreactive gastric inhibitory polypeptide (IR-GIP) concentrations and pancreatic B cell function as estimated by plasma C-peptide was evaluated in 14 Type 1 (insulin-dependent) diabetics. |
| 568 | 6364671 | Relation of immunoreactive gastric inhibitory polypeptide to changes in glycaemic control and B cell function in type 1 (insulin-dependent) diabetes mellitus. |
| 569 | 6364671 | The effect of strict glycaemic control on plasma immunoreactive gastric inhibitory polypeptide (IR-GIP) concentrations and pancreatic B cell function as estimated by plasma C-peptide was evaluated in 14 Type 1 (insulin-dependent) diabetics. |
| 570 | 6365657 | The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. |
| 571 | 6365944 | Augmented gastric inhibitory polypeptide and insulin responses to a meal after an increase in carbohydrate (sucrose) intake. |
| 572 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 573 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 574 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 575 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 576 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 577 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 578 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 579 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 580 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 581 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 582 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 583 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 584 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 585 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 586 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 587 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 588 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 589 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 590 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 591 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 592 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 593 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 594 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 595 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 596 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 597 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 598 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 599 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 600 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 601 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 602 | 6368294 | Glucose-dependent insulinotropic polypeptide augmentation of insulin. |
| 603 | 6368294 | Glucose-dependent insulinotropic polypeptide (GIP) is said to be a major physiologic factor in the augmentation of the insulin response to oral glucose. |
| 604 | 6368294 | Whether GIP promotes insulin release at physiologic concentrations of glucose or GIP, however, is questionable. |
| 605 | 6368294 | No significant enhancement of glucose-stimulated insulin secretion was seen when GIP was infused with 10 or 20 g i.v. glucose; however, with 40 g a doubling of the insulin response occurred. |
| 606 | 6368294 | The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). |
| 607 | 6368294 | The concentration of GIP and glucose required to produce significant potentiation of the insulin response appears to be in the pharmacologic, rather than physiologic, range. |
| 608 | 6369071 | The effect of normal and gestational-diabetic pregnancy on the gastroenteropancreatic (GEP) hormone response to lipid ingestion was studied in 17 women, 8 normal and 9 with gestational diabetes, by determination of the plasma concentrations of gastric inhibitory polypeptide (GIP), gut glucagon-like immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) following the ingestion of 67 g of triglyceride in late pregnancy and postpartum. |
| 609 | 6373459 | Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. |
| 610 | 6373459 | Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. |
| 611 | 6373459 | GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. |
| 612 | 6373459 | At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. |
| 613 | 6373459 | GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals. |
| 614 | 6373459 | Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. |
| 615 | 6373459 | Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. |
| 616 | 6373459 | GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. |
| 617 | 6373459 | At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. |
| 618 | 6373459 | GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals. |
| 619 | 6373459 | Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. |
| 620 | 6373459 | Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. |
| 621 | 6373459 | GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. |
| 622 | 6373459 | At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. |
| 623 | 6373459 | GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals. |
| 624 | 6373459 | Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. |
| 625 | 6373459 | Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. |
| 626 | 6373459 | GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. |
| 627 | 6373459 | At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. |
| 628 | 6373459 | GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals. |
| 629 | 6373459 | Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. |
| 630 | 6373459 | Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. |
| 631 | 6373459 | GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. |
| 632 | 6373459 | At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. |
| 633 | 6373459 | GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals. |
| 634 | 6373462 | Preceding hyperinsulinemia prevents demonstration of insulin effect on fat-induced gastric inhibitory polypeptide (GIP). |
| 635 | 6373462 | The effect of insulin on fat-induced gastric inhibitory polypeptide (GIP) release has been studied in seven healthy volunteers during euglycemic blood glucose clamping. |
| 636 | 6373462 | Preceding hyperinsulinemia prevents demonstration of insulin effect on fat-induced gastric inhibitory polypeptide (GIP). |
| 637 | 6373462 | The effect of insulin on fat-induced gastric inhibitory polypeptide (GIP) release has been studied in seven healthy volunteers during euglycemic blood glucose clamping. |
| 638 | 6373812 | Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. |
| 639 | 6373812 | In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. |
| 640 | 6373812 | Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). |
| 641 | 6373812 | In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. |
| 642 | 6373812 | In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes. |
| 643 | 6373812 | Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. |
| 644 | 6373812 | In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. |
| 645 | 6373812 | Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). |
| 646 | 6373812 | In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. |
| 647 | 6373812 | In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes. |
| 648 | 6373812 | Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. |
| 649 | 6373812 | In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. |
| 650 | 6373812 | Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). |
| 651 | 6373812 | In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. |
| 652 | 6373812 | In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes. |
| 653 | 6373812 | Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. |
| 654 | 6373812 | In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. |
| 655 | 6373812 | Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). |
| 656 | 6373812 | In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. |
| 657 | 6373812 | In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes. |
| 658 | 6373812 | Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. |
| 659 | 6373812 | In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. |
| 660 | 6373812 | Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). |
| 661 | 6373812 | In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. |
| 662 | 6373812 | In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes. |
| 663 | 6383904 | The role of GIP in aging, obesity, and non-insulin-dependent diabetes mellitus. |
| 664 | 6383904 | The effect of aging, obesity, and non-insulin-dependent diabetes mellitus on glucose-stimulated gastric inhibitory polypeptide (GIP) levels was studied in 55 male subjects, ranging in age from 19 to 84 yr, and in obesity, expressed as body mass index, from 21 to 34. |
| 665 | 6383904 | The role of GIP in aging, obesity, and non-insulin-dependent diabetes mellitus. |
| 666 | 6383904 | The effect of aging, obesity, and non-insulin-dependent diabetes mellitus on glucose-stimulated gastric inhibitory polypeptide (GIP) levels was studied in 55 male subjects, ranging in age from 19 to 84 yr, and in obesity, expressed as body mass index, from 21 to 34. |
| 667 | 6386555 | Lack of negative feed-back regulation of insulin on the responses of gastric inhibitory polypeptide, insulin, glucagon and pancreatic polypeptide to a meal in insulin treated diabetics. |
| 668 | 6386555 | The effect of insulin on the secretion of immunoreactive gastric inhibitory polypeptide, insulin (as measured by C-peptide), glucagon and pancreatic polypeptide during and after a test meal was examined in seven diabetic patients treated with high insulin doses (mean 1.12 +/- 0.12 IU/kg X 24 h) before and after a reduction of the insulin dose (to 0.62 +/- 0.04 IU/kg X 24 h, p less than 0.02). |
| 669 | 6386555 | While plasma insulin concentrations were significantly higher on the higher dose, no significant differences were found in the responses of immunoreactive gastric inhibitory polypeptide, C-peptide, glucagon and pancreatic polypeptide to the two meals. |
| 670 | 6386555 | Lack of negative feed-back regulation of insulin on the responses of gastric inhibitory polypeptide, insulin, glucagon and pancreatic polypeptide to a meal in insulin treated diabetics. |
| 671 | 6386555 | The effect of insulin on the secretion of immunoreactive gastric inhibitory polypeptide, insulin (as measured by C-peptide), glucagon and pancreatic polypeptide during and after a test meal was examined in seven diabetic patients treated with high insulin doses (mean 1.12 +/- 0.12 IU/kg X 24 h) before and after a reduction of the insulin dose (to 0.62 +/- 0.04 IU/kg X 24 h, p less than 0.02). |
| 672 | 6386555 | While plasma insulin concentrations were significantly higher on the higher dose, no significant differences were found in the responses of immunoreactive gastric inhibitory polypeptide, C-peptide, glucagon and pancreatic polypeptide to the two meals. |
| 673 | 6386555 | Lack of negative feed-back regulation of insulin on the responses of gastric inhibitory polypeptide, insulin, glucagon and pancreatic polypeptide to a meal in insulin treated diabetics. |
| 674 | 6386555 | The effect of insulin on the secretion of immunoreactive gastric inhibitory polypeptide, insulin (as measured by C-peptide), glucagon and pancreatic polypeptide during and after a test meal was examined in seven diabetic patients treated with high insulin doses (mean 1.12 +/- 0.12 IU/kg X 24 h) before and after a reduction of the insulin dose (to 0.62 +/- 0.04 IU/kg X 24 h, p less than 0.02). |
| 675 | 6386555 | While plasma insulin concentrations were significantly higher on the higher dose, no significant differences were found in the responses of immunoreactive gastric inhibitory polypeptide, C-peptide, glucagon and pancreatic polypeptide to the two meals. |
| 676 | 6388305 | Effect of source of dietary carbohydrate on plasma glucose, insulin, and gastric inhibitory polypeptide responses to test meals in subjects with noninsulin-dependent diabetes mellitus. |
| 677 | 6388305 | In order to test the clinical utility of these observations, we evaluated plasma glucose, insulin, and gastric inhibitory polypeptide responses to four major sources of carbohydrate (potato, rice, spaghetti, lentil) as part of a conventional mixed meal in patients with noninsulin-dependent diabetes mellitus. |
| 678 | 6388305 | Effect of source of dietary carbohydrate on plasma glucose, insulin, and gastric inhibitory polypeptide responses to test meals in subjects with noninsulin-dependent diabetes mellitus. |
| 679 | 6388305 | In order to test the clinical utility of these observations, we evaluated plasma glucose, insulin, and gastric inhibitory polypeptide responses to four major sources of carbohydrate (potato, rice, spaghetti, lentil) as part of a conventional mixed meal in patients with noninsulin-dependent diabetes mellitus. |
| 680 | 6400703 | In this study the effect on blood glucose, serum insulin, C-peptide, and plasma gastric inhibitory polypeptide (GIP) of giving 75 g glucose in 300 ml over 1 and 10 min (G1 and G10) was investigated in six subjects. |
| 681 | 6753106 | Compared with the controls, the methyl-prednisolone-treated rats had increased fasting levels of serum insulin, blood glucose, and plasma GIP; the alloxan-treated rats had decreased fasting levels of insulin and increased levels of fasting blood glucose and plasma GIP. |
| 682 | 6759077 | The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. |
| 683 | 6759077 | To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). |
| 684 | 6759077 | Serum insulin, glucose, and GIP were measured. |
| 685 | 6759077 | These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. |
| 686 | 6759077 | The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. |
| 687 | 6759077 | The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. |
| 688 | 6759077 | To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). |
| 689 | 6759077 | Serum insulin, glucose, and GIP were measured. |
| 690 | 6759077 | These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. |
| 691 | 6759077 | The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. |
| 692 | 6759077 | The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. |
| 693 | 6759077 | To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). |
| 694 | 6759077 | Serum insulin, glucose, and GIP were measured. |
| 695 | 6759077 | These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. |
| 696 | 6759077 | The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. |
| 697 | 6759077 | The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. |
| 698 | 6759077 | To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). |
| 699 | 6759077 | Serum insulin, glucose, and GIP were measured. |
| 700 | 6759077 | These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. |
| 701 | 6759077 | The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. |
| 702 | 6759077 | The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. |
| 703 | 6759077 | To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). |
| 704 | 6759077 | Serum insulin, glucose, and GIP were measured. |
| 705 | 6759077 | These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. |
| 706 | 6759077 | The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. |
| 707 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 708 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 709 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 710 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 711 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 712 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 713 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 714 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 715 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 716 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 717 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 718 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 719 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 720 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 721 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 722 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 723 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 724 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 725 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 726 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 727 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 728 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 729 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 730 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 731 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 732 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 733 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 734 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 735 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 736 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 737 | 6986299 | Inhibition of gastric inhibitory polypeptide (GIP) release by insulin and glucose in juvenile diabetes. |
| 738 | 6986299 | The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. |
| 739 | 6986299 | Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. |
| 740 | 6986299 | The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. |
| 741 | 6986299 | It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. |
| 742 | 6986299 | This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release. |
| 743 | 6995476 | Glucose-dependent insulin-releasing peptide or gastric inhibitory polypeptide (GIP) is released into the circulation after ingestion of a mixed meal and is thought to enhance glucose-induced insulin release. |
| 744 | 6995476 | Overnight insulin infusion normalized basal glucose levels in the MODs and induced a slight but insignificant rise in plasma GIP levels in MODs to 362 +/- 40.9 pg/ml; overnight gastric aspiration caused a further slight rise in basal GIP concentration to 392 +/- 56.6 pg/ml. |
| 745 | 6995476 | Glucose-dependent insulin-releasing peptide or gastric inhibitory polypeptide (GIP) is released into the circulation after ingestion of a mixed meal and is thought to enhance glucose-induced insulin release. |
| 746 | 6995476 | Overnight insulin infusion normalized basal glucose levels in the MODs and induced a slight but insignificant rise in plasma GIP levels in MODs to 362 +/- 40.9 pg/ml; overnight gastric aspiration caused a further slight rise in basal GIP concentration to 392 +/- 56.6 pg/ml. |
| 747 | 7013122 | Major factors may include decreased absorption of carbohydrates and amino acids, decreased oral caloric intake, increased insulin sensitivity and decreased output of gastric inhibitory polypeptide as well as the eventual weight loss. |
| 748 | 7014314 | The responses of gastric inhibitory polypeptides (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, and pancreatic glucagon to a 50-g oral glucose load were studied in late pregnancy and postpartum in 11 normal women, 10 normal weight gestational diabetics, and 10 overweight gestational diabetics. |
| 749 | 7014585 | The adult-onset diabetic group was also studied for immunoreactive GIP (IR-GIP), insulin, and glucose with a test meal before and after tolazamide therapy. |
| 750 | 7017571 | Gastric inhibitory polypeptide (GIP), a hormone located primarily in the duodenum, is the main hormonal stimulus to insulin release from the gastrointestinal tract. |
| 751 | 7017571 | The demonstration of hypersecretion of GIP in nondiabetic insulinopenic individuals adds further support to the hypothesis that insulin exerts feedback control on GIP secretion. |
| 752 | 7017571 | Gastric inhibitory polypeptide (GIP), a hormone located primarily in the duodenum, is the main hormonal stimulus to insulin release from the gastrointestinal tract. |
| 753 | 7017571 | The demonstration of hypersecretion of GIP in nondiabetic insulinopenic individuals adds further support to the hypothesis that insulin exerts feedback control on GIP secretion. |
| 754 | 7021006 | Effect of exogenous insulin on fasting serum levels of gastric inhibitory polypeptide (GIP) in juvenile diabetes. |
| 755 | 7021006 | The effect of insulin on fasting levels of immunoreactive gastric inhibitory polypeptide (IR-GIP) has been examined in insulin-dependent, juvenile-type diabetics who were well-controlled with two doses of an intermediate insulin. |
| 756 | 7021006 | It is suggested that fasting serum GIP levels increase in case of insulin deficiency because basal GIP secretion is suppressed by normal insulin levels. |
| 757 | 7021006 | Effect of exogenous insulin on fasting serum levels of gastric inhibitory polypeptide (GIP) in juvenile diabetes. |
| 758 | 7021006 | The effect of insulin on fasting levels of immunoreactive gastric inhibitory polypeptide (IR-GIP) has been examined in insulin-dependent, juvenile-type diabetics who were well-controlled with two doses of an intermediate insulin. |
| 759 | 7021006 | It is suggested that fasting serum GIP levels increase in case of insulin deficiency because basal GIP secretion is suppressed by normal insulin levels. |
| 760 | 7021006 | Effect of exogenous insulin on fasting serum levels of gastric inhibitory polypeptide (GIP) in juvenile diabetes. |
| 761 | 7021006 | The effect of insulin on fasting levels of immunoreactive gastric inhibitory polypeptide (IR-GIP) has been examined in insulin-dependent, juvenile-type diabetics who were well-controlled with two doses of an intermediate insulin. |
| 762 | 7021006 | It is suggested that fasting serum GIP levels increase in case of insulin deficiency because basal GIP secretion is suppressed by normal insulin levels. |
| 763 | 7045154 | In spite of similar IRGIP responses, the obese IGT patients did release more insulin than the obese control subjects, suggesting that incretin factors other than GIP may be operative in this condition. |
| 764 | 7045315 | In contrast, plasma C-peptide, hPP, and GIP concentrations did not change. |
| 765 | 7045315 | Following the mixed meal plasma glucose, hPP, and GIP concentrations increased similarly in the two groups of children, but no change was observed in either plasma glucagon or C-peptide concentrations in either group. |
| 766 | 7045315 | These data demonstrate that EOD and LOD are associated with insulin insufficiency alone and that abnormalities in secretion of other pancreatic islet hormone or GIP cannot be implicated in the high incidence of severe hypoglycemia observed in children with EOD. |
| 767 | 7045315 | In contrast, plasma C-peptide, hPP, and GIP concentrations did not change. |
| 768 | 7045315 | Following the mixed meal plasma glucose, hPP, and GIP concentrations increased similarly in the two groups of children, but no change was observed in either plasma glucagon or C-peptide concentrations in either group. |
| 769 | 7045315 | These data demonstrate that EOD and LOD are associated with insulin insufficiency alone and that abnormalities in secretion of other pancreatic islet hormone or GIP cannot be implicated in the high incidence of severe hypoglycemia observed in children with EOD. |
| 770 | 7045315 | In contrast, plasma C-peptide, hPP, and GIP concentrations did not change. |
| 771 | 7045315 | Following the mixed meal plasma glucose, hPP, and GIP concentrations increased similarly in the two groups of children, but no change was observed in either plasma glucagon or C-peptide concentrations in either group. |
| 772 | 7045315 | These data demonstrate that EOD and LOD are associated with insulin insufficiency alone and that abnormalities in secretion of other pancreatic islet hormone or GIP cannot be implicated in the high incidence of severe hypoglycemia observed in children with EOD. |
| 773 | 7046411 | Effect of physical form of carbohydrate on the postprandial glucose, insulin, and gastric inhibitory polypeptide responses in type 2 diabetes. |
| 774 | 7046411 | In the present study we measured the postprandial glucose, insulin, and gastric inhibitory polypeptide responses to 75 g carbohydrate administered either as glucose, unpolished (brown) rice, or ground brown rice to six recently diagnosed type 2 diabetics and six healthy subjects. |
| 775 | 7046411 | Brown rice elicited significantly lower postprandial glucose, insulin, and gastric inhibitory polypeptide responses than either ground brown rice or glucose in both groups. |
| 776 | 7046411 | Effect of physical form of carbohydrate on the postprandial glucose, insulin, and gastric inhibitory polypeptide responses in type 2 diabetes. |
| 777 | 7046411 | In the present study we measured the postprandial glucose, insulin, and gastric inhibitory polypeptide responses to 75 g carbohydrate administered either as glucose, unpolished (brown) rice, or ground brown rice to six recently diagnosed type 2 diabetics and six healthy subjects. |
| 778 | 7046411 | Brown rice elicited significantly lower postprandial glucose, insulin, and gastric inhibitory polypeptide responses than either ground brown rice or glucose in both groups. |
| 779 | 7046411 | Effect of physical form of carbohydrate on the postprandial glucose, insulin, and gastric inhibitory polypeptide responses in type 2 diabetes. |
| 780 | 7046411 | In the present study we measured the postprandial glucose, insulin, and gastric inhibitory polypeptide responses to 75 g carbohydrate administered either as glucose, unpolished (brown) rice, or ground brown rice to six recently diagnosed type 2 diabetics and six healthy subjects. |
| 781 | 7046411 | Brown rice elicited significantly lower postprandial glucose, insulin, and gastric inhibitory polypeptide responses than either ground brown rice or glucose in both groups. |
| 782 | 7118058 | In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. |
| 783 | 7118058 | No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. |
| 784 | 7118058 | In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. |
| 785 | 7118058 | No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. |
| 786 | 7556958 | Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. |
| 787 | 7556958 | Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. |
| 788 | 7556958 | The receptor protein sequence was 81% identical to that of the rat GIP receptor. |
| 789 | 7556958 | GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. |
| 790 | 7556958 | These data will help study the physiology and pathophysiology of the human GIP receptor. |
| 791 | 7556958 | Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. |
| 792 | 7556958 | Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. |
| 793 | 7556958 | The receptor protein sequence was 81% identical to that of the rat GIP receptor. |
| 794 | 7556958 | GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. |
| 795 | 7556958 | These data will help study the physiology and pathophysiology of the human GIP receptor. |
| 796 | 7556958 | Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. |
| 797 | 7556958 | Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. |
| 798 | 7556958 | The receptor protein sequence was 81% identical to that of the rat GIP receptor. |
| 799 | 7556958 | GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. |
| 800 | 7556958 | These data will help study the physiology and pathophysiology of the human GIP receptor. |
| 801 | 7556958 | Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. |
| 802 | 7556958 | Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. |
| 803 | 7556958 | The receptor protein sequence was 81% identical to that of the rat GIP receptor. |
| 804 | 7556958 | GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. |
| 805 | 7556958 | These data will help study the physiology and pathophysiology of the human GIP receptor. |
| 806 | 7556958 | Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. |
| 807 | 7556958 | Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. |
| 808 | 7556958 | The receptor protein sequence was 81% identical to that of the rat GIP receptor. |
| 809 | 7556958 | GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. |
| 810 | 7556958 | These data will help study the physiology and pathophysiology of the human GIP receptor. |
| 811 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 812 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 813 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 814 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 815 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 816 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 817 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 818 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 819 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 820 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 821 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 822 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 823 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 824 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 825 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 826 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 827 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 828 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 829 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 830 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 831 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 832 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 833 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 834 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 835 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 836 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 837 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 838 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 839 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 840 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 841 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 842 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 843 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 844 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 845 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 846 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 847 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 848 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 849 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 850 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 851 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 852 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 853 | 7589426 | Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. |
| 854 | 7589426 | Glucose-dependent insulinotropic polypeptide (GIP) plays an important role in the regulation of postprandial insulin secretion and proinsulin gene expression of pancreatic beta-cells. |
| 855 | 7589426 | This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. |
| 856 | 7589426 | Homology to the GIP receptor from rat or hamster was 79% and 81%, respectively. |
| 857 | 7589426 | At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. |
| 858 | 7589426 | Northern analysis revealed one transcript of human GIP receptor mRNA with an apparent size of 5.5 kb. |
| 859 | 7589426 | The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. |
| 860 | 7664683 | In the present study we cloned a rat islet GIP receptor complementary DNA (GIP-R1) to answer several important questions regarding the ligand-binding and intracellular signaling properties of the GP receptor. |
| 861 | 7664683 | Surprisingly, exendin-(9-39) [Ex-(9-39)], a GLP-1 receptor antagonist, and Ex-4-(1-39), a GLP-1 receptor agonist, demonstrated some affinity for the GIP receptor, with 39% and 21% displacement of [125I]spGIP, respectively, at 1 microM. |
| 862 | 7664683 | In the present study we cloned a rat islet GIP receptor complementary DNA (GIP-R1) to answer several important questions regarding the ligand-binding and intracellular signaling properties of the GP receptor. |
| 863 | 7664683 | Surprisingly, exendin-(9-39) [Ex-(9-39)], a GLP-1 receptor antagonist, and Ex-4-(1-39), a GLP-1 receptor agonist, demonstrated some affinity for the GIP receptor, with 39% and 21% displacement of [125I]spGIP, respectively, at 1 microM. |
| 864 | 7755955 | Plasma glucose, serum insulin (IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. |
| 865 | 7813808 | Anesthetized rats were challenged by an intraduodenal glucose infusion to evaluate maximally occurring GLP-1 and gastric inhibitory polypeptide (GIP) plasma levels. |
| 866 | 7813808 | Exendin (9-39) amide abolished the insulin-stimulatory effect of 60 pmol of GLP-1 or of the GLP-1 agonist exendin-4 (0.5 nmol) injected as bolus, respectively. |
| 867 | 7813808 | In contrast, the GLP-1 antagonist left the insulin response after an intravenous glucose or glucose plus GIP (60 pmol) load unaltered. |
| 868 | 7813808 | Anesthetized rats were challenged by an intraduodenal glucose infusion to evaluate maximally occurring GLP-1 and gastric inhibitory polypeptide (GIP) plasma levels. |
| 869 | 7813808 | Exendin (9-39) amide abolished the insulin-stimulatory effect of 60 pmol of GLP-1 or of the GLP-1 agonist exendin-4 (0.5 nmol) injected as bolus, respectively. |
| 870 | 7813808 | In contrast, the GLP-1 antagonist left the insulin response after an intravenous glucose or glucose plus GIP (60 pmol) load unaltered. |
| 871 | 7895557 | Serum insulin, plasma glucose, and GIP levels were measured in fasting and postprandial blood samples collected at 15-min intervals for 2 hr. |
| 872 | 7988423 | Secretin or cholecystokinin did not stimulate the secretion of GLP-1. |
| 873 | 7988423 | Bombesin (10(-9)-10(-7) M) provoked a dose-dependent release of GLP-1, consisting of an early peak, followed by a sustained response. |
| 874 | 7988423 | Tetrodotoxin did not modify the bethanechol-, isoproterenol-, calcitonin gene-related peptide-, or bombesin-induced GLP-1 release. |
| 875 | 7988423 | In conclusion, the present study conducted with the isolated vascularly perfused rat colon shows that there are interactions between the two most potent incretins, GIP and GLP-1, probably through an enteroendocrine pathway. |
| 876 | 8001623 | To facilitate this already established data on the effects of induced malabsorption on gut hormones such as gastric inhibitory polypeptide (GIP) in connection with preliminary findings which deal with the new incretin hormone glucagon-like peptide 1 (7-36) amide (GLP-1) are discussed. |
| 877 | 8001623 | The slowing of nutrient (i.e. glucose) absorption by therapeutic means (for example, acarbose) could supplement a new approach in the treatment of type 2 diabetics which would utilize the well-preserved insulinotropic activity of GLP-1 in these patients, its glucagon-lowering effect, and its possible inhibition of gastric emptying rates, the latter helping to reduce the requirement for rapid insulin secretory responses as is intended while using alpha-glucosidase inhibitor treatment. |
| 878 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 879 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 880 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 881 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 882 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 883 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 884 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 885 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 886 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 887 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 888 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 889 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 890 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 891 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 892 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 893 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 894 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 895 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 896 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 897 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 898 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 899 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 900 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 901 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 902 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 903 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 904 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 905 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 906 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 907 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 908 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 909 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 910 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 911 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 912 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 913 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 914 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 915 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 916 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 917 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 918 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 919 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 920 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 921 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 922 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 923 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 924 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 925 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 926 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 927 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 928 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 929 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 930 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 931 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 932 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 933 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 934 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 935 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 936 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 937 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 938 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 939 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 940 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 941 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 942 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 943 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 944 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 945 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 946 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 947 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 948 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 949 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 950 | 8036284 | The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-37) in normal and diabetic subjects. |
| 951 | 8036284 | The leading gut hormone candidates are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP-1). |
| 952 | 8036284 | To determine the relative insulinotropic activity of these peptides, we infused GLP-1(7-37) and GIP into normal subjects and patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 953 | 8036284 | In normal subjects during euglycemia, GLP-1(7-37) stimulated insulin release, whereas GIP did not. |
| 954 | 8036284 | During the second hour, either GIP, GLP-1(7-37), or both were infused in normal healthy volunteers and in patients with NIDDM. |
| 955 | 8036284 | GIP at a dose of 1, 2 or 4 pmol/kg/min augmented the 90-120 min insulin response by 69, 841 and 920 pmol/l, while GLP-1(7-37), at a dose of 1.5 pmol/kg/min augmented the insulin response by 2106 pmol/l. |
| 956 | 8036284 | In the diabetic subjects, GIP had no effect, while GLP-1(7-37) augmented the insulin response by 929 pmol/l. |
| 957 | 8036284 | We conclude that in normal healthy subjects, GLP-1(7-37), on a molar basis, is several times more potent than GIP at equivalent glycemic conditions. |
| 958 | 8036284 | In NIDDM, GIP had no insulinotropic effect, while GLP-1(7-37) had a marked effect. |
| 959 | 8036744 | Stimulation of insulin secretion and insulin gene expression by gastric inhibitory polypeptide. |
| 960 | 8077330 | To study whether the increased glucose levels in the amniotic fluid during diabetic pregnancies induce an early maturation of the hormonal enteroinsular axis, we measured blood glucose levels and plasma concentrations of C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide (GIP) in cord blood from 18 newborn infants of insulin-treated diabetic mothers (IDM) and 18 infants of nondiabetic mothers. |
| 961 | 8125072 | GLP-1 hormone is released into the circulation from intestinal L cells in response to meals and is the most potent incretin hormone known; GLP-1 and GIP appear to account for most, if not all, of the intestinal incretin effect in the augmentation of glucose-stimulated insulin secretion. |
| 962 | 8125072 | Analyses of the mechanisms of action of GLP-1 and of glucose on isolated cultured rat beta cells using patch-clamp techniques to record ion channel activities has led to the glucose competence concept in which the combined glucose-signaling and GLP-1/cAMP-signaling pathways are required to affect depolarization of beta cells and to thereby stimulate insulin secretion. |
| 963 | 8125072 | Because of the discoveries that GLP-1 stimulates both secretion and production of insulin, and that the actions of GLP-1 are entirely glucose-dependent, GLP-1 may provide unique advantages over the sulfonylurea drugs in the treatment of NIDDM. |
| 964 | 8329730 | The release of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) immunoreactivity and B cell secretory responses (IR insulin and C-peptide) to oral (50 g) and "isoglycaemic" intravenous glucose (identical glycaemic profile) were measured by radioimmunoassay. |
| 965 | 8329730 | In both groups GIP and GLP-1 increased after oral but not after intravenous glucose, and B cell secretory responses were significantly smaller (by 55.2 +/- 7.7% and 46.5 +/- 12.5%, respectively) with "isoglycaemic" intravenous glucose infusions. |
| 966 | 8329730 | The release of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) immunoreactivity and B cell secretory responses (IR insulin and C-peptide) to oral (50 g) and "isoglycaemic" intravenous glucose (identical glycaemic profile) were measured by radioimmunoassay. |
| 967 | 8329730 | In both groups GIP and GLP-1 increased after oral but not after intravenous glucose, and B cell secretory responses were significantly smaller (by 55.2 +/- 7.7% and 46.5 +/- 12.5%, respectively) with "isoglycaemic" intravenous glucose infusions. |
| 968 | 8380389 | Using the glucose-responsive hamster beta-cell line (hamster insulin tumor cells), we examined the cellular mechanisms by which gastric inhibitory polypeptide (GIP) and glucagon-like peptide I(7-37) (GLP-I) potentiate glucose-stimulated insulin secretion. |
| 969 | 8380389 | When added to glucose-stimulated cells, GIP and GLP-I increased cAMP levels and further increased insulin secretion. |
| 970 | 8380389 | Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. |
| 971 | 8380389 | This study establishes that GIP and GLP-I potentiate glucose-stimulated insulin secretion by increasing extracellular Ca2+ influx through voltage-dependent Ca2+ channels. |
| 972 | 8380389 | Using the glucose-responsive hamster beta-cell line (hamster insulin tumor cells), we examined the cellular mechanisms by which gastric inhibitory polypeptide (GIP) and glucagon-like peptide I(7-37) (GLP-I) potentiate glucose-stimulated insulin secretion. |
| 973 | 8380389 | When added to glucose-stimulated cells, GIP and GLP-I increased cAMP levels and further increased insulin secretion. |
| 974 | 8380389 | Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. |
| 975 | 8380389 | This study establishes that GIP and GLP-I potentiate glucose-stimulated insulin secretion by increasing extracellular Ca2+ influx through voltage-dependent Ca2+ channels. |
| 976 | 8380389 | Using the glucose-responsive hamster beta-cell line (hamster insulin tumor cells), we examined the cellular mechanisms by which gastric inhibitory polypeptide (GIP) and glucagon-like peptide I(7-37) (GLP-I) potentiate glucose-stimulated insulin secretion. |
| 977 | 8380389 | When added to glucose-stimulated cells, GIP and GLP-I increased cAMP levels and further increased insulin secretion. |
| 978 | 8380389 | Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. |
| 979 | 8380389 | This study establishes that GIP and GLP-I potentiate glucose-stimulated insulin secretion by increasing extracellular Ca2+ influx through voltage-dependent Ca2+ channels. |
| 980 | 8380389 | Using the glucose-responsive hamster beta-cell line (hamster insulin tumor cells), we examined the cellular mechanisms by which gastric inhibitory polypeptide (GIP) and glucagon-like peptide I(7-37) (GLP-I) potentiate glucose-stimulated insulin secretion. |
| 981 | 8380389 | When added to glucose-stimulated cells, GIP and GLP-I increased cAMP levels and further increased insulin secretion. |
| 982 | 8380389 | Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. |
| 983 | 8380389 | This study establishes that GIP and GLP-I potentiate glucose-stimulated insulin secretion by increasing extracellular Ca2+ influx through voltage-dependent Ca2+ channels. |
| 984 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 985 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 986 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 987 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 988 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 989 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 990 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 991 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 992 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 993 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 994 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 995 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 996 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 997 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 998 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 999 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 1000 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 1001 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 1002 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 1003 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 1004 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 1005 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 1006 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 1007 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 1008 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 1009 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 1010 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 1011 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 1012 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 1013 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 1014 | 8419907 | Dual effects of gastric inhibitory polypeptide on insulin secretion. |
| 1015 | 8419907 | The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. |
| 1016 | 8419907 | If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). |
| 1017 | 8419907 | If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. |
| 1018 | 8419907 | In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). |
| 1019 | 8419907 | These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. |
| 1020 | 8420760 | Blood samples were obtained at 15-min intervals for measurement of glucose, insulin, CCK-8, and gastric inhibitory polypeptide (GIP) concentrations. |
| 1021 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1022 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1023 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1024 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1025 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1026 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1027 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1028 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1029 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1030 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1031 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1032 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1033 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1034 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1035 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1036 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1037 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1038 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1039 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1040 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1041 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1042 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1043 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1044 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1045 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1046 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1047 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1048 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1049 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1050 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1051 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1052 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1053 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1054 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1055 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1056 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1057 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1058 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1059 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1060 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1061 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1062 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1063 | 8423228 | Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. |
| 1064 | 8423228 | The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. |
| 1065 | 8423228 | Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. |
| 1066 | 8423228 | Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. |
| 1067 | 8423228 | Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). |
| 1068 | 8423228 | Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. |
| 1069 | 8423228 | In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. |
| 1070 | 8435987 | Hypersecretion of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide in obese patients. |
| 1071 | 8435987 | To investigate the involvement of the potent insulinotropic hormones gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1) in the postprandial hyperinsulinaemia of obesity, we examined the changes in plasma levels of GIP and tGLP-1 by an oral glucose tolerance test (OGTT) in nine normal subjects (controls), nine obese subjects without glucose intolerance (Group A), and six obese mild diabetic patients (Group B). |
| 1072 | 8435987 | These results suggest that the combined augmentation of plasma GIP and tGLP-1 responses were involved in the delayed and considerable increases in plasma insulin after glucose ingestion in obese diabetic patients. |
| 1073 | 8435987 | Hypersecretion of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide in obese patients. |
| 1074 | 8435987 | To investigate the involvement of the potent insulinotropic hormones gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1) in the postprandial hyperinsulinaemia of obesity, we examined the changes in plasma levels of GIP and tGLP-1 by an oral glucose tolerance test (OGTT) in nine normal subjects (controls), nine obese subjects without glucose intolerance (Group A), and six obese mild diabetic patients (Group B). |
| 1075 | 8435987 | These results suggest that the combined augmentation of plasma GIP and tGLP-1 responses were involved in the delayed and considerable increases in plasma insulin after glucose ingestion in obese diabetic patients. |
| 1076 | 8435987 | Hypersecretion of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide in obese patients. |
| 1077 | 8435987 | To investigate the involvement of the potent insulinotropic hormones gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1) in the postprandial hyperinsulinaemia of obesity, we examined the changes in plasma levels of GIP and tGLP-1 by an oral glucose tolerance test (OGTT) in nine normal subjects (controls), nine obese subjects without glucose intolerance (Group A), and six obese mild diabetic patients (Group B). |
| 1078 | 8435987 | These results suggest that the combined augmentation of plasma GIP and tGLP-1 responses were involved in the delayed and considerable increases in plasma insulin after glucose ingestion in obese diabetic patients. |
| 1079 | 8480468 | Fasting levels of pancreatic polypeptide, pancreatic glucagon, total glucagon, glucagon-like peptide-1 7-36 amide, and gastric inhibitory polypeptide were normal in all patient groups. |
| 1080 | 8480468 | In conclusion, at cystic fibrosis (a) insulin secretion is impaired even when glucose tolerance and insulin sensitivity are within the normal range, (b) the glucagon test gives valid estimates of residual beta cell function, (c) pancreatic polypeptide response to oral glucose is absent, (d) glucagon suppressibility decreases with decreasing glucose tolerance, and (e) the enteroinsular axis is intact. |
| 1081 | 8536820 | Voglibose (AO-128) is an efficient alpha-glucosidase inhibitor and mobilizes the endogenous GLP-1 reserve. |
| 1082 | 8536820 | The alpha-glucosidase inhibitor voglibose (AO-128) was designed to prevent rapid postprandial blood glucose rises in non-insulin-dependent diabetics. |
| 1083 | 8536820 | Blood was drawn at regular intervals up to 180 min after a standardized breakfast to analyze the levels of glucose, insulin, C peptide, gastric inhibitory polypeptide, and glucagon-like peptide 1 (GLP-1). |
| 1084 | 8549871 | The present study shows expression at the RNA level in beta-cells of receptors for glucagon, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide I(7-36) amide (GLP-I), while RNA from islet alpha-cells hybridized only with GIP receptor cDNA. |
| 1085 | 8549871 | In conclusion, these data show that stimulation of glucagon, GLP-I, and GIP receptors in rat beta-cells causes cAMP production required for insulin release, while adenylate cyclase in alpha-cells is positively regulated by GIP. |
| 1086 | 8549871 | The present study shows expression at the RNA level in beta-cells of receptors for glucagon, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide I(7-36) amide (GLP-I), while RNA from islet alpha-cells hybridized only with GIP receptor cDNA. |
| 1087 | 8549871 | In conclusion, these data show that stimulation of glucagon, GLP-I, and GIP receptors in rat beta-cells causes cAMP production required for insulin release, while adenylate cyclase in alpha-cells is positively regulated by GIP. |
| 1088 | 8586147 | Glucagon-like peptide-1 and control of insulin secretion. |
| 1089 | 8586147 | The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). |
| 1090 | 8586147 | GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. |
| 1091 | 8586147 | GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. |
| 1092 | 8586147 | Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. |
| 1093 | 8586147 | Glucagon-like peptide-1 and control of insulin secretion. |
| 1094 | 8586147 | The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). |
| 1095 | 8586147 | GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. |
| 1096 | 8586147 | GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. |
| 1097 | 8586147 | Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. |
| 1098 | 8586147 | Glucagon-like peptide-1 and control of insulin secretion. |
| 1099 | 8586147 | The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). |
| 1100 | 8586147 | GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. |
| 1101 | 8586147 | GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. |
| 1102 | 8586147 | Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. |
| 1103 | 8586147 | Glucagon-like peptide-1 and control of insulin secretion. |
| 1104 | 8586147 | The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). |
| 1105 | 8586147 | GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. |
| 1106 | 8586147 | GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. |
| 1107 | 8586147 | Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. |
| 1108 | 8590785 | Response of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide to glucose ingestion in non-insulin dependent diabetes mellitus. |
| 1109 | 8590785 | Gastric inhibitory polypeptide (tGIP) and truncated glucagon like peptide-1 (GLP-1) are potent gastrointestinal insulinotropic factors (incretin), are most released after a meal or ingestion of glucose in man and animals. |
| 1110 | 8590785 | To investigate whether sulfonylurea (SU) affects the secretion of incretin, the modulation of plasma GIP and tGLP-1 levels following glucose ingestion in non-insulin-dependent diabetic type 2 patients with or without SU therapy was studied. |
| 1111 | 8590785 | Plasma GIP was measured by radioimmunoassay (RIA) with R65 antibody, and GLP-1 was measured by RIA with N-terminal-directed antiserum R1043 (GLP-1NT) and C-terminal-directed antiserum R2337 (GLP-1CT). |
| 1112 | 8590785 | Response of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide to glucose ingestion in non-insulin dependent diabetes mellitus. |
| 1113 | 8590785 | Gastric inhibitory polypeptide (tGIP) and truncated glucagon like peptide-1 (GLP-1) are potent gastrointestinal insulinotropic factors (incretin), are most released after a meal or ingestion of glucose in man and animals. |
| 1114 | 8590785 | To investigate whether sulfonylurea (SU) affects the secretion of incretin, the modulation of plasma GIP and tGLP-1 levels following glucose ingestion in non-insulin-dependent diabetic type 2 patients with or without SU therapy was studied. |
| 1115 | 8590785 | Plasma GIP was measured by radioimmunoassay (RIA) with R65 antibody, and GLP-1 was measured by RIA with N-terminal-directed antiserum R1043 (GLP-1NT) and C-terminal-directed antiserum R2337 (GLP-1CT). |
| 1116 | 8590785 | Response of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide to glucose ingestion in non-insulin dependent diabetes mellitus. |
| 1117 | 8590785 | Gastric inhibitory polypeptide (tGIP) and truncated glucagon like peptide-1 (GLP-1) are potent gastrointestinal insulinotropic factors (incretin), are most released after a meal or ingestion of glucose in man and animals. |
| 1118 | 8590785 | To investigate whether sulfonylurea (SU) affects the secretion of incretin, the modulation of plasma GIP and tGLP-1 levels following glucose ingestion in non-insulin-dependent diabetic type 2 patients with or without SU therapy was studied. |
| 1119 | 8590785 | Plasma GIP was measured by radioimmunoassay (RIA) with R65 antibody, and GLP-1 was measured by RIA with N-terminal-directed antiserum R1043 (GLP-1NT) and C-terminal-directed antiserum R2337 (GLP-1CT). |
| 1120 | 8590785 | Response of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide to glucose ingestion in non-insulin dependent diabetes mellitus. |
| 1121 | 8590785 | Gastric inhibitory polypeptide (tGIP) and truncated glucagon like peptide-1 (GLP-1) are potent gastrointestinal insulinotropic factors (incretin), are most released after a meal or ingestion of glucose in man and animals. |
| 1122 | 8590785 | To investigate whether sulfonylurea (SU) affects the secretion of incretin, the modulation of plasma GIP and tGLP-1 levels following glucose ingestion in non-insulin-dependent diabetic type 2 patients with or without SU therapy was studied. |
| 1123 | 8590785 | Plasma GIP was measured by radioimmunoassay (RIA) with R65 antibody, and GLP-1 was measured by RIA with N-terminal-directed antiserum R1043 (GLP-1NT) and C-terminal-directed antiserum R2337 (GLP-1CT). |
| 1124 | 8832801 | Nutrient-induced secretion and metabolic effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. |
| 1125 | 8897861 | Decreased glucose-induced cAMP and insulin release in islets of diabetic rats: reversal by IBMX, glucagon, GIP. |
| 1126 | 8897861 | Somatostatin, prostaglandin E2, UK-14304, or galanin inhibited cAMP accumulation and insulin release to the same extent in both types of islets. |
| 1127 | 8897861 | The addition of IBMX, glucagon, or gastric inhibitory polypeptide (GIP) to perifused islets of diabetic rats amplified their insulin response to glucose, and a clear biphasic pattern of the release was regained. |
| 1128 | 8897861 | Decreased glucose-induced cAMP and insulin release in islets of diabetic rats: reversal by IBMX, glucagon, GIP. |
| 1129 | 8897861 | Somatostatin, prostaglandin E2, UK-14304, or galanin inhibited cAMP accumulation and insulin release to the same extent in both types of islets. |
| 1130 | 8897861 | The addition of IBMX, glucagon, or gastric inhibitory polypeptide (GIP) to perifused islets of diabetic rats amplified their insulin response to glucose, and a clear biphasic pattern of the release was regained. |
| 1131 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1132 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1133 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1134 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1135 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1136 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1137 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1138 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1139 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1140 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1141 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1142 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1143 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1144 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1145 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1146 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1147 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1148 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1149 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1150 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1151 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1152 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1153 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1154 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1155 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1156 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1157 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1158 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1159 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1160 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1161 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1162 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1163 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1164 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1165 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1166 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1167 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1168 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1169 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1170 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1171 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1172 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1173 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1174 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1175 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1176 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1177 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1178 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1179 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1180 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1181 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1182 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1183 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1184 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1185 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1186 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1187 | 8920677 | [Gastric inhibitory polypeptide (GIP) and GIP receptor (GIPR)]. |
| 1188 | 8920677 | Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. |
| 1189 | 8920677 | In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. |
| 1190 | 8920677 | It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). |
| 1191 | 8920677 | We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. |
| 1192 | 8920677 | The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. |
| 1193 | 8920677 | Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. |
| 1194 | 8920677 | RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells. |
| 1195 | 8921824 | Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)--evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins. |
| 1196 | 8921824 | The incremental glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses (areas under curves; AUCs) were determined during a standard 180-min 75-g oral glucose tolerance test in a group of 12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) and 13 matched controls without family history of diabetes using highly sensitive and specific radioimmunoassay hormone assays. |
| 1197 | 8921824 | Fasting plasma GLP-1 and GIP concentrations were similar in all groups. |
| 1198 | 8921824 | Gender was identified as the major independent covariate for incremental glucose, insulin, GIP and GLP-1 responses, with higher values of all parameters in females. |
| 1199 | 8921824 | Incremental GLP-1 responses correlated with incremental insulin responses in the combined study population (N = 37; R = 0.42, p = 0.01). |
| 1200 | 8921824 | In conclusion, a decreased intestinal GLP-1 secretion may contribute to the abnormal insulin secretion during oral glucose ingestion in NIDDM twins. |
| 1201 | 8921824 | However, decreased secretion of gut incretin hormones (GLP-1 or GIP) does not explain all of the defects of pancreatic insulin secretion in NIDDM patients/twins or in non-diabetic individuals (identical twins) with a genetic predisposition to NIDDM. |
| 1202 | 8921824 | Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)--evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins. |
| 1203 | 8921824 | The incremental glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses (areas under curves; AUCs) were determined during a standard 180-min 75-g oral glucose tolerance test in a group of 12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) and 13 matched controls without family history of diabetes using highly sensitive and specific radioimmunoassay hormone assays. |
| 1204 | 8921824 | Fasting plasma GLP-1 and GIP concentrations were similar in all groups. |
| 1205 | 8921824 | Gender was identified as the major independent covariate for incremental glucose, insulin, GIP and GLP-1 responses, with higher values of all parameters in females. |
| 1206 | 8921824 | Incremental GLP-1 responses correlated with incremental insulin responses in the combined study population (N = 37; R = 0.42, p = 0.01). |
| 1207 | 8921824 | In conclusion, a decreased intestinal GLP-1 secretion may contribute to the abnormal insulin secretion during oral glucose ingestion in NIDDM twins. |
| 1208 | 8921824 | However, decreased secretion of gut incretin hormones (GLP-1 or GIP) does not explain all of the defects of pancreatic insulin secretion in NIDDM patients/twins or in non-diabetic individuals (identical twins) with a genetic predisposition to NIDDM. |
| 1209 | 8921824 | Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)--evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins. |
| 1210 | 8921824 | The incremental glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses (areas under curves; AUCs) were determined during a standard 180-min 75-g oral glucose tolerance test in a group of 12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) and 13 matched controls without family history of diabetes using highly sensitive and specific radioimmunoassay hormone assays. |
| 1211 | 8921824 | Fasting plasma GLP-1 and GIP concentrations were similar in all groups. |
| 1212 | 8921824 | Gender was identified as the major independent covariate for incremental glucose, insulin, GIP and GLP-1 responses, with higher values of all parameters in females. |
| 1213 | 8921824 | Incremental GLP-1 responses correlated with incremental insulin responses in the combined study population (N = 37; R = 0.42, p = 0.01). |
| 1214 | 8921824 | In conclusion, a decreased intestinal GLP-1 secretion may contribute to the abnormal insulin secretion during oral glucose ingestion in NIDDM twins. |
| 1215 | 8921824 | However, decreased secretion of gut incretin hormones (GLP-1 or GIP) does not explain all of the defects of pancreatic insulin secretion in NIDDM patients/twins or in non-diabetic individuals (identical twins) with a genetic predisposition to NIDDM. |
| 1216 | 8921824 | Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)--evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins. |
| 1217 | 8921824 | The incremental glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses (areas under curves; AUCs) were determined during a standard 180-min 75-g oral glucose tolerance test in a group of 12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) and 13 matched controls without family history of diabetes using highly sensitive and specific radioimmunoassay hormone assays. |
| 1218 | 8921824 | Fasting plasma GLP-1 and GIP concentrations were similar in all groups. |
| 1219 | 8921824 | Gender was identified as the major independent covariate for incremental glucose, insulin, GIP and GLP-1 responses, with higher values of all parameters in females. |
| 1220 | 8921824 | Incremental GLP-1 responses correlated with incremental insulin responses in the combined study population (N = 37; R = 0.42, p = 0.01). |
| 1221 | 8921824 | In conclusion, a decreased intestinal GLP-1 secretion may contribute to the abnormal insulin secretion during oral glucose ingestion in NIDDM twins. |
| 1222 | 8921824 | However, decreased secretion of gut incretin hormones (GLP-1 or GIP) does not explain all of the defects of pancreatic insulin secretion in NIDDM patients/twins or in non-diabetic individuals (identical twins) with a genetic predisposition to NIDDM. |
| 1223 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1224 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1225 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1226 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1227 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1228 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1229 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1230 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1231 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1232 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1233 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1234 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1235 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1236 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1237 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1238 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1239 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1240 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1241 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1242 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1243 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1244 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1245 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1246 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1247 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1248 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1249 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1250 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1251 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1252 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1253 | 8922354 | Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. |
| 1254 | 8922354 | Gastric inhibitory polypeptide (GIP) potently stimulates insulin secretion from pancreatic islets in the presence of glucose as an incretin. |
| 1255 | 8922354 | Because the insulinotropic effect of GIP is reduced in NIDDM, it should be clarified whether defects in the GIP receptor gene contribute to the impaired insulin secretion in NIDDM. |
| 1256 | 8922354 | Using genomic DNA samples from Japanese NIDDM and non-NIDDM subjects, we have investigated the entire coding region of the GIP receptor gene by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). |
| 1257 | 8922354 | Investigation of the function of GIP receptor with either of these mutations reveals a half-maximal stimulation value of GIP-induced cAMP response in Chinese hamster ovary cells expressing the GIP receptor with Gly198Cys of 6.3 +/- 1.2 x 10(-10) mol/l (n = 3), which was considerably higher than that of the normal GIP receptor, 9.4 +/- 3.8 x 10(-12) mol/l GIP (n = 3), whereas that of the GIP receptor with Glu354Gln was not significantly different from that of the normal GIP receptor. |
| 1258 | 8922354 | To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. |
| 1259 | 8928774 | In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. |
| 1260 | 8928774 | The response to glucagon-like peptide-1 (GLP-1) was preserved, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. |
| 1261 | 8928774 | Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. |
| 1262 | 8928774 | The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line. |
| 1263 | 8928774 | In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. |
| 1264 | 8928774 | The response to glucagon-like peptide-1 (GLP-1) was preserved, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. |
| 1265 | 8928774 | Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. |
| 1266 | 8928774 | The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line. |
| 1267 | 8928774 | In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. |
| 1268 | 8928774 | The response to glucagon-like peptide-1 (GLP-1) was preserved, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. |
| 1269 | 8928774 | Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. |
| 1270 | 8928774 | The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line. |
| 1271 | 8928774 | In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. |
| 1272 | 8928774 | The response to glucagon-like peptide-1 (GLP-1) was preserved, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. |
| 1273 | 8928774 | Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. |
| 1274 | 8928774 | The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line. |
| 1275 | 8988521 | Postprandial glucose-dependent insulinotropic polypeptide and insulin responses in patients with chronic pancreatitis with and without secondary diabetes. |
| 1276 | 9054467 | To elucidate the question of whether production of the insulinotropic gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) is altered by a diabetic metabolic state, their intestinal expression pattern was evaluated. |
| 1277 | 9054467 | In conclusion, incretin hormone expression (GIP and GLP-1) follows specific patterns throughout the gut and is unaltered by the diabetic state. |
| 1278 | 9054467 | To elucidate the question of whether production of the insulinotropic gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) is altered by a diabetic metabolic state, their intestinal expression pattern was evaluated. |
| 1279 | 9054467 | In conclusion, incretin hormone expression (GIP and GLP-1) follows specific patterns throughout the gut and is unaltered by the diabetic state. |
| 1280 | 9075801 | Protein kinase A-dependent stimulation of exocytosis in mouse pancreatic beta-cells by glucose-dependent insulinotropic polypeptide. |
| 1281 | 9075801 | The mechanisms by which glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin secretion were investigated by measurements of whole-cell Ca2+ currents, the cytoplasmic Ca2+ concentration, and cell capacitance as an indicator of exocytosis in individual mouse pancreatic beta-cells maintained in short-term culture. |
| 1282 | 9075801 | The stimulatory effect of GIP on exocytosis was blocked by pretreatment with the specific protein kinase A (PKA) inhibitor Rp-8-Br-cAMPS. |
| 1283 | 9075801 | Collectively, our data indicate that the insulinotropic hormone GIP stimulates insulin secretion from pancreatic beta-cells, through the cAMP/PKA signaling pathway, by interacting with the secretory machinery at a level distal to an elevation in [Ca2+]i. |
| 1284 | 9075801 | Protein kinase A-dependent stimulation of exocytosis in mouse pancreatic beta-cells by glucose-dependent insulinotropic polypeptide. |
| 1285 | 9075801 | The mechanisms by which glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin secretion were investigated by measurements of whole-cell Ca2+ currents, the cytoplasmic Ca2+ concentration, and cell capacitance as an indicator of exocytosis in individual mouse pancreatic beta-cells maintained in short-term culture. |
| 1286 | 9075801 | The stimulatory effect of GIP on exocytosis was blocked by pretreatment with the specific protein kinase A (PKA) inhibitor Rp-8-Br-cAMPS. |
| 1287 | 9075801 | Collectively, our data indicate that the insulinotropic hormone GIP stimulates insulin secretion from pancreatic beta-cells, through the cAMP/PKA signaling pathway, by interacting with the secretory machinery at a level distal to an elevation in [Ca2+]i. |
| 1288 | 9075801 | Protein kinase A-dependent stimulation of exocytosis in mouse pancreatic beta-cells by glucose-dependent insulinotropic polypeptide. |
| 1289 | 9075801 | The mechanisms by which glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin secretion were investigated by measurements of whole-cell Ca2+ currents, the cytoplasmic Ca2+ concentration, and cell capacitance as an indicator of exocytosis in individual mouse pancreatic beta-cells maintained in short-term culture. |
| 1290 | 9075801 | The stimulatory effect of GIP on exocytosis was blocked by pretreatment with the specific protein kinase A (PKA) inhibitor Rp-8-Br-cAMPS. |
| 1291 | 9075801 | Collectively, our data indicate that the insulinotropic hormone GIP stimulates insulin secretion from pancreatic beta-cells, through the cAMP/PKA signaling pathway, by interacting with the secretory machinery at a level distal to an elevation in [Ca2+]i. |
| 1292 | 9075801 | Protein kinase A-dependent stimulation of exocytosis in mouse pancreatic beta-cells by glucose-dependent insulinotropic polypeptide. |
| 1293 | 9075801 | The mechanisms by which glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin secretion were investigated by measurements of whole-cell Ca2+ currents, the cytoplasmic Ca2+ concentration, and cell capacitance as an indicator of exocytosis in individual mouse pancreatic beta-cells maintained in short-term culture. |
| 1294 | 9075801 | The stimulatory effect of GIP on exocytosis was blocked by pretreatment with the specific protein kinase A (PKA) inhibitor Rp-8-Br-cAMPS. |
| 1295 | 9075801 | Collectively, our data indicate that the insulinotropic hormone GIP stimulates insulin secretion from pancreatic beta-cells, through the cAMP/PKA signaling pathway, by interacting with the secretory machinery at a level distal to an elevation in [Ca2+]i. |
| 1296 | 9133546 | Glucagon-like peptide I and glucose-dependent insulinotropic polypeptide stimulate Ca2+-induced secretion in rat alpha-cells by a protein kinase A-mediated mechanism. |
| 1297 | 9133546 | The stimulatory actions of GLP-I(7-36) amide and GIP were mimicked by forskolin and antagonized by the protein kinase A (PKA)-inhibitor Rp-8-Br-cAMPS. |
| 1298 | 9133546 | The islet hormone somatostatin inhibited the stimulatory action of GLP-I(7-36) amide and GIP via a cyclic AMP-independent mechanism, whereas insulin had no effect on exocytosis. |
| 1299 | 9133546 | Glucagon-like peptide I and glucose-dependent insulinotropic polypeptide stimulate Ca2+-induced secretion in rat alpha-cells by a protein kinase A-mediated mechanism. |
| 1300 | 9133546 | The stimulatory actions of GLP-I(7-36) amide and GIP were mimicked by forskolin and antagonized by the protein kinase A (PKA)-inhibitor Rp-8-Br-cAMPS. |
| 1301 | 9133546 | The islet hormone somatostatin inhibited the stimulatory action of GLP-I(7-36) amide and GIP via a cyclic AMP-independent mechanism, whereas insulin had no effect on exocytosis. |
| 1302 | 9133546 | Glucagon-like peptide I and glucose-dependent insulinotropic polypeptide stimulate Ca2+-induced secretion in rat alpha-cells by a protein kinase A-mediated mechanism. |
| 1303 | 9133546 | The stimulatory actions of GLP-I(7-36) amide and GIP were mimicked by forskolin and antagonized by the protein kinase A (PKA)-inhibitor Rp-8-Br-cAMPS. |
| 1304 | 9133546 | The islet hormone somatostatin inhibited the stimulatory action of GLP-I(7-36) amide and GIP via a cyclic AMP-independent mechanism, whereas insulin had no effect on exocytosis. |
| 1305 | 9162612 | Venous blood samples were taken via an indwelling cannula in a forearm vein at fasting and at eight postprandial times and then analysed for blood glucose, plasma insulin, C-peptide, and gastric inhibitory polypeptide (GIP). |
| 1306 | 9162612 | Guar gum bread significantly reduced the postprandial rise in blood glucose, plasma insulin, and, except for bread containing low MW guar gum, plasma GIP levels compared to the control. |
| 1307 | 9162612 | Venous blood samples were taken via an indwelling cannula in a forearm vein at fasting and at eight postprandial times and then analysed for blood glucose, plasma insulin, C-peptide, and gastric inhibitory polypeptide (GIP). |
| 1308 | 9162612 | Guar gum bread significantly reduced the postprandial rise in blood glucose, plasma insulin, and, except for bread containing low MW guar gum, plasma GIP levels compared to the control. |
| 1309 | 9202216 | In the present study, to test the possibility that the impaired insulin secretion induced by triphenyltin compounds could result from an impaired Ca2+ response in pancreatic beta-cells, we investigated the effect of triphenyltin-chloride (TPTCl) administration on the changes in the cytoplasmic Ca2+ concentration ([Ca2+]i) induced by secretagogues, such as glucose, high K+, gastric inhibitory polypeptide (GIP), and acetylcholine (ACh) in hamster pancreatic beta-cells. |
| 1310 | 9202216 | TPTCl administration also impaired the insulin secretion in islet cells induced by 27.8 mM glucose, 100 nM GIP in the presence of 5.5 mM glucose, and 100 microM ACh in the presence of 5.5 mM glucose (P < 0.05, N = 9-16). |
| 1311 | 9202216 | In the present study, to test the possibility that the impaired insulin secretion induced by triphenyltin compounds could result from an impaired Ca2+ response in pancreatic beta-cells, we investigated the effect of triphenyltin-chloride (TPTCl) administration on the changes in the cytoplasmic Ca2+ concentration ([Ca2+]i) induced by secretagogues, such as glucose, high K+, gastric inhibitory polypeptide (GIP), and acetylcholine (ACh) in hamster pancreatic beta-cells. |
| 1312 | 9202216 | TPTCl administration also impaired the insulin secretion in islet cells induced by 27.8 mM glucose, 100 nM GIP in the presence of 5.5 mM glucose, and 100 microM ACh in the presence of 5.5 mM glucose (P < 0.05, N = 9-16). |
| 1313 | 9221612 | In addition to the classical incretin hormone "Gastric inhibitory polypeptide-1" (GIP), "Glucagon-like peptide-1" (GLP-1) is very interesting to investigators today. |
| 1314 | 9221612 | GLP-1 stimulates glucose-dependent insulin secretion, decreases plasma glucagon levels, delays gastric emptying, and putatively exerts an additional effect on peripheral glucose utilization. |
| 1315 | 9228508 | Considering minor variations in the nutritional values of the diets, IR-insulin, IR-C-peptide, IR-glucose-dependent insulinotropic polypeptide (GIP), and IR-glucagon-like peptide. 1 (GLP-1) in plasma did not significantly differ between the study groups. |
| 1316 | 9272099 | Reduced gastric inhibitory polypeptide but normal glucagon-like peptide 1 response to oral glucose in postmenopausal women with impaired glucose tolerance. |
| 1317 | 9285204 | Glucagon-like peptide 1 (GLP-1) is a physiological incretin hormone in normal humans explaining in part the augmented insulin response after oral versus intravenous glucose administration. |
| 1318 | 9285204 | In addition, GLP-1 also lowers glucagon concentrations, slows gastric emptying, stimulates (pro)insulin biosynthesis, reduces food intake upon intracerebroventricular administration in animals, and may, in addition, enhance insulin sensitivity. |
| 1319 | 9285204 | Therefore, GLP-1, in many aspects, opposes the Type 2-diabetic phenotype characterized by disturbed glucose-induced insulin secretory capacity, hyperglucagonaemia, moderate insulin deficiency, accelerated gastric emptying, overeating (obesity) and insulin resistance. |
| 1320 | 9285204 | In contrast, GLP-1 glucose-dependently stimulates insulin secretion in diet- and sulfonylurea-treated Type 2-diabetic patients and also in patients under insulin therapy long after sulfonylurea secondary failure. |
| 1321 | 9285204 | Interference with sucrose digestion using alpha-glucosidase inhibition moves nutrients into distal parts of the gastrointestinal tract and, thereby, prolongs and augments GLP-1 release. |
| 1322 | 9285204 | Enprostil, a prostaglandin E2 analogue, fully suppresses GIP responses, while only marginally affecting insulin secretion and glucose tolerance after oral glucose, suggesting compensatory hypersecretion of additional insulinotropic peptides, possibly including GLP-1. |
| 1323 | 9392159 | [Gastric inhibitory polypeptide (GIP) receptor]. |
| 1324 | 9397146 | GLP-1 and gastric inhibitory peptide (GIP) which has also been termed glucose-dependent insulinotropic peptide appear to account for most of the incretin effect in the augmentation of glucose-stimulated insulin secretion. |
| 1325 | 9397146 | It is proposed that at least one factor contributing to the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) is desensitization of the GLP-1 receptor on beta-cells. |
| 1326 | 9397146 | At pharmacological doses, infusion of GLP-1, but not of GLP, can improve and enhance postprandial insulin response in NIDDM patients. |
| 1327 | 9397146 | The observations that GLP-1 induces both secretion and production of insulin, and that its activities are mainly glucose-dependent, led to the suggestion that GLP-1 may present a unique advantage over sulfonylurea drugs in the treatment of NIDDM. |
| 1328 | 9421375 | More importantly, GLP-1(7-36) amide (via generation of cyclic AMP and activation of protein kinase A) potentiated exocytosis at a site distal to a rise in the cytoplasmic Ca2+ concentration. |
| 1329 | 9421375 | The present data suggest that the strong insulinotropic action of GLP-1(7-36) amide and GIP in humans results from its interaction with several proximal as well as distal important regulatory steps in the stimulus-secretion coupling. |
| 1330 | 9421376 | In a previous study, we showed that cAMP production in beta-cells depends on the expression of receptors for glucagon, glucagon-like peptide 1(7-36) amide [GLP-1(7-36) amide], and glucose-dependent insulinotropic polypeptide. |
| 1331 | 9421376 | Glucagon binding was partially displaced by 1 micromol/l des-His1-[Glu9]glucagon-amide, a glucagon receptor antagonist, and by 1 micromol/l GLP-1. |
| 1332 | 9528997 | However, neither basal or GIP stimulated GLP-1 secretion were affected by ambient glucose concentrations from 5-25 mM. |
| 1333 | 9528997 | The ability of GIP to stimulate GLP-1 secretion is probably mediated through activation of protein kinase A. |
| 1334 | 9648827 | Enhanced glucose-dependent insulinotropic polypeptide secretion and insulinotropic action in glucagon-like peptide 1 receptor -/- mice. |
| 1335 | 9648827 | Despite the physiological importance of the enteroinsular axis, disruption of glucagon-like peptide (GLP)-1 action is associated with only modest glucose intolerance in GLP-1 receptor -/- (GLP-1R -/-) mice. |
| 1336 | 9648827 | We show here that GLP-1R -/- mice exhibit compensatory changes in the enteroinsular axis via increased glucose-dependent insulinotropic polypeptide (GIP) secretion and enhanced GIP action. |
| 1337 | 9648827 | Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02). |
| 1338 | 9648827 | Furthermore, GIP perfusion of mice pancreas and isolated islets in the presence of elevated glucose concentrations elicited a significantly greater insulin response in GLP-1R -/- than in +/+ mice (P < or = 0.02-0.05). |
| 1339 | 9648827 | In contrast, no significant perturbation in the insulin response to perfused glucagon was detected under conditions of low (4.4 mmol/l) or high (16.6 mmol/l) glucose in GLP-1R -/- mice. |
| 1340 | 9648827 | Total pancreatic insulin but not glucagon content was significantly reduced in GLP-1R -/- compared with in +/+ mice (77 +/- 9 vs. 121 +/- 10 pmol/mg protein; P < or = 0.005). |
| 1341 | 9648827 | These observations suggest that upregulation of the GIP component of the enteroinsular axis, at the levels of GIP secretion and action, modifies the phenotype resulting from interruption of the insulinotropic activity of GLP-1 in vivo. |
| 1342 | 9648827 | Enhanced glucose-dependent insulinotropic polypeptide secretion and insulinotropic action in glucagon-like peptide 1 receptor -/- mice. |
| 1343 | 9648827 | Despite the physiological importance of the enteroinsular axis, disruption of glucagon-like peptide (GLP)-1 action is associated with only modest glucose intolerance in GLP-1 receptor -/- (GLP-1R -/-) mice. |
| 1344 | 9648827 | We show here that GLP-1R -/- mice exhibit compensatory changes in the enteroinsular axis via increased glucose-dependent insulinotropic polypeptide (GIP) secretion and enhanced GIP action. |
| 1345 | 9648827 | Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02). |
| 1346 | 9648827 | Furthermore, GIP perfusion of mice pancreas and isolated islets in the presence of elevated glucose concentrations elicited a significantly greater insulin response in GLP-1R -/- than in +/+ mice (P < or = 0.02-0.05). |
| 1347 | 9648827 | In contrast, no significant perturbation in the insulin response to perfused glucagon was detected under conditions of low (4.4 mmol/l) or high (16.6 mmol/l) glucose in GLP-1R -/- mice. |
| 1348 | 9648827 | Total pancreatic insulin but not glucagon content was significantly reduced in GLP-1R -/- compared with in +/+ mice (77 +/- 9 vs. 121 +/- 10 pmol/mg protein; P < or = 0.005). |
| 1349 | 9648827 | These observations suggest that upregulation of the GIP component of the enteroinsular axis, at the levels of GIP secretion and action, modifies the phenotype resulting from interruption of the insulinotropic activity of GLP-1 in vivo. |
| 1350 | 9648827 | Enhanced glucose-dependent insulinotropic polypeptide secretion and insulinotropic action in glucagon-like peptide 1 receptor -/- mice. |
| 1351 | 9648827 | Despite the physiological importance of the enteroinsular axis, disruption of glucagon-like peptide (GLP)-1 action is associated with only modest glucose intolerance in GLP-1 receptor -/- (GLP-1R -/-) mice. |
| 1352 | 9648827 | We show here that GLP-1R -/- mice exhibit compensatory changes in the enteroinsular axis via increased glucose-dependent insulinotropic polypeptide (GIP) secretion and enhanced GIP action. |
| 1353 | 9648827 | Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02). |
| 1354 | 9648827 | Furthermore, GIP perfusion of mice pancreas and isolated islets in the presence of elevated glucose concentrations elicited a significantly greater insulin response in GLP-1R -/- than in +/+ mice (P < or = 0.02-0.05). |
| 1355 | 9648827 | In contrast, no significant perturbation in the insulin response to perfused glucagon was detected under conditions of low (4.4 mmol/l) or high (16.6 mmol/l) glucose in GLP-1R -/- mice. |
| 1356 | 9648827 | Total pancreatic insulin but not glucagon content was significantly reduced in GLP-1R -/- compared with in +/+ mice (77 +/- 9 vs. 121 +/- 10 pmol/mg protein; P < or = 0.005). |
| 1357 | 9648827 | These observations suggest that upregulation of the GIP component of the enteroinsular axis, at the levels of GIP secretion and action, modifies the phenotype resulting from interruption of the insulinotropic activity of GLP-1 in vivo. |
| 1358 | 9648827 | Enhanced glucose-dependent insulinotropic polypeptide secretion and insulinotropic action in glucagon-like peptide 1 receptor -/- mice. |
| 1359 | 9648827 | Despite the physiological importance of the enteroinsular axis, disruption of glucagon-like peptide (GLP)-1 action is associated with only modest glucose intolerance in GLP-1 receptor -/- (GLP-1R -/-) mice. |
| 1360 | 9648827 | We show here that GLP-1R -/- mice exhibit compensatory changes in the enteroinsular axis via increased glucose-dependent insulinotropic polypeptide (GIP) secretion and enhanced GIP action. |
| 1361 | 9648827 | Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02). |
| 1362 | 9648827 | Furthermore, GIP perfusion of mice pancreas and isolated islets in the presence of elevated glucose concentrations elicited a significantly greater insulin response in GLP-1R -/- than in +/+ mice (P < or = 0.02-0.05). |
| 1363 | 9648827 | In contrast, no significant perturbation in the insulin response to perfused glucagon was detected under conditions of low (4.4 mmol/l) or high (16.6 mmol/l) glucose in GLP-1R -/- mice. |
| 1364 | 9648827 | Total pancreatic insulin but not glucagon content was significantly reduced in GLP-1R -/- compared with in +/+ mice (77 +/- 9 vs. 121 +/- 10 pmol/mg protein; P < or = 0.005). |
| 1365 | 9648827 | These observations suggest that upregulation of the GIP component of the enteroinsular axis, at the levels of GIP secretion and action, modifies the phenotype resulting from interruption of the insulinotropic activity of GLP-1 in vivo. |
| 1366 | 9648827 | Enhanced glucose-dependent insulinotropic polypeptide secretion and insulinotropic action in glucagon-like peptide 1 receptor -/- mice. |
| 1367 | 9648827 | Despite the physiological importance of the enteroinsular axis, disruption of glucagon-like peptide (GLP)-1 action is associated with only modest glucose intolerance in GLP-1 receptor -/- (GLP-1R -/-) mice. |
| 1368 | 9648827 | We show here that GLP-1R -/- mice exhibit compensatory changes in the enteroinsular axis via increased glucose-dependent insulinotropic polypeptide (GIP) secretion and enhanced GIP action. |
| 1369 | 9648827 | Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02). |
| 1370 | 9648827 | Furthermore, GIP perfusion of mice pancreas and isolated islets in the presence of elevated glucose concentrations elicited a significantly greater insulin response in GLP-1R -/- than in +/+ mice (P < or = 0.02-0.05). |
| 1371 | 9648827 | In contrast, no significant perturbation in the insulin response to perfused glucagon was detected under conditions of low (4.4 mmol/l) or high (16.6 mmol/l) glucose in GLP-1R -/- mice. |
| 1372 | 9648827 | Total pancreatic insulin but not glucagon content was significantly reduced in GLP-1R -/- compared with in +/+ mice (77 +/- 9 vs. 121 +/- 10 pmol/mg protein; P < or = 0.005). |
| 1373 | 9648827 | These observations suggest that upregulation of the GIP component of the enteroinsular axis, at the levels of GIP secretion and action, modifies the phenotype resulting from interruption of the insulinotropic activity of GLP-1 in vivo. |
| 1374 | 9703325 | The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP)-1 act on the pancreas to potentiate glucose-induced insulin secretion (enteroinsular axis). |
| 1375 | 9703325 | These results showed that inhibiting DP IV activity with Ile-thiazolidide blocked the formation of NH2-terminally truncated GIP and GLP-1. |
| 1376 | 9703325 | This was attributed to the glucose-lowering actions of increasing the circulating half-lives of the endogenously released incretins GIP and, particularly, GLP-1. |
| 1377 | 9703325 | The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP)-1 act on the pancreas to potentiate glucose-induced insulin secretion (enteroinsular axis). |
| 1378 | 9703325 | These results showed that inhibiting DP IV activity with Ile-thiazolidide blocked the formation of NH2-terminally truncated GIP and GLP-1. |
| 1379 | 9703325 | This was attributed to the glucose-lowering actions of increasing the circulating half-lives of the endogenously released incretins GIP and, particularly, GLP-1. |
| 1380 | 9703325 | The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (GLP)-1 act on the pancreas to potentiate glucose-induced insulin secretion (enteroinsular axis). |
| 1381 | 9703325 | These results showed that inhibiting DP IV activity with Ile-thiazolidide blocked the formation of NH2-terminally truncated GIP and GLP-1. |
| 1382 | 9703325 | This was attributed to the glucose-lowering actions of increasing the circulating half-lives of the endogenously released incretins GIP and, particularly, GLP-1. |
| 1383 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1384 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1385 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1386 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1387 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1388 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1389 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1390 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1391 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1392 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1393 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1394 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1395 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1396 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1397 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1398 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1399 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1400 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1401 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1402 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1403 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1404 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1405 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1406 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1407 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1408 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1409 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1410 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1411 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1412 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1413 | 9794107 | Discovery of amino acid variants in the human glucose-dependent insulinotropic polypeptide (GIP) receptor: the impact on the pancreatic beta cell responses and functional expression studies in Chinese hamster fibroblast cells. |
| 1414 | 9794107 | The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. |
| 1415 | 9794107 | The insulinotropic effect of GLP-1 is maintained in patients with Type II (non-insulin-dependent) diabetes mellitus, whereas, for unknown reasons, the effect of GIP is diminished or lacking. |
| 1416 | 9794107 | We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. |
| 1417 | 9794107 | Investigation of the function of the two GIP receptor variants in Chinese hamster fibroblasts showed, however, that the GIP-induced cAMP formation and the binding of GIP to cells expressing the variant receptors were not different from the findings in cells expressing the wildtype GIP receptor. |
| 1418 | 9794107 | In conclusion, amino acid variants in the GIP receptor are not associated with random Type II diabetes in patients of Danish Caucasian origin or with altered GIP binding and GIP-induced cAMP production when stably transfected in Chinese hamster fibroblasts. |
| 1419 | 9820111 | Findings on the effects of GIP indicate that its incretory effect on stimulation of insulin secretion under conditions of hyperglycaemia is more important than the formerly known effect of enterogastrone. |
| 1420 | 9833938 | Reduced insulin secretion has been described as part of normal ageing although there is no information on age-related changes in the secretion of the major insulinotropic hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (7-36 amide) (GLP-1). |
| 1421 | 9833938 | Total integrated responses for GIP and GLP-1 were considerably greater in the older subjects. |
| 1422 | 9833938 | We hypothesise that an age-related impairment of insulin secretion to insulinotropic hormones, GIP and GLP-1, contributes to a reduction in glucose tolerance in this age group. |
| 1423 | 9833938 | The pronounced compensatory increase in postprandial secretion of GIP and GLP-1 provides further evidence not only for the negative feedback relation between incretin and insulin secretion but also for the importance of the entero-insular axis in the regulation of insulin secretion. |
| 1424 | 9833938 | Reduced insulin secretion has been described as part of normal ageing although there is no information on age-related changes in the secretion of the major insulinotropic hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (7-36 amide) (GLP-1). |
| 1425 | 9833938 | Total integrated responses for GIP and GLP-1 were considerably greater in the older subjects. |
| 1426 | 9833938 | We hypothesise that an age-related impairment of insulin secretion to insulinotropic hormones, GIP and GLP-1, contributes to a reduction in glucose tolerance in this age group. |
| 1427 | 9833938 | The pronounced compensatory increase in postprandial secretion of GIP and GLP-1 provides further evidence not only for the negative feedback relation between incretin and insulin secretion but also for the importance of the entero-insular axis in the regulation of insulin secretion. |
| 1428 | 9833938 | Reduced insulin secretion has been described as part of normal ageing although there is no information on age-related changes in the secretion of the major insulinotropic hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (7-36 amide) (GLP-1). |
| 1429 | 9833938 | Total integrated responses for GIP and GLP-1 were considerably greater in the older subjects. |
| 1430 | 9833938 | We hypothesise that an age-related impairment of insulin secretion to insulinotropic hormones, GIP and GLP-1, contributes to a reduction in glucose tolerance in this age group. |
| 1431 | 9833938 | The pronounced compensatory increase in postprandial secretion of GIP and GLP-1 provides further evidence not only for the negative feedback relation between incretin and insulin secretion but also for the importance of the entero-insular axis in the regulation of insulin secretion. |
| 1432 | 9833938 | Reduced insulin secretion has been described as part of normal ageing although there is no information on age-related changes in the secretion of the major insulinotropic hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide (7-36 amide) (GLP-1). |
| 1433 | 9833938 | Total integrated responses for GIP and GLP-1 were considerably greater in the older subjects. |
| 1434 | 9833938 | We hypothesise that an age-related impairment of insulin secretion to insulinotropic hormones, GIP and GLP-1, contributes to a reduction in glucose tolerance in this age group. |
| 1435 | 9833938 | The pronounced compensatory increase in postprandial secretion of GIP and GLP-1 provides further evidence not only for the negative feedback relation between incretin and insulin secretion but also for the importance of the entero-insular axis in the regulation of insulin secretion. |
| 1436 | 9934817 | The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin. |
| 1437 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 1438 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 1439 | 9934817 | There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin. |
| 1440 | 9934817 | In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls. |
| 1441 | 9934817 | The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin. |
| 1442 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 1443 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 1444 | 9934817 | There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin. |
| 1445 | 9934817 | In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls. |
| 1446 | 10094118 | The incretins glucose-dependent insulinotropic polypeptide (GIP1-42) and truncated forms of glucagon-like peptide-1 (GLP-1) are hormones released from the gut in response to ingested nutrients, which act on the pancreas to potentiate glucose-induced insulin secretion. |
| 1447 | 10102692 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis that, like glucagon-like peptide 1(7-36) amide (tGLP-1), has a functional profile of possible therapeutic value for type 2 diabetes. |
| 1448 | 10102692 | The present study examined the ability of NH2-terminal modification of human GIP to protect from plasma degradation and enhance insulin-releasing and antihyperglycemic activity. |
| 1449 | 10102692 | This was associated with a significantly greater and more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng x ml(-1) x min(-1); P < 0.05). |
| 1450 | 10102692 | These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degradation and exhibits enhanced antihyperglycemic activity and insulin-releasing action in vivo. |
| 1451 | 10102692 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis that, like glucagon-like peptide 1(7-36) amide (tGLP-1), has a functional profile of possible therapeutic value for type 2 diabetes. |
| 1452 | 10102692 | The present study examined the ability of NH2-terminal modification of human GIP to protect from plasma degradation and enhance insulin-releasing and antihyperglycemic activity. |
| 1453 | 10102692 | This was associated with a significantly greater and more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng x ml(-1) x min(-1); P < 0.05). |
| 1454 | 10102692 | These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degradation and exhibits enhanced antihyperglycemic activity and insulin-releasing action in vivo. |
| 1455 | 10102692 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis that, like glucagon-like peptide 1(7-36) amide (tGLP-1), has a functional profile of possible therapeutic value for type 2 diabetes. |
| 1456 | 10102692 | The present study examined the ability of NH2-terminal modification of human GIP to protect from plasma degradation and enhance insulin-releasing and antihyperglycemic activity. |
| 1457 | 10102692 | This was associated with a significantly greater and more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng x ml(-1) x min(-1); P < 0.05). |
| 1458 | 10102692 | These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degradation and exhibits enhanced antihyperglycemic activity and insulin-releasing action in vivo. |
| 1459 | 10102692 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis that, like glucagon-like peptide 1(7-36) amide (tGLP-1), has a functional profile of possible therapeutic value for type 2 diabetes. |
| 1460 | 10102692 | The present study examined the ability of NH2-terminal modification of human GIP to protect from plasma degradation and enhance insulin-releasing and antihyperglycemic activity. |
| 1461 | 10102692 | This was associated with a significantly greater and more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng x ml(-1) x min(-1); P < 0.05). |
| 1462 | 10102692 | These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degradation and exhibits enhanced antihyperglycemic activity and insulin-releasing action in vivo. |
| 1463 | 10235607 | There was no statistical difference between obese diabetic mice and lean controls regarding the numbers and CSI of antral gastrin/CCK-, somatostatin- and serotonin-; and duodenal secretin-, gastric inhibitory peptide (GIP)-, CCK/gastrin-, and somatostatin-IR cells; nor was there any difference regarding nuclear area, with the exception of the antral somatostatin- and duodenal GIP-IR cells. |
| 1464 | 10331404 | Forskolin, an activator of adenylyl cyclase, raised intracellular cAMP levels and enhanced KCl-induced (Ca2+ -stimulated) insulin release in the presence, but not in the absence, of glucose. |
| 1465 | 10331404 | This action of cAMP is physiologically relevant, because not only forskolin but also glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, and pituitary adenylyl cyclase activating polypeptide exerted similar actions. |
| 1466 | 10331404 | In conclusion, the cAMP/protein kinase A pathway has no direct effect on Ca2+ -stimulated insulin exocytosis. |
| 1467 | 10455124 | Characterization of the carboxyl-terminal domain of the rat glucose-dependent insulinotropic polypeptide (GIP) receptor. |
| 1468 | 10455124 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone involved in the regulation of insulin secretion. |
| 1469 | 10455124 | In non-insulin-dependent diabetes mellitus insulin responses to GIP are blunted, possibly due to altered signal transduction or reduced receptor number. |
| 1470 | 10455124 | The majority of the GIP receptor CT is therefore not required for signaling, a minimum chain length of approximately 405 amino acids is needed for receptor expression, and serines 426 and 427 are important for regulating rate of receptor internalization. |
| 1471 | 10455124 | Characterization of the carboxyl-terminal domain of the rat glucose-dependent insulinotropic polypeptide (GIP) receptor. |
| 1472 | 10455124 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone involved in the regulation of insulin secretion. |
| 1473 | 10455124 | In non-insulin-dependent diabetes mellitus insulin responses to GIP are blunted, possibly due to altered signal transduction or reduced receptor number. |
| 1474 | 10455124 | The majority of the GIP receptor CT is therefore not required for signaling, a minimum chain length of approximately 405 amino acids is needed for receptor expression, and serines 426 and 427 are important for regulating rate of receptor internalization. |
| 1475 | 10455124 | Characterization of the carboxyl-terminal domain of the rat glucose-dependent insulinotropic polypeptide (GIP) receptor. |
| 1476 | 10455124 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone involved in the regulation of insulin secretion. |
| 1477 | 10455124 | In non-insulin-dependent diabetes mellitus insulin responses to GIP are blunted, possibly due to altered signal transduction or reduced receptor number. |
| 1478 | 10455124 | The majority of the GIP receptor CT is therefore not required for signaling, a minimum chain length of approximately 405 amino acids is needed for receptor expression, and serines 426 and 427 are important for regulating rate of receptor internalization. |
| 1479 | 10455124 | Characterization of the carboxyl-terminal domain of the rat glucose-dependent insulinotropic polypeptide (GIP) receptor. |
| 1480 | 10455124 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone involved in the regulation of insulin secretion. |
| 1481 | 10455124 | In non-insulin-dependent diabetes mellitus insulin responses to GIP are blunted, possibly due to altered signal transduction or reduced receptor number. |
| 1482 | 10455124 | The majority of the GIP receptor CT is therefore not required for signaling, a minimum chain length of approximately 405 amino acids is needed for receptor expression, and serines 426 and 427 are important for regulating rate of receptor internalization. |
| 1483 | 10571117 | Immunocytochemical evidence for a paracrine interaction between GIP and GLP-1-producing cells in canine small intestine. |
| 1484 | 10571117 | We have recently demonstrated that glucose-dependent insulinotropic peptide (GIP) stimulated GLP-1 secretion from canine ileal L cells in culture. |
| 1485 | 10571117 | Immunocytochemical evidence for a paracrine interaction between GIP and GLP-1-producing cells in canine small intestine. |
| 1486 | 10571117 | We have recently demonstrated that glucose-dependent insulinotropic peptide (GIP) stimulated GLP-1 secretion from canine ileal L cells in culture. |
| 1487 | 10611300 | Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic beta cells. |
| 1488 | 10611300 | GIPR-/- mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. |
| 1489 | 10611300 | Although blood glucose levels after meal ingestion are not increased by high-fat diet in GIPR+/+ mice because of compensatory higher insulin secretion, they are significantly increased in GIPR-/- mice because of the lack of such enhancement. |
| 1490 | 10611300 | Accordingly, early insulin secretion mediated by GIP determines glucose tolerance after oral glucose load in vivo, and because GIP plays an important role in the compensatory enhancement of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis may contribute to the pathogenesis of diabetes. |
| 1491 | 10611300 | Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic beta cells. |
| 1492 | 10611300 | GIPR-/- mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. |
| 1493 | 10611300 | Although blood glucose levels after meal ingestion are not increased by high-fat diet in GIPR+/+ mice because of compensatory higher insulin secretion, they are significantly increased in GIPR-/- mice because of the lack of such enhancement. |
| 1494 | 10611300 | Accordingly, early insulin secretion mediated by GIP determines glucose tolerance after oral glucose load in vivo, and because GIP plays an important role in the compensatory enhancement of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis may contribute to the pathogenesis of diabetes. |
| 1495 | 10634963 | Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1). |
| 1496 | 10666005 | Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. |
| 1497 | 10666005 | The GIP receptor is a G-protein-coupled receptor belonging to the family of secretin/VIP receptors. |
| 1498 | 10666005 | GIP receptor mRNA is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex, and brain, suggesting it may have other functions in addition to the ones mentioned above. |
| 1499 | 10666005 | In addition to stimulating insulin release, GIP has been shown to amplify the effect of insulin on target tissues. |
| 1500 | 10666005 | In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. |
| 1501 | 10666005 | Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. |
| 1502 | 10666005 | The GIP receptor is a G-protein-coupled receptor belonging to the family of secretin/VIP receptors. |
| 1503 | 10666005 | GIP receptor mRNA is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex, and brain, suggesting it may have other functions in addition to the ones mentioned above. |
| 1504 | 10666005 | In addition to stimulating insulin release, GIP has been shown to amplify the effect of insulin on target tissues. |
| 1505 | 10666005 | In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. |
| 1506 | 10666005 | Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. |
| 1507 | 10666005 | The GIP receptor is a G-protein-coupled receptor belonging to the family of secretin/VIP receptors. |
| 1508 | 10666005 | GIP receptor mRNA is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex, and brain, suggesting it may have other functions in addition to the ones mentioned above. |
| 1509 | 10666005 | In addition to stimulating insulin release, GIP has been shown to amplify the effect of insulin on target tissues. |
| 1510 | 10666005 | In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. |
| 1511 | 10666005 | Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. |
| 1512 | 10666005 | The GIP receptor is a G-protein-coupled receptor belonging to the family of secretin/VIP receptors. |
| 1513 | 10666005 | GIP receptor mRNA is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex, and brain, suggesting it may have other functions in addition to the ones mentioned above. |
| 1514 | 10666005 | In addition to stimulating insulin release, GIP has been shown to amplify the effect of insulin on target tissues. |
| 1515 | 10666005 | In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. |
| 1516 | 10666005 | Accordingly, it was later renamed glucose-dependent insulinotropic polypeptide because its action on insulin release depends upon an increase in circulating levels of glucose. |
| 1517 | 10666005 | The GIP receptor is a G-protein-coupled receptor belonging to the family of secretin/VIP receptors. |
| 1518 | 10666005 | GIP receptor mRNA is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex, and brain, suggesting it may have other functions in addition to the ones mentioned above. |
| 1519 | 10666005 | In addition to stimulating insulin release, GIP has been shown to amplify the effect of insulin on target tissues. |
| 1520 | 10666005 | In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. |
| 1521 | 10720037 | Cholecystokinin (CCK) is a gut hormone and a neuropeptide that has the capacity to stimulate insulin secretion. |
| 1522 | 10720037 | In contrast, the increase in the circulating levels of gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (GLP-1), or glucagon after meal ingestion was not significantly affected by CCK-8. |
| 1523 | 10766455 | Transforming growth factor alpha (TGF-alpha) increased basal, but not glucose-stimulated, insulin release and insulin content in islets cultured in low glucose. |
| 1524 | 10766455 | Gastrin, expressed in islets during fetal life, did not affect basal or glucose-stimulated insulin release, or insulin content, in islets maintained in either low or high glucose. |
| 1525 | 10766455 | The addition of gastrin to TGF-alpha did not affect the results obtained with the latter peptide. |
| 1526 | 10766455 | Gastrin-releasing peptide failed to influence basal or glucose-responsive insulin secretory rates, and insulin content, at either glucose concentration during culture. |
| 1527 | 10766455 | The somatostatin analog Sandostatin (octreotide acetate) neither influenced basal nor stimulated short-term insulin release at any glucose concentration present during culture, whereas the hormone significantly decreased the insulin content of islets cultured in high glucose. |
| 1528 | 10766455 | Culture with gastric inhibitory peptide (GIP) or glucagon-like peptide I (GLP-1), two proposed incretins, did not affect short-term insulin secretion in response to 3.3 or 16.7 mM glucose irrespective of the ambient glucose concentration during culture. |
| 1529 | 10766455 | To the contrary, GLP-1, but not GIP, increased the content of insulin in islets cultured in low glucose. |
| 1530 | 10766455 | We suggest that GH and TGF-alpha stimulate, while somatostatin, through paracrine interaction, may inhibit, these processes. |
| 1531 | 10766455 | Transforming growth factor alpha (TGF-alpha) increased basal, but not glucose-stimulated, insulin release and insulin content in islets cultured in low glucose. |
| 1532 | 10766455 | Gastrin, expressed in islets during fetal life, did not affect basal or glucose-stimulated insulin release, or insulin content, in islets maintained in either low or high glucose. |
| 1533 | 10766455 | The addition of gastrin to TGF-alpha did not affect the results obtained with the latter peptide. |
| 1534 | 10766455 | Gastrin-releasing peptide failed to influence basal or glucose-responsive insulin secretory rates, and insulin content, at either glucose concentration during culture. |
| 1535 | 10766455 | The somatostatin analog Sandostatin (octreotide acetate) neither influenced basal nor stimulated short-term insulin release at any glucose concentration present during culture, whereas the hormone significantly decreased the insulin content of islets cultured in high glucose. |
| 1536 | 10766455 | Culture with gastric inhibitory peptide (GIP) or glucagon-like peptide I (GLP-1), two proposed incretins, did not affect short-term insulin secretion in response to 3.3 or 16.7 mM glucose irrespective of the ambient glucose concentration during culture. |
| 1537 | 10766455 | To the contrary, GLP-1, but not GIP, increased the content of insulin in islets cultured in low glucose. |
| 1538 | 10766455 | We suggest that GH and TGF-alpha stimulate, while somatostatin, through paracrine interaction, may inhibit, these processes. |
| 1539 | 10823914 | Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26. |
| 1540 | 10823914 | This enzyme activity has been implicated in the regulation of the biological activity of multiple hormones and chemokines, including the insulinotropic peptides glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 1541 | 10823914 | Levels of glucose-stimulated circulating insulin and the intact insulinotropic form of GLP-1 are increased in CD26(-/-) mice. |
| 1542 | 10823914 | This inhibitor also improved glucose tolerance in GLP-1 receptor(-/-) mice, indicating that CD26 contributes to blood glucose regulation by controlling the activity of GLP-1 as well as additional substrates. |
| 1543 | 10828847 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. |
| 1544 | 10828847 | The present study has examined the ability of Tyr(1)-glucitol GIP to be protected from plasma degradation and to enhance insulin-releasing and antihyperglycaemic activity in 20- to 25-week-old obese diabetic ob/ob mice. |
| 1545 | 10828847 | This was associated with a significantly greater and more protracted insulin response following Tyr(1)-glucitol GIP than GIP (AUC, 491+/-118 vs 180+/-33 ng/ml.min; P<0.05). |
| 1546 | 10828847 | Administration of Tyr(1)-glucitol GIP also enhanced the glucose-lowering ability of 50 units/kg insulin (218.4+/-30.2 vs insulin alone 133.9+/-16.2 mmol/l.min; P<0.05). |
| 1547 | 10828847 | These data demonstrate that Tyr(1)-glucitol GIP displays resistance to plasma DPP IV degradation in a commonly used animal model of type 2 diabetes, resulting in enhanced antihyperglycaemic activity and insulin-releasing action in vivo. |
| 1548 | 10828847 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. |
| 1549 | 10828847 | The present study has examined the ability of Tyr(1)-glucitol GIP to be protected from plasma degradation and to enhance insulin-releasing and antihyperglycaemic activity in 20- to 25-week-old obese diabetic ob/ob mice. |
| 1550 | 10828847 | This was associated with a significantly greater and more protracted insulin response following Tyr(1)-glucitol GIP than GIP (AUC, 491+/-118 vs 180+/-33 ng/ml.min; P<0.05). |
| 1551 | 10828847 | Administration of Tyr(1)-glucitol GIP also enhanced the glucose-lowering ability of 50 units/kg insulin (218.4+/-30.2 vs insulin alone 133.9+/-16.2 mmol/l.min; P<0.05). |
| 1552 | 10828847 | These data demonstrate that Tyr(1)-glucitol GIP displays resistance to plasma DPP IV degradation in a commonly used animal model of type 2 diabetes, resulting in enhanced antihyperglycaemic activity and insulin-releasing action in vivo. |
| 1553 | 10828847 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. |
| 1554 | 10828847 | The present study has examined the ability of Tyr(1)-glucitol GIP to be protected from plasma degradation and to enhance insulin-releasing and antihyperglycaemic activity in 20- to 25-week-old obese diabetic ob/ob mice. |
| 1555 | 10828847 | This was associated with a significantly greater and more protracted insulin response following Tyr(1)-glucitol GIP than GIP (AUC, 491+/-118 vs 180+/-33 ng/ml.min; P<0.05). |
| 1556 | 10828847 | Administration of Tyr(1)-glucitol GIP also enhanced the glucose-lowering ability of 50 units/kg insulin (218.4+/-30.2 vs insulin alone 133.9+/-16.2 mmol/l.min; P<0.05). |
| 1557 | 10828847 | These data demonstrate that Tyr(1)-glucitol GIP displays resistance to plasma DPP IV degradation in a commonly used animal model of type 2 diabetes, resulting in enhanced antihyperglycaemic activity and insulin-releasing action in vivo. |
| 1558 | 10828847 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. |
| 1559 | 10828847 | The present study has examined the ability of Tyr(1)-glucitol GIP to be protected from plasma degradation and to enhance insulin-releasing and antihyperglycaemic activity in 20- to 25-week-old obese diabetic ob/ob mice. |
| 1560 | 10828847 | This was associated with a significantly greater and more protracted insulin response following Tyr(1)-glucitol GIP than GIP (AUC, 491+/-118 vs 180+/-33 ng/ml.min; P<0.05). |
| 1561 | 10828847 | Administration of Tyr(1)-glucitol GIP also enhanced the glucose-lowering ability of 50 units/kg insulin (218.4+/-30.2 vs insulin alone 133.9+/-16.2 mmol/l.min; P<0.05). |
| 1562 | 10828847 | These data demonstrate that Tyr(1)-glucitol GIP displays resistance to plasma DPP IV degradation in a commonly used animal model of type 2 diabetes, resulting in enhanced antihyperglycaemic activity and insulin-releasing action in vivo. |
| 1563 | 10828847 | Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. |
| 1564 | 10828847 | The present study has examined the ability of Tyr(1)-glucitol GIP to be protected from plasma degradation and to enhance insulin-releasing and antihyperglycaemic activity in 20- to 25-week-old obese diabetic ob/ob mice. |
| 1565 | 10828847 | This was associated with a significantly greater and more protracted insulin response following Tyr(1)-glucitol GIP than GIP (AUC, 491+/-118 vs 180+/-33 ng/ml.min; P<0.05). |
| 1566 | 10828847 | Administration of Tyr(1)-glucitol GIP also enhanced the glucose-lowering ability of 50 units/kg insulin (218.4+/-30.2 vs insulin alone 133.9+/-16.2 mmol/l.min; P<0.05). |
| 1567 | 10828847 | These data demonstrate that Tyr(1)-glucitol GIP displays resistance to plasma DPP IV degradation in a commonly used animal model of type 2 diabetes, resulting in enhanced antihyperglycaemic activity and insulin-releasing action in vivo. |
| 1568 | 10893327 | Glucagon-like peptide-1 improves insulin and proinsulin binding on RINm5F cells and human monocytes. |
| 1569 | 10893327 | The present study tested the hypothesis that GLP-1 may modulate insulin receptor binding. |
| 1570 | 10893327 | In addition, we investigated the effect of GLP-1 on insulin receptor binding on monocytes isolated from type 1 and type 2 diabetes patients and healthy volunteers. |
| 1571 | 10893327 | In RINm5F cells, GLP-1 increased the capacity and affinity of insulin binding in a time- and concentration-dependent manner. |
| 1572 | 10893327 | The GLP-1 receptor agonist exendin-4 showed similar effects, whereas the receptor antagonist exendin-(9---39) amide inhibited the GLP-1-induced increase in insulin receptor binding. |
| 1573 | 10893327 | The GLP-1 effect was potentiated by the adenylyl cyclase activator forskolin and the stable cAMP analog Sp-5, 6-dichloro-1-beta-D-ribofuranosyl-benzimidazole-3', 5'-monophosphorothioate but was antagonized by the intracellular Ca(2+) chelator 1,2-bis(0-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM. |
| 1574 | 10893327 | Glucagon, gastric inhibitory peptide (GIP), and GIP-(1---30) did not affect insulin binding. |
| 1575 | 10893327 | In isolated monocytes, 24 h incubation with 100 nM GLP-1 significantly (P<0.05) increased the diminished number of high-capacity/low-affinity insulin binding sites per cell in type 1 diabetics (9,000+/-3,200 vs. 18,500+/-3,600) and in type 2 diabetics (15,700+/-2,100 vs. 28,900+/-1,800) compared with nondiabetic control subjects (25,100+/-2,700 vs. 26,200+/-4,200). |
| 1576 | 10893327 | Diabetologia 39: 421-432, 1996), we further investigated the effect of GLP-1 on proinsulin binding in RINm5F cells and monocytes. |
| 1577 | 10893327 | In both cell types, GLP-1 induced a significant increase in proinsulin binding. |
| 1578 | 10893327 | We conclude that, in RINm5F cells and in isolated human monocytes, GLP-1 specifically increases the number of high-capacity insulin binding sites that may be functional proinsulin receptors. |
| 1579 | 10975043 | Blood glucose peak following a meal is modulated by gut hormones incretin effect, essentially GIP and GLP1. |
| 1580 | 11110661 | A tumor-derived K-cell line was induced to produce human insulin by providing the cells with the human insulin gene linked to the 5'-regulatory region of the gene encoding glucose-dependent insulinotropic polypeptide (GIP). |
| 1581 | 11116211 | The purified N-terminal fragment (hereafter referred to as NT) of the GLP-1R produced in either insect (Sf9) or mammalian (COS-7) cells was shown to bind GLP-1. |
| 1582 | 11116211 | The GLP-1R NT protein attached to beads bound GLP-1, but with lower affinity (inhibitory concentration (IC(50)): 4.5 x 10(-7) M) than wild-type (WT) GLP-1R (IC(50): 5.2 x 10(-9)M). |
| 1583 | 11116211 | The low affinity of GLP-1R NT suggested that other receptor domains may contribute to GLP-1 binding. |
| 1584 | 11116211 | This was supported by studies using chimeric glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptors. |
| 1585 | 11116211 | GIP(1-151)/GLP-1R, but not GIP(1-222)/GLP-1R, exhibited specific GLP-1 binding and GLP-1-induced cAMP production, suggesting that the region encompassing transmembrane (TM) domain 1 through to TM3 was required for binding. |
| 1586 | 11116211 | These studies indicate that the NT domain of the GLP-1R is able to bind GLP-1, but charged residues concentrated at the distal TM2/extracellular loop-1 (EC1) interface (K197, D198, K202) and in EC1 (D215 and R227) probably contribute to the binding determinants of the GLP-1R. |
| 1587 | 11116211 | The purified N-terminal fragment (hereafter referred to as NT) of the GLP-1R produced in either insect (Sf9) or mammalian (COS-7) cells was shown to bind GLP-1. |
| 1588 | 11116211 | The GLP-1R NT protein attached to beads bound GLP-1, but with lower affinity (inhibitory concentration (IC(50)): 4.5 x 10(-7) M) than wild-type (WT) GLP-1R (IC(50): 5.2 x 10(-9)M). |
| 1589 | 11116211 | The low affinity of GLP-1R NT suggested that other receptor domains may contribute to GLP-1 binding. |
| 1590 | 11116211 | This was supported by studies using chimeric glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptors. |
| 1591 | 11116211 | GIP(1-151)/GLP-1R, but not GIP(1-222)/GLP-1R, exhibited specific GLP-1 binding and GLP-1-induced cAMP production, suggesting that the region encompassing transmembrane (TM) domain 1 through to TM3 was required for binding. |
| 1592 | 11116211 | These studies indicate that the NT domain of the GLP-1R is able to bind GLP-1, but charged residues concentrated at the distal TM2/extracellular loop-1 (EC1) interface (K197, D198, K202) and in EC1 (D215 and R227) probably contribute to the binding determinants of the GLP-1R. |
| 1593 | 11158012 | Aberrant gastric inhibitory polypeptide (GIP) receptor expression in bilaterally hyperplastic adrenals or unilateral adrenal adenomas is a rare form of adrenal hyperfunction. |
| 1594 | 11158012 | In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. |
| 1595 | 11158012 | The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. |
| 1596 | 11158012 | Thus, aberrant expression of the GIP receptor does not exclusively involve cells of a zona fasciculata phenotype, as previously reported, but may also occur in other types of differentiated adrenocortical cells. |
| 1597 | 11158012 | Aberrant gastric inhibitory polypeptide (GIP) receptor expression in bilaterally hyperplastic adrenals or unilateral adrenal adenomas is a rare form of adrenal hyperfunction. |
| 1598 | 11158012 | In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. |
| 1599 | 11158012 | The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. |
| 1600 | 11158012 | Thus, aberrant expression of the GIP receptor does not exclusively involve cells of a zona fasciculata phenotype, as previously reported, but may also occur in other types of differentiated adrenocortical cells. |
| 1601 | 11158012 | Aberrant gastric inhibitory polypeptide (GIP) receptor expression in bilaterally hyperplastic adrenals or unilateral adrenal adenomas is a rare form of adrenal hyperfunction. |
| 1602 | 11158012 | In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. |
| 1603 | 11158012 | The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. |
| 1604 | 11158012 | Thus, aberrant expression of the GIP receptor does not exclusively involve cells of a zona fasciculata phenotype, as previously reported, but may also occur in other types of differentiated adrenocortical cells. |
| 1605 | 11158012 | Aberrant gastric inhibitory polypeptide (GIP) receptor expression in bilaterally hyperplastic adrenals or unilateral adrenal adenomas is a rare form of adrenal hyperfunction. |
| 1606 | 11158012 | In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. |
| 1607 | 11158012 | The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. |
| 1608 | 11158012 | Thus, aberrant expression of the GIP receptor does not exclusively involve cells of a zona fasciculata phenotype, as previously reported, but may also occur in other types of differentiated adrenocortical cells. |
| 1609 | 11181530 | Tissue levels of GLP-1 and plasma insulin and glucagon levels were not different between the two groups. |
| 1610 | 11181530 | Preexposure to oleic acid but not to palmitic acid significantly increased GIP-induced GLP-1 secretion when compared with controls (55 +/- 12% vs. 34 +/- 9%, P < 0.01). |
| 1611 | 11246881 | AUC(INT) for GLP-1 averaged 48 +/- 2% (for patients) versus 51 +/- 5% (for control subjects) of AUC(TOT). |
| 1612 | 11246881 | The measurement of intact incretin hormones revealed that total as well as intact GIP responses were minimally decreased in patients with type 2 diabetes, whereas the late intact GLP-1 response was strongly reduced, supporting the hypothesis that an impaired function of GLP-1 as a transmitter in the enteroinsular axis contributes to the inappropriate insulin secretion in type 2 diabetes. |
| 1613 | 11284388 | In addition to, but independent of its serine type catalytic activity, DPPIV binds closely to the soluble extracellular enzyme adenosine deaminase. |
| 1614 | 11284388 | Other known substrates which are subject in vitro to receptor-specific changes induced by DPPIV truncation include neuropeptides such as substance P, peptidE YY and neuropeptide Y. |
| 1615 | 11284388 | On the other hand, DPPIV mediated cleavage of the N-terminal His-Ala or Tyr-Ala dipeptides from circulating incretin hormones like, glucagon-like peptides (GLP)-1 and -2, gastric inhibitory polypeptide (GIP), all members of the enteroglucagon/GRF superfamily, results in their biological inactivation in vitro and in vivo. |
| 1616 | 11284388 | Administration of specific DPPIV inhibitors closes this pathway of incretin degradation and greatly enhances insulin secretion. |
| 1617 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1618 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1619 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1620 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1621 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1622 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1623 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1624 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1625 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1626 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1627 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1628 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1629 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1630 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1631 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1632 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1633 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1634 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1635 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1636 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1637 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1638 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1639 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1640 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1641 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1642 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1643 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1644 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1645 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1646 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1647 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1648 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1649 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1650 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1651 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1652 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1653 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1654 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1655 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1656 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1657 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1658 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1659 | 11334402 | Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone that is released postprandially from the small intestine and acts in concert with glucagon-like peptide (GLP)-1 to potentiate glucose-induced insulin secretion from the pancreatic beta-cell. |
| 1660 | 11334402 | In type 2 diabetes, there is a decreased responsiveness of the pancreas to GIP; however, the insulin response to GLP-1 remains intact. |
| 1661 | 11334402 | The literature suggests that the ineffectiveness of GIP in type 2 diabetes may be a result of chronic homologous desensitization of the GIP receptor. |
| 1662 | 11334402 | The hypothesis of the present study is that one cause of decreased responsiveness to GIP in type 2 diabetes is an inappropriate expression of the GIP receptor in the pancreatic islet. |
| 1663 | 11334402 | GIP also potently stimulated first-phase insulin secretion from isolated perifused islets (10.3 +/- 3.0 x basal), and GIP and GLP-1 potentiated insulin secretion from the perfused pancreas (6 x control area under the curve [AUC]) from lean animals. |
| 1664 | 11334402 | GIP yielded no significant effect in the Vancouver diabetic fatty Zucker (VDF) rat pancreases, whereas GLP-1 elicited an eightfold increase of insulin secretion from the perfused VDF pancreas. |
| 1665 | 11334402 | Finally, the expression of both GIP receptor mRNA and protein was decreased in islets from VDF rats. |
| 1666 | 11334405 | The preabsorptive insulin response was not accompanied by any increase in circulating levels of gastric inhibitory polypeptide (GIP) or glucagon-like peptide 1 (GLP-1). |
| 1667 | 11334405 | In conclusion, 1) the early preabsorptive insulin response to meal ingestion in humans can be largely attributed to autonomic activation mediated by noncholinergic and cholinergic mechanisms, 2) this cephalic insulin response is required for a normal postprandial glucose tolerance, and 3) GIP and GLP-1 do not contribute to the preabsorptive cephalic phase insulin response to meal ingestion. |
| 1668 | 11334405 | The preabsorptive insulin response was not accompanied by any increase in circulating levels of gastric inhibitory polypeptide (GIP) or glucagon-like peptide 1 (GLP-1). |
| 1669 | 11334405 | In conclusion, 1) the early preabsorptive insulin response to meal ingestion in humans can be largely attributed to autonomic activation mediated by noncholinergic and cholinergic mechanisms, 2) this cephalic insulin response is required for a normal postprandial glucose tolerance, and 3) GIP and GLP-1 do not contribute to the preabsorptive cephalic phase insulin response to meal ingestion. |
| 1670 | 11343800 | Due to the requirement for an elevated glucose concentration for activity, the incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1, have potential in the treatment of non-insulin-dependent diabetes mellitus. |
| 1671 | 11343800 | Peptides were screened for stimulation of cyclic AMP (cAMP) accumulation in Chinese hamster ovary cells transfected with the rat islet GIP receptor. |
| 1672 | 11343800 | Competitive-binding displacement studies indicated that these peptides were low-affinity ligands for the GIP receptor. |
| 1673 | 11343800 | Intravenous infusion of GIP(1-42) (1 pmol/min/100 g) with a concurrent intraperitoneal glucose load (1 g/kg) significantly reduced circulating blood glucose excursions through stimulation of insulin release. |
| 1674 | 11343800 | Due to the requirement for an elevated glucose concentration for activity, the incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1, have potential in the treatment of non-insulin-dependent diabetes mellitus. |
| 1675 | 11343800 | Peptides were screened for stimulation of cyclic AMP (cAMP) accumulation in Chinese hamster ovary cells transfected with the rat islet GIP receptor. |
| 1676 | 11343800 | Competitive-binding displacement studies indicated that these peptides were low-affinity ligands for the GIP receptor. |
| 1677 | 11343800 | Intravenous infusion of GIP(1-42) (1 pmol/min/100 g) with a concurrent intraperitoneal glucose load (1 g/kg) significantly reduced circulating blood glucose excursions through stimulation of insulin release. |
| 1678 | 11343800 | Due to the requirement for an elevated glucose concentration for activity, the incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1, have potential in the treatment of non-insulin-dependent diabetes mellitus. |
| 1679 | 11343800 | Peptides were screened for stimulation of cyclic AMP (cAMP) accumulation in Chinese hamster ovary cells transfected with the rat islet GIP receptor. |
| 1680 | 11343800 | Competitive-binding displacement studies indicated that these peptides were low-affinity ligands for the GIP receptor. |
| 1681 | 11343800 | Intravenous infusion of GIP(1-42) (1 pmol/min/100 g) with a concurrent intraperitoneal glucose load (1 g/kg) significantly reduced circulating blood glucose excursions through stimulation of insulin release. |
| 1682 | 11343800 | Due to the requirement for an elevated glucose concentration for activity, the incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1, have potential in the treatment of non-insulin-dependent diabetes mellitus. |
| 1683 | 11343800 | Peptides were screened for stimulation of cyclic AMP (cAMP) accumulation in Chinese hamster ovary cells transfected with the rat islet GIP receptor. |
| 1684 | 11343800 | Competitive-binding displacement studies indicated that these peptides were low-affinity ligands for the GIP receptor. |
| 1685 | 11343800 | Intravenous infusion of GIP(1-42) (1 pmol/min/100 g) with a concurrent intraperitoneal glucose load (1 g/kg) significantly reduced circulating blood glucose excursions through stimulation of insulin release. |
| 1686 | 11460578 | Of the known gut hormones only gastric inhibitory polypeptide (GIP) and glucagon-like polypeptide-1 (GLP-1 [7-36] amide) fulfill this definition. |
| 1687 | 11460578 | --The incretin effect (i.e. the ratio between the integrated insulin response to an oral glucose load and an isoglycaemic intravenous glucose infusion) is markedly diminished in patients with type 2 diabetes mellitus, while the plasma levels of GIP and GLP-1 and their responses to nutrients are in the normal range. |
| 1688 | 11460578 | This insensitivity of the diabetic B-cells towards incretins can be overcome by supraphysiological (pharmacological) concentrations of GLP-1 [7-36], however not of GIP. |
| 1689 | 11460578 | At present methods are being developed to improve the pharmacokinetics of GLP-1 by inhibition of the cleaving enzyme dipeptidyl peptidase IV (DPP-IV) or by synthesis of DPP-IV resistant GLP-1 analogues. |
| 1690 | 11460578 | Of the known gut hormones only gastric inhibitory polypeptide (GIP) and glucagon-like polypeptide-1 (GLP-1 [7-36] amide) fulfill this definition. |
| 1691 | 11460578 | --The incretin effect (i.e. the ratio between the integrated insulin response to an oral glucose load and an isoglycaemic intravenous glucose infusion) is markedly diminished in patients with type 2 diabetes mellitus, while the plasma levels of GIP and GLP-1 and their responses to nutrients are in the normal range. |
| 1692 | 11460578 | This insensitivity of the diabetic B-cells towards incretins can be overcome by supraphysiological (pharmacological) concentrations of GLP-1 [7-36], however not of GIP. |
| 1693 | 11460578 | At present methods are being developed to improve the pharmacokinetics of GLP-1 by inhibition of the cleaving enzyme dipeptidyl peptidase IV (DPP-IV) or by synthesis of DPP-IV resistant GLP-1 analogues. |
| 1694 | 11460578 | Of the known gut hormones only gastric inhibitory polypeptide (GIP) and glucagon-like polypeptide-1 (GLP-1 [7-36] amide) fulfill this definition. |
| 1695 | 11460578 | --The incretin effect (i.e. the ratio between the integrated insulin response to an oral glucose load and an isoglycaemic intravenous glucose infusion) is markedly diminished in patients with type 2 diabetes mellitus, while the plasma levels of GIP and GLP-1 and their responses to nutrients are in the normal range. |
| 1696 | 11460578 | This insensitivity of the diabetic B-cells towards incretins can be overcome by supraphysiological (pharmacological) concentrations of GLP-1 [7-36], however not of GIP. |
| 1697 | 11460578 | At present methods are being developed to improve the pharmacokinetics of GLP-1 by inhibition of the cleaving enzyme dipeptidyl peptidase IV (DPP-IV) or by synthesis of DPP-IV resistant GLP-1 analogues. |
| 1698 | 11502801 | To elucidate the causes of the diminished incretin effect in type 2 diabetes mellitus we investigated the secretion of the incretin hormones, glucagon-like peptide-1 and glucose- dependent insulinotropic polypeptide and measured nonesterified fatty acids, and plasma concentrations of insulin, C peptide, pancreatic polypeptide, and glucose during a 4-h mixed meal test in 54 heterogeneous type 2 diabetic patients, 33 matched control subjects with normal glucose tolerance, and 15 unmatched subjects with impaired glucose tolerance. |
| 1699 | 11502801 | In a multiple regression analysis, a model with diabetes, body mass index, male sex, insulin area under the curve (negative influence), glucose-dependent insulinotropic polypeptide area under the curve (negative influence), and glucagon area under the curve (positive influence) explained 42% of the variability of the glucagon-like peptide-1 response. |
| 1700 | 11502801 | To elucidate the causes of the diminished incretin effect in type 2 diabetes mellitus we investigated the secretion of the incretin hormones, glucagon-like peptide-1 and glucose- dependent insulinotropic polypeptide and measured nonesterified fatty acids, and plasma concentrations of insulin, C peptide, pancreatic polypeptide, and glucose during a 4-h mixed meal test in 54 heterogeneous type 2 diabetic patients, 33 matched control subjects with normal glucose tolerance, and 15 unmatched subjects with impaired glucose tolerance. |
| 1701 | 11502801 | In a multiple regression analysis, a model with diabetes, body mass index, male sex, insulin area under the curve (negative influence), glucose-dependent insulinotropic polypeptide area under the curve (negative influence), and glucagon area under the curve (positive influence) explained 42% of the variability of the glucagon-like peptide-1 response. |
| 1702 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1703 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1704 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1705 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1706 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1707 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1708 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1709 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1710 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1711 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1712 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1713 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1714 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1715 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1716 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1717 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1718 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1719 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1720 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1721 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1722 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1723 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1724 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1725 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1726 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1727 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1728 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1729 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1730 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1731 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1732 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1733 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1734 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1735 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1736 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1737 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1738 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1739 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1740 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1741 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1742 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1743 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1744 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1745 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1746 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1747 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1748 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1749 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1750 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1751 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1752 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1753 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1754 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1755 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1756 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1757 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1758 | 11518806 | Glucose-dependent insulinotropic polypeptide is a growth factor for beta (INS-1) cells by pleiotropic signaling. |
| 1759 | 11518806 | Activation of the G-protein-coupled receptor for glucose-dependent insulinotropic polypeptide facilitates insulin-release from pancreatic beta-cells. |
| 1760 | 11518806 | In the present study, we examined whether glucose-dependent insulinotropic polypeptide also acts as a growth factor for the beta-cell line INS-1. |
| 1761 | 11518806 | Glucose-dependent insulinotropic polypeptide stimulated the signaling modules of PKA/cAMP regulatory element binder, MAPK, and PI3K/protein kinase B in a glucose- and dose-dependent manner. |
| 1762 | 11518806 | Janus kinase 2 and signal transducer and activators of transcription 5/6 pathways were not stimulated by glucose-dependent insulinotropic polypeptide. |
| 1763 | 11518806 | Activation of PI3K by glucose-dependent insulinotropic polypeptide and glucose was associated with insulin receptor substrate isoforms insulin receptor substrate-2 and growth factor bound-2 associated binder-1 and PI3K isoforms p85alpha, p110alpha, p110beta, and p110gamma. |
| 1764 | 11518806 | Downstream of PI3K, glucose-dependent insulinotropic polypeptide-stimulated protein kinase Balpha and protein kinase Bbeta isoforms and phosphorylated glycogen synthase kinase-3, forkhead transcription factor FKHR, and p70S6K. |
| 1765 | 11518806 | These data indicate that glucose-dependent insulinotropic polypeptide functions synergistically with glucose as a pleiotropic growth factor for insulin-producing beta-cells, which may play a role for metabolic adaptations of insulin-producing cells during type II diabetes. |
| 1766 | 11522498 | There was a small but significant increase in postprandial cholecystokinin (CCK) in responders, and fasting gastric inhibitory peptide (GIP) levels were significantly increased in responders and all patients after treatment. |
| 1767 | 11679427 | With exogenous GIP, patients with type 2 diabetes responded with a lower increment (Delta) in insulin (P = 0.0003) and C-peptide concentrations (P < 0.0001) than control subjects. |
| 1768 | 11679427 | The GIP effects in first-degree relatives were diminished compared with control subjects (Delta insulin: P = 0.04; Delta C-peptide: P = 0.016) but significantly higher than in patients with type 2 diabetes (P < or = 0.05). |
| 1769 | 11679427 | With exogenous GIP, patients with type 2 diabetes responded with a lower increment (Delta) in insulin (P = 0.0003) and C-peptide concentrations (P < 0.0001) than control subjects. |
| 1770 | 11679427 | The GIP effects in first-degree relatives were diminished compared with control subjects (Delta insulin: P = 0.04; Delta C-peptide: P = 0.016) but significantly higher than in patients with type 2 diabetes (P < or = 0.05). |
| 1771 | 11697865 | We observed an increased mRNA expression of insulin, proendocrine gene neurogenin 3, and beta-cell transcription factor Pdx1 when the cells were grown on bovine collagen I gels. |
| 1772 | 11697865 | Application of GIP, GLP-1 derivative NN2211, and activin-A/betacellulin to IMPAN cells in normal culture did not lead to endocrine differentiation. |
| 1773 | 11713984 | To day it is well established that the most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP, previously known as gastric inhibitory polypeptide) and glucagon-like peptide-1 (GLP-1) from the upper and lower small intestinal mucosa, respectively. |
| 1774 | 11713984 | The reason for this seems to be twofold: an impaired secretion of GLP-1 and a severely impaired insulinotropic effect of GIP in these patients. |
| 1775 | 11713984 | To day it is well established that the most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP, previously known as gastric inhibitory polypeptide) and glucagon-like peptide-1 (GLP-1) from the upper and lower small intestinal mucosa, respectively. |
| 1776 | 11713984 | The reason for this seems to be twofold: an impaired secretion of GLP-1 and a severely impaired insulinotropic effect of GIP in these patients. |
| 1777 | 11820780 | In CHL cells expressing the human GIP receptor, (Pro(3))GIP antagonized the cyclic adenosine monophosphate (cAMP) stimulatory ability of 10(-7) M native GIP, with an IC(50) value of 2.6 microM. |
| 1778 | 11820780 | In the clonal pancreatic beta cell line BRIN-BD11, (Pro(3))GIP over the concentration range 10(-13) to 10(-8) M dose dependently inhibited GIP-stimulated (10(-7) M) insulin release (1.2- to 1.7-fold; P < 0.05 to P < 0.001). |
| 1779 | 11820780 | In obese diabetic (ob/ob) mice, intraperitoneal administration of (Pro(3))GIP (25 nmol/kg body wt) countered the ability of native GIP to stimulate plasma insulin (2.4-fold decrease; P < 0.001) and lower the glycemic excursion (1.5-fold decrease; P < 0.001) induced by a glucose load (18 mmol/kg body wt). |
| 1780 | 11820780 | Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. |
| 1781 | 11820780 | In CHL cells expressing the human GIP receptor, (Pro(3))GIP antagonized the cyclic adenosine monophosphate (cAMP) stimulatory ability of 10(-7) M native GIP, with an IC(50) value of 2.6 microM. |
| 1782 | 11820780 | In the clonal pancreatic beta cell line BRIN-BD11, (Pro(3))GIP over the concentration range 10(-13) to 10(-8) M dose dependently inhibited GIP-stimulated (10(-7) M) insulin release (1.2- to 1.7-fold; P < 0.05 to P < 0.001). |
| 1783 | 11820780 | In obese diabetic (ob/ob) mice, intraperitoneal administration of (Pro(3))GIP (25 nmol/kg body wt) countered the ability of native GIP to stimulate plasma insulin (2.4-fold decrease; P < 0.001) and lower the glycemic excursion (1.5-fold decrease; P < 0.001) induced by a glucose load (18 mmol/kg body wt). |
| 1784 | 11820780 | Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. |
| 1785 | 11820780 | In CHL cells expressing the human GIP receptor, (Pro(3))GIP antagonized the cyclic adenosine monophosphate (cAMP) stimulatory ability of 10(-7) M native GIP, with an IC(50) value of 2.6 microM. |
| 1786 | 11820780 | In the clonal pancreatic beta cell line BRIN-BD11, (Pro(3))GIP over the concentration range 10(-13) to 10(-8) M dose dependently inhibited GIP-stimulated (10(-7) M) insulin release (1.2- to 1.7-fold; P < 0.05 to P < 0.001). |
| 1787 | 11820780 | In obese diabetic (ob/ob) mice, intraperitoneal administration of (Pro(3))GIP (25 nmol/kg body wt) countered the ability of native GIP to stimulate plasma insulin (2.4-fold decrease; P < 0.001) and lower the glycemic excursion (1.5-fold decrease; P < 0.001) induced by a glucose load (18 mmol/kg body wt). |
| 1788 | 11820780 | Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. |
| 1789 | 11820780 | In CHL cells expressing the human GIP receptor, (Pro(3))GIP antagonized the cyclic adenosine monophosphate (cAMP) stimulatory ability of 10(-7) M native GIP, with an IC(50) value of 2.6 microM. |
| 1790 | 11820780 | In the clonal pancreatic beta cell line BRIN-BD11, (Pro(3))GIP over the concentration range 10(-13) to 10(-8) M dose dependently inhibited GIP-stimulated (10(-7) M) insulin release (1.2- to 1.7-fold; P < 0.05 to P < 0.001). |
| 1791 | 11820780 | In obese diabetic (ob/ob) mice, intraperitoneal administration of (Pro(3))GIP (25 nmol/kg body wt) countered the ability of native GIP to stimulate plasma insulin (2.4-fold decrease; P < 0.001) and lower the glycemic excursion (1.5-fold decrease; P < 0.001) induced by a glucose load (18 mmol/kg body wt). |
| 1792 | 11820780 | Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. |
| 1793 | 11855690 | The glucose intolerance of ageing may be due, in part, to decreased insulin sensitivity of pancreatic / cells to insulinotropic gut hormones (GLP1/GIP) and in part to alterations of hepatic glucose production. |
| 1794 | 11872663 | A series of synthetic GIP peptides modified at the NH(2)-terminus were screened in vitro for resistance to dipeptidyl peptidase IV (DP IV) degradation and potency to stimulate cyclic AMP and affinity for the transfected rat GIP receptor. |
| 1795 | 11872663 | , or fa/fa Vancouver Diabetic Fatty (VDF) Zucker rats, both GIP and [D-Ala(2)]GIP significantly reduced glycemic excursions during a concurrent oral glucose tolerance test via stimulation of insulin release. |
| 1796 | 11872663 | A series of synthetic GIP peptides modified at the NH(2)-terminus were screened in vitro for resistance to dipeptidyl peptidase IV (DP IV) degradation and potency to stimulate cyclic AMP and affinity for the transfected rat GIP receptor. |
| 1797 | 11872663 | , or fa/fa Vancouver Diabetic Fatty (VDF) Zucker rats, both GIP and [D-Ala(2)]GIP significantly reduced glycemic excursions during a concurrent oral glucose tolerance test via stimulation of insulin release. |
| 1798 | 11916911 | The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are responsible for >50% of nutrient-stimulated insulin secretion. |
| 1799 | 11916911 | After being released into the circulation, GIP and GLP-1 are rapidly inactivated by the circulating enzyme dipeptidyl peptidase IV (DP IV). |
| 1800 | 11916911 | The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are responsible for >50% of nutrient-stimulated insulin secretion. |
| 1801 | 11916911 | After being released into the circulation, GIP and GLP-1 are rapidly inactivated by the circulating enzyme dipeptidyl peptidase IV (DP IV). |
| 1802 | 12068290 | Wild-type mice fed a high-fat diet exhibited both hypersecretion of GIP and extreme visceral and subcutaneous fat deposition with insulin resistance. |
| 1803 | 12068290 | In contrast, mice lacking the GIP receptor (Gipr(-/-)) fed a high-fat diet were clearly protected from both the obesity and the insulin resistance. |
| 1804 | 12068290 | Moreover, double-homozygous mice (Gipr(-/-), Lep(ob)/Lep(ob)) generated by crossbreeding Gipr(-/-) and obese ob/ob (Lep(ob)/Lep(ob)) mice gained less weight and had lower adiposity than Lep(ob)/Lep(ob) mice. |
| 1805 | 12068290 | Wild-type mice fed a high-fat diet exhibited both hypersecretion of GIP and extreme visceral and subcutaneous fat deposition with insulin resistance. |
| 1806 | 12068290 | In contrast, mice lacking the GIP receptor (Gipr(-/-)) fed a high-fat diet were clearly protected from both the obesity and the insulin resistance. |
| 1807 | 12068290 | Moreover, double-homozygous mice (Gipr(-/-), Lep(ob)/Lep(ob)) generated by crossbreeding Gipr(-/-) and obese ob/ob (Lep(ob)/Lep(ob)) mice gained less weight and had lower adiposity than Lep(ob)/Lep(ob) mice. |
| 1808 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1809 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1810 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1811 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1812 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1813 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1814 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1815 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1816 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1817 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1818 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1819 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1820 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1821 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1822 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1823 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1824 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1825 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1826 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1827 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1828 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1829 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1830 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1831 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1832 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1833 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1834 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1835 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1836 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1837 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1838 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1839 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1840 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1841 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1842 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1843 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1844 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1845 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1846 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1847 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1848 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1849 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1850 | 12102645 | Gastric inhibitory polypeptide analogues: do they have a therapeutic role in diabetes mellitus similar to that of glucagon-like Peptide-1? |
| 1851 | 12102645 | Gastric inhibitory polypeptide (GIP, also called glucose-dependent insulinotropic polypeptide) and glucagon-like peptide-1 (GLP-1) are peptide hormones from the gut that enhance nutrient-stimulated insulin secretion (the 'incretin' effect). |
| 1852 | 12102645 | Judging from experiments in mice with targeted deletions of GIP and GLP-1 receptors, the incretin effect is essential for normal glucose tolerance. |
| 1853 | 12102645 | The explanation seems to be that both the secretion of GLP-1 and the effect of GIP are impaired (whereas both the secretion of GIP and the effect of GLP-1 are near normal). |
| 1854 | 12102645 | The known genetic variations in the GIP receptor sequence are not associated with type 2 diabetes mellitus, but a defective insulinotropic effect of GIP may be found in first degree relatives of the patients, suggesting a genetic background for the defect. |
| 1855 | 12102645 | Whereas GLP-1 and its analogues are attractive as therapeutic agents for type 2 diabetes mellitus, analogues of GIP are unlikely to be effective. |
| 1856 | 12102645 | On the other hand, GIP seems to play an important role in lipid metabolism, promoting the disposal of ingested lipids, and mice with a targeted deletion of the GIP receptor do not become obese when exposed to a high-fat diet. |
| 1857 | 12137960 | This so-called "incretin effect" is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). |
| 1858 | 12137960 | In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. |
| 1859 | 12137960 | However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. |
| 1860 | 12137960 | This so-called "incretin effect" is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). |
| 1861 | 12137960 | In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. |
| 1862 | 12137960 | However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. |
| 1863 | 12137960 | This so-called "incretin effect" is primarily conferred by Glucagon-like peptide 1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). |
| 1864 | 12137960 | In contrast to GLP-1, GIP has lost most of its insulinotropic effect in type 2 diabetic patients. |
| 1865 | 12137960 | However, the physiological importance of GIP in the regulation of insulin secretion has been shown to even exceed that of GLP-1. |
| 1866 | 12145765 | To investigate the relative effects of fructose and glucose on blood glucose, plasma insulin and incretin (glucagon-like peptide-1 [GLP-1] and gastric inhibitory peptide [GIP]) concentrations, and acute food intake, 10 (6 men, 4 women) patients with diet-controlled type 2 diabetes (diabetic) (44 to 71 years) and 10 age and body mass index (BMI)-matched (6 men, 4 women) nondiabetic, control subjects with varying degrees of glucose tolerance (nondiabetic), were studied on 3 days. |
| 1867 | 12150711 | Enhanced cAMP generation and insulin-releasing potency of two novel Tyr1-modified enzyme-resistant forms of glucose-dependent insulinotropic polypeptide is associated with significant antihyperglycaemic activity in spontaneous obesity-diabetes. |
| 1868 | 12150711 | Glucose-dependent insulinotropic polypeptide (GIP) is an important incretin hormone, which potentiates glucose-induced insulin secretion. |
| 1869 | 12150711 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, both analogues exhibited a 2-fold increase in cAMP-generating potency compared with native GIP (EC(50) values of 9.4, 10.0 and 18.2 nM respectively). |
| 1870 | 12150711 | This was associated with a significantly greater AUC for insulin (2.1-fold; P <0.001) for both analogues compared with native GIP. |
| 1871 | 12150711 | Enhanced cAMP generation and insulin-releasing potency of two novel Tyr1-modified enzyme-resistant forms of glucose-dependent insulinotropic polypeptide is associated with significant antihyperglycaemic activity in spontaneous obesity-diabetes. |
| 1872 | 12150711 | Glucose-dependent insulinotropic polypeptide (GIP) is an important incretin hormone, which potentiates glucose-induced insulin secretion. |
| 1873 | 12150711 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, both analogues exhibited a 2-fold increase in cAMP-generating potency compared with native GIP (EC(50) values of 9.4, 10.0 and 18.2 nM respectively). |
| 1874 | 12150711 | This was associated with a significantly greater AUC for insulin (2.1-fold; P <0.001) for both analogues compared with native GIP. |
| 1875 | 12150711 | Enhanced cAMP generation and insulin-releasing potency of two novel Tyr1-modified enzyme-resistant forms of glucose-dependent insulinotropic polypeptide is associated with significant antihyperglycaemic activity in spontaneous obesity-diabetes. |
| 1876 | 12150711 | Glucose-dependent insulinotropic polypeptide (GIP) is an important incretin hormone, which potentiates glucose-induced insulin secretion. |
| 1877 | 12150711 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, both analogues exhibited a 2-fold increase in cAMP-generating potency compared with native GIP (EC(50) values of 9.4, 10.0 and 18.2 nM respectively). |
| 1878 | 12150711 | This was associated with a significantly greater AUC for insulin (2.1-fold; P <0.001) for both analogues compared with native GIP. |
| 1879 | 12150711 | Enhanced cAMP generation and insulin-releasing potency of two novel Tyr1-modified enzyme-resistant forms of glucose-dependent insulinotropic polypeptide is associated with significant antihyperglycaemic activity in spontaneous obesity-diabetes. |
| 1880 | 12150711 | Glucose-dependent insulinotropic polypeptide (GIP) is an important incretin hormone, which potentiates glucose-induced insulin secretion. |
| 1881 | 12150711 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, both analogues exhibited a 2-fold increase in cAMP-generating potency compared with native GIP (EC(50) values of 9.4, 10.0 and 18.2 nM respectively). |
| 1882 | 12150711 | This was associated with a significantly greater AUC for insulin (2.1-fold; P <0.001) for both analogues compared with native GIP. |
| 1883 | 12196458 | Upon release into circulation, the potent insulin secretagogues glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are rapidly cleaved and inactivated by the enzyme dipeptidyl peptidase IV (DP IV). |
| 1884 | 12196458 | Long-term administration of specific DP IV inhibitors, so as to enhance circulating active GIP and GLP-1 levels, has been shown to improve glucose tolerance and beta-cell glucose responsiveness and to reduce hyperinsulinemia in the Vancouver diabetic fatty (VDF) rat model of type 2 diabetes. |
| 1885 | 12196458 | Upon release into circulation, the potent insulin secretagogues glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are rapidly cleaved and inactivated by the enzyme dipeptidyl peptidase IV (DP IV). |
| 1886 | 12196458 | Long-term administration of specific DP IV inhibitors, so as to enhance circulating active GIP and GLP-1 levels, has been shown to improve glucose tolerance and beta-cell glucose responsiveness and to reduce hyperinsulinemia in the Vancouver diabetic fatty (VDF) rat model of type 2 diabetes. |
| 1887 | 12242461 | Improved stability, insulin-releasing activity and antidiabetic potential of two novel N-terminal analogues of gastric inhibitory polypeptide: N-acetyl-GIP and pGlu-GIP. |
| 1888 | 12369712 | Role of protein kinase C, PI3-kinase and tyrosine kinase in activation of MAP kinase by glucose and agonists of G-protein coupled receptors in INS-1 cells. |
| 1889 | 12369712 | The interplay of protein kinase C (PKC), PI3-kinase and cellular tyrosine kinase with MAP kinase activity using inhibitors and compounds such as glucose, phorbol 12-myristate 13-acetate (PMA) and agonists of G-protein coupled receptors like gastrin releasing peptide (GRP), oxytocin (OT) and glucose-dependent insulinotropic peptide (GIP) was investigated in INS-1 cells, an insulin secreting cell line. |
| 1890 | 12369712 | MAP kinase activity was determined by using a peptide derived from the EGF receptor as a MAP kinase substrate and [32P]ATP. |
| 1891 | 12369712 | Glucose as well as GRP, OT and GIP exhibited a time-dependent increase in MAP kinase activity with a maximum at time point 2.5 min. |
| 1892 | 12369712 | The flavone PD 098059 is known to bind to the inactive forms of MEK1 (MAPK/ERK-Kinase) thus preventing activation by upstream activators. 20 microM PD 098059 (IC50 = 5 microM) inhibited MAP kinase stimulated by either glucose, GRP, OT, GIP or PMA. |
| 1893 | 12369712 | Inhibiton ("downregulation") of PKC by a long term (22 h) pretreatment with 1 microM PMA did not influence MAP kinase activity when augmented by either of the above mentioned compound. |
| 1894 | 12369712 | To investigate whether PI3-kinase and cellular tyrosine kinase are involved in G-protein mediated effects on MAP kinase, inhibitors were used: 100 nM wortmannin (PI3-kinase inhibitor) reduced the effects of GRP, OT and GIP but not that of PMA; 100 microM genistein (tyrosine kinase inhibitor) inhibited the stimulatory effect of either above mentioned compound on MAP kinase activation. |
| 1895 | 12369712 | Inhibition of MAP kinase by 20 microM PD 098059 did not influence insulin secretion modulated by either compound (glucose, GRP, OT or GIP). [3H]Thymidine incorporation, however, was severely inhibited by PD 098059. |
| 1896 | 12369712 | Thus MAP kinase is important for INS-1 cell proliferation but not for its insulin secretory response with respect to major initiators and modulators of insulin release. |
| 1897 | 12369712 | The data indicate that MAP kinase is active and under the control of MAP kinase. |
| 1898 | 12369712 | PKC is upstream of a genistein-sensitive tyrosine kinase and probably downstream of a PI3-kinase in INS-1 cells. |
| 1899 | 12475913 | A novel pathway for regulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta cells. |
| 1900 | 12475913 | Glucose-dependent insulinotropic polypeptide (GIP) is secreted postprandially and acts in concert with glucose to stimulate insulin secretion from the pancreas. |
| 1901 | 12475913 | Here, we describe a novel pathway for the regulation of GIP receptor (GIPR) expression within clonal beta-cell lines, pancreatic islets, and in vivo. |
| 1902 | 12475913 | High (25 mM) glucose was able to significantly reduce GIPR mRNA levels in INS(832/13) cells after only 6 h. |
| 1903 | 12475913 | In contrast, palmitic acid (2 mM) and WY 14643 (100 microM) stimulated approximate doublings of GIPR expression in INS(832/13) cells under low (5.5 mM), but not high (25 mM), glucose conditions, suggesting that fat can regulate GIPR expression via PPARalpha in a glucose-dependent manner. |
| 1904 | 12475913 | Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. |
| 1905 | 12475913 | Finally, in hyperglycemic clamped rats, there was a 70% reduction in GIPR expression in the islets and a 71% reduction in GIP-stimulated insulin secretion from the perfused pancreas. |
| 1906 | 12475913 | Thus, evidence is presented that the GIPR is controlled at normoglycemia by the fatty acid load on the islet; however, when exposed to hyperglycemic conditions, the GIPR is down-regulated, which may contribute to the decreased responsiveness to GIP that is observed in type 2 diabetes. |
| 1907 | 12475913 | A novel pathway for regulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta cells. |
| 1908 | 12475913 | Glucose-dependent insulinotropic polypeptide (GIP) is secreted postprandially and acts in concert with glucose to stimulate insulin secretion from the pancreas. |
| 1909 | 12475913 | Here, we describe a novel pathway for the regulation of GIP receptor (GIPR) expression within clonal beta-cell lines, pancreatic islets, and in vivo. |
| 1910 | 12475913 | High (25 mM) glucose was able to significantly reduce GIPR mRNA levels in INS(832/13) cells after only 6 h. |
| 1911 | 12475913 | In contrast, palmitic acid (2 mM) and WY 14643 (100 microM) stimulated approximate doublings of GIPR expression in INS(832/13) cells under low (5.5 mM), but not high (25 mM), glucose conditions, suggesting that fat can regulate GIPR expression via PPARalpha in a glucose-dependent manner. |
| 1912 | 12475913 | Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. |
| 1913 | 12475913 | Finally, in hyperglycemic clamped rats, there was a 70% reduction in GIPR expression in the islets and a 71% reduction in GIP-stimulated insulin secretion from the perfused pancreas. |
| 1914 | 12475913 | Thus, evidence is presented that the GIPR is controlled at normoglycemia by the fatty acid load on the islet; however, when exposed to hyperglycemic conditions, the GIPR is down-regulated, which may contribute to the decreased responsiveness to GIP that is observed in type 2 diabetes. |
| 1915 | 12475913 | A novel pathway for regulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta cells. |
| 1916 | 12475913 | Glucose-dependent insulinotropic polypeptide (GIP) is secreted postprandially and acts in concert with glucose to stimulate insulin secretion from the pancreas. |
| 1917 | 12475913 | Here, we describe a novel pathway for the regulation of GIP receptor (GIPR) expression within clonal beta-cell lines, pancreatic islets, and in vivo. |
| 1918 | 12475913 | High (25 mM) glucose was able to significantly reduce GIPR mRNA levels in INS(832/13) cells after only 6 h. |
| 1919 | 12475913 | In contrast, palmitic acid (2 mM) and WY 14643 (100 microM) stimulated approximate doublings of GIPR expression in INS(832/13) cells under low (5.5 mM), but not high (25 mM), glucose conditions, suggesting that fat can regulate GIPR expression via PPARalpha in a glucose-dependent manner. |
| 1920 | 12475913 | Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. |
| 1921 | 12475913 | Finally, in hyperglycemic clamped rats, there was a 70% reduction in GIPR expression in the islets and a 71% reduction in GIP-stimulated insulin secretion from the perfused pancreas. |
| 1922 | 12475913 | Thus, evidence is presented that the GIPR is controlled at normoglycemia by the fatty acid load on the islet; however, when exposed to hyperglycemic conditions, the GIPR is down-regulated, which may contribute to the decreased responsiveness to GIP that is observed in type 2 diabetes. |
| 1923 | 12475913 | A novel pathway for regulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta cells. |
| 1924 | 12475913 | Glucose-dependent insulinotropic polypeptide (GIP) is secreted postprandially and acts in concert with glucose to stimulate insulin secretion from the pancreas. |
| 1925 | 12475913 | Here, we describe a novel pathway for the regulation of GIP receptor (GIPR) expression within clonal beta-cell lines, pancreatic islets, and in vivo. |
| 1926 | 12475913 | High (25 mM) glucose was able to significantly reduce GIPR mRNA levels in INS(832/13) cells after only 6 h. |
| 1927 | 12475913 | In contrast, palmitic acid (2 mM) and WY 14643 (100 microM) stimulated approximate doublings of GIPR expression in INS(832/13) cells under low (5.5 mM), but not high (25 mM), glucose conditions, suggesting that fat can regulate GIPR expression via PPARalpha in a glucose-dependent manner. |
| 1928 | 12475913 | Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. |
| 1929 | 12475913 | Finally, in hyperglycemic clamped rats, there was a 70% reduction in GIPR expression in the islets and a 71% reduction in GIP-stimulated insulin secretion from the perfused pancreas. |
| 1930 | 12475913 | Thus, evidence is presented that the GIPR is controlled at normoglycemia by the fatty acid load on the islet; however, when exposed to hyperglycemic conditions, the GIPR is down-regulated, which may contribute to the decreased responsiveness to GIP that is observed in type 2 diabetes. |
| 1931 | 12475913 | A novel pathway for regulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta cells. |
| 1932 | 12475913 | Glucose-dependent insulinotropic polypeptide (GIP) is secreted postprandially and acts in concert with glucose to stimulate insulin secretion from the pancreas. |
| 1933 | 12475913 | Here, we describe a novel pathway for the regulation of GIP receptor (GIPR) expression within clonal beta-cell lines, pancreatic islets, and in vivo. |
| 1934 | 12475913 | High (25 mM) glucose was able to significantly reduce GIPR mRNA levels in INS(832/13) cells after only 6 h. |
| 1935 | 12475913 | In contrast, palmitic acid (2 mM) and WY 14643 (100 microM) stimulated approximate doublings of GIPR expression in INS(832/13) cells under low (5.5 mM), but not high (25 mM), glucose conditions, suggesting that fat can regulate GIPR expression via PPARalpha in a glucose-dependent manner. |
| 1936 | 12475913 | Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. |
| 1937 | 12475913 | Finally, in hyperglycemic clamped rats, there was a 70% reduction in GIPR expression in the islets and a 71% reduction in GIP-stimulated insulin secretion from the perfused pancreas. |
| 1938 | 12475913 | Thus, evidence is presented that the GIPR is controlled at normoglycemia by the fatty acid load on the islet; however, when exposed to hyperglycemic conditions, the GIPR is down-regulated, which may contribute to the decreased responsiveness to GIP that is observed in type 2 diabetes. |
| 1939 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1940 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1941 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1942 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1943 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1944 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1945 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1946 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1947 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1948 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1949 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1950 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1951 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1952 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1953 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1954 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1955 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1956 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1957 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1958 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1959 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1960 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1961 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1962 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1963 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1964 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1965 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1966 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1967 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1968 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1969 | 12525257 | The therapeutic potential of glucagon-like peptide-1 (GLP-1) in improving glycaemic control in diabetes has been widely studied, but the potential beneficial effects of glucose-dependent insulinotropic polypeptide (GIP) have until recently been almost overlooked. |
| 1970 | 12525257 | One of the major problems, however, in exploiting either GIP or GLP-1 as potential therapeutic agents is their short duration of action, due to enzymatic degradation in vivo by dipeptidylpeptidase IV (DPP IV). |
| 1971 | 12525257 | Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. |
| 1972 | 12525257 | In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. |
| 1973 | 12525257 | In the pancreatic BRIN-BD11 beta-cell line, (Gly2)GIP and (Ser2)GIP (10(-8) M) evoked significant increases (1.2- and 1.5-fold respectively; P<0.01 to P<0.001) in insulinotropic activity compared with GIP. |
| 1974 | 12525257 | This enhanced glucose-lowering ability was coupled to a significantly raised (P<0.01) and more protracted insulin response compared with GIP. |
| 1975 | 12540373 | The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. |
| 1976 | 12540373 | Both GLP-1 receptor and GIP receptor knockout mice (GLP-1R(-/-) and GIPR(-/-), respectively) have been generated to investigate the physiological importance of this axis. |
| 1977 | 12540373 | Although reduced GIP action is a component of type 2 diabetes, GIPR-deficient mice exhibit only moderately impaired glucose tolerance. |
| 1978 | 12540373 | Although serum total GLP-1 levels in GIPR knockout mice were unaltered, insulin responses to GLP-1 from pancreas perfusions and static islet incubations were significantly greater (40-60%) in GIPR(-/-) than in wild-type (GIPR(+/+)) mice. |
| 1979 | 12540373 | Pancreatic insulin content and gene expression were reduced in GIPR(-/-) mice compared with GIPR(+/+) mice. |
| 1980 | 12540373 | In conclusion, GIPR(-/-) mice exhibit altered islet structure and topography and increased islet sensitivity to GLP-1 despite a decrease in pancreatic insulin content and gene expression. |
| 1981 | 12540373 | The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. |
| 1982 | 12540373 | Both GLP-1 receptor and GIP receptor knockout mice (GLP-1R(-/-) and GIPR(-/-), respectively) have been generated to investigate the physiological importance of this axis. |
| 1983 | 12540373 | Although reduced GIP action is a component of type 2 diabetes, GIPR-deficient mice exhibit only moderately impaired glucose tolerance. |
| 1984 | 12540373 | Although serum total GLP-1 levels in GIPR knockout mice were unaltered, insulin responses to GLP-1 from pancreas perfusions and static islet incubations were significantly greater (40-60%) in GIPR(-/-) than in wild-type (GIPR(+/+)) mice. |
| 1985 | 12540373 | Pancreatic insulin content and gene expression were reduced in GIPR(-/-) mice compared with GIPR(+/+) mice. |
| 1986 | 12540373 | In conclusion, GIPR(-/-) mice exhibit altered islet structure and topography and increased islet sensitivity to GLP-1 despite a decrease in pancreatic insulin content and gene expression. |
| 1987 | 12540373 | The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. |
| 1988 | 12540373 | Both GLP-1 receptor and GIP receptor knockout mice (GLP-1R(-/-) and GIPR(-/-), respectively) have been generated to investigate the physiological importance of this axis. |
| 1989 | 12540373 | Although reduced GIP action is a component of type 2 diabetes, GIPR-deficient mice exhibit only moderately impaired glucose tolerance. |
| 1990 | 12540373 | Although serum total GLP-1 levels in GIPR knockout mice were unaltered, insulin responses to GLP-1 from pancreas perfusions and static islet incubations were significantly greater (40-60%) in GIPR(-/-) than in wild-type (GIPR(+/+)) mice. |
| 1991 | 12540373 | Pancreatic insulin content and gene expression were reduced in GIPR(-/-) mice compared with GIPR(+/+) mice. |
| 1992 | 12540373 | In conclusion, GIPR(-/-) mice exhibit altered islet structure and topography and increased islet sensitivity to GLP-1 despite a decrease in pancreatic insulin content and gene expression. |
| 1993 | 12602781 | The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay. |
| 1994 | 12602781 | The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls. |
| 1995 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 1996 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 1997 | 12602781 | Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals. |
| 1998 | 12602781 | The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay. |
| 1999 | 12602781 | The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls. |
| 2000 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 2001 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 2002 | 12602781 | Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals. |
| 2003 | 12602781 | The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay. |
| 2004 | 12602781 | The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls. |
| 2005 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 2006 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 2007 | 12602781 | Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals. |
| 2008 | 12606516 | Recent studies into the physiology of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have added stimulation of beta-cell growth, differentiation, and cell survival to well-documented, potent insulinotropic effects. |
| 2009 | 12606516 | We hypothesized that enhancement of the cytoprotective and beta-cell regenerative effects of GIP and GLP-1 might extend the therapeutic potential of DP IV inhibitors to include type 1 diabetes. |
| 2010 | 12606516 | In vitro studies using a beta-(INS-1) cell line showed a dose-dependent prevention of STZ-induced apoptotic cell-death by both GIP and GLP-1, supporting a role for the incretins in eliciting the in vivo results. |
| 2011 | 12606516 | Recent studies into the physiology of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have added stimulation of beta-cell growth, differentiation, and cell survival to well-documented, potent insulinotropic effects. |
| 2012 | 12606516 | We hypothesized that enhancement of the cytoprotective and beta-cell regenerative effects of GIP and GLP-1 might extend the therapeutic potential of DP IV inhibitors to include type 1 diabetes. |
| 2013 | 12606516 | In vitro studies using a beta-(INS-1) cell line showed a dose-dependent prevention of STZ-induced apoptotic cell-death by both GIP and GLP-1, supporting a role for the incretins in eliciting the in vivo results. |
| 2014 | 12606516 | Recent studies into the physiology of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have added stimulation of beta-cell growth, differentiation, and cell survival to well-documented, potent insulinotropic effects. |
| 2015 | 12606516 | We hypothesized that enhancement of the cytoprotective and beta-cell regenerative effects of GIP and GLP-1 might extend the therapeutic potential of DP IV inhibitors to include type 1 diabetes. |
| 2016 | 12606516 | In vitro studies using a beta-(INS-1) cell line showed a dose-dependent prevention of STZ-induced apoptotic cell-death by both GIP and GLP-1, supporting a role for the incretins in eliciting the in vivo results. |
| 2017 | 12628351 | Because of the insulinotropic action of GIP, this hormone has been considered as a potential therapy of type 2 diabetes, where insulin secretion is inadequate. |
| 2018 | 12628351 | However, a recent study using GIP receptor knockout mice suggests that inhibition of GIP signalling might be a new target for anti-obesity drugs. |
| 2019 | 12628351 | Because of the insulinotropic action of GIP, this hormone has been considered as a potential therapy of type 2 diabetes, where insulin secretion is inadequate. |
| 2020 | 12628351 | However, a recent study using GIP receptor knockout mice suggests that inhibition of GIP signalling might be a new target for anti-obesity drugs. |
| 2021 | 12641488 | Glucagon-like peptide 1 and gastric inhibitory polypeptide: potential applications in type 2 diabetes mellitus. |
| 2022 | 12641488 | Although the insulinotropic actions of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) have been known for almost 2 decades, the incretin hormones have not yet become available for clinical application. |
| 2023 | 12641488 | Various analogues of GLP-1 and GIP have been generated in order to achieve resistance to DPP IV degradation. |
| 2024 | 12641488 | The natural GLP-1 receptor agonist exendin-4, found in the saliva of the Gila monster, has a longer biological half-life after subcutaneous injection than GLP-1, and inhibition of DPP IV using, for example, pyrrolidine derivatives provides elevated concentrations of intact, biologically active GIP and GLP-1 endogenously released from the gut. |
| 2025 | 12641488 | Glucagon-like peptide 1 and gastric inhibitory polypeptide: potential applications in type 2 diabetes mellitus. |
| 2026 | 12641488 | Although the insulinotropic actions of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) have been known for almost 2 decades, the incretin hormones have not yet become available for clinical application. |
| 2027 | 12641488 | Various analogues of GLP-1 and GIP have been generated in order to achieve resistance to DPP IV degradation. |
| 2028 | 12641488 | The natural GLP-1 receptor agonist exendin-4, found in the saliva of the Gila monster, has a longer biological half-life after subcutaneous injection than GLP-1, and inhibition of DPP IV using, for example, pyrrolidine derivatives provides elevated concentrations of intact, biologically active GIP and GLP-1 endogenously released from the gut. |
| 2029 | 12641488 | Glucagon-like peptide 1 and gastric inhibitory polypeptide: potential applications in type 2 diabetes mellitus. |
| 2030 | 12641488 | Although the insulinotropic actions of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) have been known for almost 2 decades, the incretin hormones have not yet become available for clinical application. |
| 2031 | 12641488 | Various analogues of GLP-1 and GIP have been generated in order to achieve resistance to DPP IV degradation. |
| 2032 | 12641488 | The natural GLP-1 receptor agonist exendin-4, found in the saliva of the Gila monster, has a longer biological half-life after subcutaneous injection than GLP-1, and inhibition of DPP IV using, for example, pyrrolidine derivatives provides elevated concentrations of intact, biologically active GIP and GLP-1 endogenously released from the gut. |
| 2033 | 12641488 | Glucagon-like peptide 1 and gastric inhibitory polypeptide: potential applications in type 2 diabetes mellitus. |
| 2034 | 12641488 | Although the insulinotropic actions of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) have been known for almost 2 decades, the incretin hormones have not yet become available for clinical application. |
| 2035 | 12641488 | Various analogues of GLP-1 and GIP have been generated in order to achieve resistance to DPP IV degradation. |
| 2036 | 12641488 | The natural GLP-1 receptor agonist exendin-4, found in the saliva of the Gila monster, has a longer biological half-life after subcutaneous injection than GLP-1, and inhibition of DPP IV using, for example, pyrrolidine derivatives provides elevated concentrations of intact, biologically active GIP and GLP-1 endogenously released from the gut. |
| 2037 | 12788877 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones secreted in response to meal ingestion, thereby enhancing postprandial insulin secretion. |
| 2038 | 12788877 | Both in diabetic patients and in healthy subjects, significant increases in GLP-1 and GIP concentrations were seen after ingestion of both meals. |
| 2039 | 12788877 | Both type 1 and type 2 diabetic patients had normal GIP responses, compared with healthy subjects, whereas decreased GLP-1 responses were seen in type 2 diabetic patients, compared with matched obese healthy subjects. |
| 2040 | 12788877 | Increased fasting concentrations of GIP and an early enhanced postprandial GIP response were seen in obese, compared with lean healthy subjects, whereas GLP-1 responses were the same in the two groups. beta-cell sensitivity to glucose, evaluated as the slope of insulin secretion rates vs. plasma glucose concentration, tended to increase in both type 2 diabetic patients (29%, P = 0.19) and obese healthy subjects (22% P = 0.04) during the large meal, compared with the small meal, perhaps reflecting the increased incretin response. |
| 2041 | 12788877 | We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. |
| 2042 | 12788877 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones secreted in response to meal ingestion, thereby enhancing postprandial insulin secretion. |
| 2043 | 12788877 | Both in diabetic patients and in healthy subjects, significant increases in GLP-1 and GIP concentrations were seen after ingestion of both meals. |
| 2044 | 12788877 | Both type 1 and type 2 diabetic patients had normal GIP responses, compared with healthy subjects, whereas decreased GLP-1 responses were seen in type 2 diabetic patients, compared with matched obese healthy subjects. |
| 2045 | 12788877 | Increased fasting concentrations of GIP and an early enhanced postprandial GIP response were seen in obese, compared with lean healthy subjects, whereas GLP-1 responses were the same in the two groups. beta-cell sensitivity to glucose, evaluated as the slope of insulin secretion rates vs. plasma glucose concentration, tended to increase in both type 2 diabetic patients (29%, P = 0.19) and obese healthy subjects (22% P = 0.04) during the large meal, compared with the small meal, perhaps reflecting the increased incretin response. |
| 2046 | 12788877 | We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. |
| 2047 | 12788877 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones secreted in response to meal ingestion, thereby enhancing postprandial insulin secretion. |
| 2048 | 12788877 | Both in diabetic patients and in healthy subjects, significant increases in GLP-1 and GIP concentrations were seen after ingestion of both meals. |
| 2049 | 12788877 | Both type 1 and type 2 diabetic patients had normal GIP responses, compared with healthy subjects, whereas decreased GLP-1 responses were seen in type 2 diabetic patients, compared with matched obese healthy subjects. |
| 2050 | 12788877 | Increased fasting concentrations of GIP and an early enhanced postprandial GIP response were seen in obese, compared with lean healthy subjects, whereas GLP-1 responses were the same in the two groups. beta-cell sensitivity to glucose, evaluated as the slope of insulin secretion rates vs. plasma glucose concentration, tended to increase in both type 2 diabetic patients (29%, P = 0.19) and obese healthy subjects (22% P = 0.04) during the large meal, compared with the small meal, perhaps reflecting the increased incretin response. |
| 2051 | 12788877 | We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. |
| 2052 | 12788877 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones secreted in response to meal ingestion, thereby enhancing postprandial insulin secretion. |
| 2053 | 12788877 | Both in diabetic patients and in healthy subjects, significant increases in GLP-1 and GIP concentrations were seen after ingestion of both meals. |
| 2054 | 12788877 | Both type 1 and type 2 diabetic patients had normal GIP responses, compared with healthy subjects, whereas decreased GLP-1 responses were seen in type 2 diabetic patients, compared with matched obese healthy subjects. |
| 2055 | 12788877 | Increased fasting concentrations of GIP and an early enhanced postprandial GIP response were seen in obese, compared with lean healthy subjects, whereas GLP-1 responses were the same in the two groups. beta-cell sensitivity to glucose, evaluated as the slope of insulin secretion rates vs. plasma glucose concentration, tended to increase in both type 2 diabetic patients (29%, P = 0.19) and obese healthy subjects (22% P = 0.04) during the large meal, compared with the small meal, perhaps reflecting the increased incretin response. |
| 2056 | 12788877 | We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. |
| 2057 | 12788877 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones secreted in response to meal ingestion, thereby enhancing postprandial insulin secretion. |
| 2058 | 12788877 | Both in diabetic patients and in healthy subjects, significant increases in GLP-1 and GIP concentrations were seen after ingestion of both meals. |
| 2059 | 12788877 | Both type 1 and type 2 diabetic patients had normal GIP responses, compared with healthy subjects, whereas decreased GLP-1 responses were seen in type 2 diabetic patients, compared with matched obese healthy subjects. |
| 2060 | 12788877 | Increased fasting concentrations of GIP and an early enhanced postprandial GIP response were seen in obese, compared with lean healthy subjects, whereas GLP-1 responses were the same in the two groups. beta-cell sensitivity to glucose, evaluated as the slope of insulin secretion rates vs. plasma glucose concentration, tended to increase in both type 2 diabetic patients (29%, P = 0.19) and obese healthy subjects (22% P = 0.04) during the large meal, compared with the small meal, perhaps reflecting the increased incretin response. |
| 2061 | 12788877 | We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. |
| 2062 | 12789546 | GIP is a secreted protein, known to be released from the small intestine, which potentiates glucose-induced insulin secretion from the pancreas. |
| 2063 | 12789546 | However, the expression of GIP and its receptor (GIPR) has not been previously noted in the rat retina. |
| 2064 | 12789546 | We here demonstrate for the first time the expression of GIP and GIPR in the rat retina. |
| 2065 | 12789546 | And we also revealed some genetic events in the early stage of diabetic retinopathy including the de novo increment of GIP and GIPR expression in the retina. |
| 2066 | 12789546 | GIP is a secreted protein, known to be released from the small intestine, which potentiates glucose-induced insulin secretion from the pancreas. |
| 2067 | 12789546 | However, the expression of GIP and its receptor (GIPR) has not been previously noted in the rat retina. |
| 2068 | 12789546 | We here demonstrate for the first time the expression of GIP and GIPR in the rat retina. |
| 2069 | 12789546 | And we also revealed some genetic events in the early stage of diabetic retinopathy including the de novo increment of GIP and GIPR expression in the retina. |
| 2070 | 12789546 | GIP is a secreted protein, known to be released from the small intestine, which potentiates glucose-induced insulin secretion from the pancreas. |
| 2071 | 12789546 | However, the expression of GIP and its receptor (GIPR) has not been previously noted in the rat retina. |
| 2072 | 12789546 | We here demonstrate for the first time the expression of GIP and GIPR in the rat retina. |
| 2073 | 12789546 | And we also revealed some genetic events in the early stage of diabetic retinopathy including the de novo increment of GIP and GIPR expression in the retina. |
| 2074 | 12789546 | GIP is a secreted protein, known to be released from the small intestine, which potentiates glucose-induced insulin secretion from the pancreas. |
| 2075 | 12789546 | However, the expression of GIP and its receptor (GIPR) has not been previously noted in the rat retina. |
| 2076 | 12789546 | We here demonstrate for the first time the expression of GIP and GIPR in the rat retina. |
| 2077 | 12789546 | And we also revealed some genetic events in the early stage of diabetic retinopathy including the de novo increment of GIP and GIPR expression in the retina. |
| 2078 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2079 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2080 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2081 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2082 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2083 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2084 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2085 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2086 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2087 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2088 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2089 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2090 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2091 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2092 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2093 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2094 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2095 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2096 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2097 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2098 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2099 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2100 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2101 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2102 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2103 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2104 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2105 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2106 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2107 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2108 | 12800091 | Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. |
| 2109 | 12800091 | Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. |
| 2110 | 12800091 | However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. |
| 2111 | 12800091 | In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. |
| 2112 | 12800091 | In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. |
| 2113 | 12800091 | In obese diabetic (ob/ob) mice, GIP and (Sar(2))GIP significantly increased (1.4-fold to 1.5-fold; P <.05) plasma insulin concentrations, whereas (Abu(2))GIP exerted only minor effects. |
| 2114 | 12806222 | Enteroinsular signaling: perspectives on the role of the gastrointestinal hormones glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide in normal and abnormal glucose metabolism. |
| 2115 | 12901855 | Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released postprandially into the circulation in response to feeding, producing a glucose-dependent stimulation of insulin secretion. |
| 2116 | 12901855 | A major drawback to achieving this goal has been the rapid degradation of circulating GIP by the ubiquitous enzyme, dipeptidylpeptidase IV (DPP IV). |
| 2117 | 12901855 | Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released postprandially into the circulation in response to feeding, producing a glucose-dependent stimulation of insulin secretion. |
| 2118 | 12901855 | A major drawback to achieving this goal has been the rapid degradation of circulating GIP by the ubiquitous enzyme, dipeptidylpeptidase IV (DPP IV). |
| 2119 | 12975025 | In humans, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the most important incretins. |
| 2120 | 12975025 | This has been most successful for GLP-1, which exerts antidiabetogenic properties in subjects with type 2 diabetes by stimulating insulin secretion, increasing beta-cell mass, inhibiting glucagon secretion, delaying gastric emptying, and inducing satiety. |
| 2121 | 12975025 | However, GLP-1 is rapidly degraded by the enzyme dipeptidyl peptidase IV (DPPIV), making it unattractive as a therapeutic agent because of a very short half-life. |
| 2122 | 12975025 | Successful strategies to overcome this difficulty are the use of DPPIV-resistant GLP-1 receptor agonists, such as NN2211 or exendin-4, and the use of inhibitors of DPPIV, such as NVPDPP728 and P32/98. |
| 2123 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2124 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2125 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2126 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2127 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2128 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2129 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2130 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2131 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2132 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2133 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2134 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2135 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2136 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2137 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2138 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2139 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2140 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2141 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2142 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2143 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2144 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2145 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2146 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2147 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2148 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2149 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2150 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2151 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2152 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2153 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2154 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2155 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2156 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2157 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2158 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2159 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2160 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2161 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2162 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2163 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2164 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2165 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2166 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2167 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2168 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2169 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2170 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2171 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2172 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2173 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2174 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2175 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2176 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2177 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2178 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2179 | 14557471 | The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. |
| 2180 | 14557471 | The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. |
| 2181 | 14557471 | The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. |
| 2182 | 14557471 | All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. |
| 2183 | 14557471 | The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. |
| 2184 | 14557471 | In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. |
| 2185 | 14557471 | Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. |
| 2186 | 14557471 | In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. |
| 2187 | 14593618 | These gluco-incretin hormones are GLP-1 (glucagon-like peptide-1) and GIP (gluco-dependent insulinotropic polypeptide). |
| 2188 | 14607102 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a gastrointestinal hormone, which modulates physiological insulin secretion. |
| 2189 | 14607102 | In addition, observations in transgenic GIP receptor deficient mice indicate that GIP directly links overnutrition to obesity, therein playing a crucial role in the development of obesity and related metabolic disorders. |
| 2190 | 14607102 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a gastrointestinal hormone, which modulates physiological insulin secretion. |
| 2191 | 14607102 | In addition, observations in transgenic GIP receptor deficient mice indicate that GIP directly links overnutrition to obesity, therein playing a crucial role in the development of obesity and related metabolic disorders. |
| 2192 | 14630571 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are important in blood glucose regulation. |
| 2193 | 14630571 | The concept of DPPIV inhibition as a treatment for type 2 diabetes was evaluated in a new large animal model of insulin-deficient diabetes and reduced beta-cell mass, the nicotinamide (NIA) (67 mg/kg) and streptozotocin (STZ) (125 mg/kg)-treated minipig, using the DPPIV inhibitor, valine pyrrolidide (VP) (50 mg/kg). |
| 2194 | 14630571 | VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 +/- 1880 to 9208 +/- 3267 pM x min; P <.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 +/- 480 to 1582 +/- 353 mM x min; P =.05). |
| 2195 | 14630571 | GIP seems to contribute to the antihyperglycemic effect of VP in this model; however, additional mechanisms for the effect of DPPIV inhibition cannot be excluded. |
| 2196 | 14630571 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are important in blood glucose regulation. |
| 2197 | 14630571 | The concept of DPPIV inhibition as a treatment for type 2 diabetes was evaluated in a new large animal model of insulin-deficient diabetes and reduced beta-cell mass, the nicotinamide (NIA) (67 mg/kg) and streptozotocin (STZ) (125 mg/kg)-treated minipig, using the DPPIV inhibitor, valine pyrrolidide (VP) (50 mg/kg). |
| 2198 | 14630571 | VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 +/- 1880 to 9208 +/- 3267 pM x min; P <.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 +/- 480 to 1582 +/- 353 mM x min; P =.05). |
| 2199 | 14630571 | GIP seems to contribute to the antihyperglycemic effect of VP in this model; however, additional mechanisms for the effect of DPPIV inhibition cannot be excluded. |
| 2200 | 14630571 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are important in blood glucose regulation. |
| 2201 | 14630571 | The concept of DPPIV inhibition as a treatment for type 2 diabetes was evaluated in a new large animal model of insulin-deficient diabetes and reduced beta-cell mass, the nicotinamide (NIA) (67 mg/kg) and streptozotocin (STZ) (125 mg/kg)-treated minipig, using the DPPIV inhibitor, valine pyrrolidide (VP) (50 mg/kg). |
| 2202 | 14630571 | VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 +/- 1880 to 9208 +/- 3267 pM x min; P <.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 +/- 480 to 1582 +/- 353 mM x min; P =.05). |
| 2203 | 14630571 | GIP seems to contribute to the antihyperglycemic effect of VP in this model; however, additional mechanisms for the effect of DPPIV inhibition cannot be excluded. |
| 2204 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2205 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2206 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2207 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2208 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2209 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2210 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2211 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2212 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2213 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2214 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2215 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2216 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2217 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2218 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2219 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2220 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2221 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2222 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2223 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2224 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2225 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2226 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2227 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2228 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2229 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2230 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2231 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2232 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2233 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2234 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2235 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2236 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2237 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2238 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2239 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2240 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2241 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2242 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2243 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2244 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2245 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2246 | 14669159 | Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects. |
| 2247 | 14669159 | Insulin secretion following the intravenous infusion of gastric inhibitory polypeptide (GIP) is diminished in patients with type 2 diabetes and at least a subgroup of their first-degree relatives at hyperglycemic clamp conditions. |
| 2248 | 14669159 | Forty-five first-degree relatives of patients with type 2 diabetes and 33 matched control subjects were studied with (1) a 75-g oral glucose tolerance test (OGTT) and (2) an intravenous bolus injection of 20 pmol GIP/kg BW with blood samples drawn over 30 minutes for determination of plasma glucose, insulin, C-peptide, and GIP. |
| 2249 | 14669159 | Insulin secretion was stimulated after the administration of 20 and of 60 pmol GIP/kg BW in the dose-response experiments (P <.0001). |
| 2250 | 14669159 | GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects (P <.0001), but there was difference between groups (P =.64 and P =.87, respectively). |
| 2251 | 14669159 | Integrated insulin and C-peptide responses after GIP administration significantly correlated with the respective insulin and C-peptide responses after glucose ingestion (insulin, r = 0.78, P <.0001; C-peptide, r = 0.35, P =.0015). |
| 2252 | 14669159 | Therefore, a reduced GIP-induced insulin secretion in patients with type 2 diabetes and their first-degree relatives at hyperglycemia is more likely due to a general defect of B-cell function than to a specific defect of the GIP action. |
| 2253 | 14678954 | Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). |
| 2254 | 14678954 | There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. |
| 2255 | 14678954 | The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1. |
| 2256 | 14678954 | Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). |
| 2257 | 14678954 | There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. |
| 2258 | 14678954 | The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1. |
| 2259 | 14678954 | Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). |
| 2260 | 14678954 | There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. |
| 2261 | 14678954 | The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1. |
| 2262 | 14681845 | Stevioside tended to decrease glucagon levels, while it did not significantly alter the area under the insulin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide curves. |
| 2263 | 14681846 | The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are important hormones from the gut that enhance nutrient-stimulated insulin secretion. |
| 2264 | 14681846 | Isocaloric amounts of carbohydrate and alcohol suppressed equally the postprandial free fatty acid levels, but carbohydrate increased the postprandial glucose, GIP, and insulin levels the most. |
| 2265 | 14681846 | The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are important hormones from the gut that enhance nutrient-stimulated insulin secretion. |
| 2266 | 14681846 | Isocaloric amounts of carbohydrate and alcohol suppressed equally the postprandial free fatty acid levels, but carbohydrate increased the postprandial glucose, GIP, and insulin levels the most. |
| 2267 | 14964537 | Preoperatively, 20 MO patients with DM-II were evaluated for demographics and fasting levels of the following: glucose, insulin, C-peptide, glucagon, cortisol, gastric inhibitory polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). |
| 2268 | 14968296 | This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 2269 | 14968296 | In studies of the mechanism of the impaired incretin effect in Type 2 diabetic patients, it has been found that the secretion of GIP is generally normal, whereas the secretion of GLP-1 is reduced, presumably as a consequence of the diabetic state. |
| 2270 | 14968296 | It might be of even greater importance that the effect of GLP-1 is preserved whereas the effect of GIP is severely impaired. |
| 2271 | 14968296 | The preserved effect of GLP-1 has inspired attempts to treat Type 2 diabetes with GLP-1 or analogues thereof, and intravenous GLP-1 administration has been shown to be able to near-normalize both fasting and postprandial glycaemic concentrations in the patients, perhaps because the treatment compensates for both the impaired secretion of GLP-1 and the impaired action of GIP. |
| 2272 | 14968296 | This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 2273 | 14968296 | In studies of the mechanism of the impaired incretin effect in Type 2 diabetic patients, it has been found that the secretion of GIP is generally normal, whereas the secretion of GLP-1 is reduced, presumably as a consequence of the diabetic state. |
| 2274 | 14968296 | It might be of even greater importance that the effect of GLP-1 is preserved whereas the effect of GIP is severely impaired. |
| 2275 | 14968296 | The preserved effect of GLP-1 has inspired attempts to treat Type 2 diabetes with GLP-1 or analogues thereof, and intravenous GLP-1 administration has been shown to be able to near-normalize both fasting and postprandial glycaemic concentrations in the patients, perhaps because the treatment compensates for both the impaired secretion of GLP-1 and the impaired action of GIP. |
| 2276 | 14968296 | This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 2277 | 14968296 | In studies of the mechanism of the impaired incretin effect in Type 2 diabetic patients, it has been found that the secretion of GIP is generally normal, whereas the secretion of GLP-1 is reduced, presumably as a consequence of the diabetic state. |
| 2278 | 14968296 | It might be of even greater importance that the effect of GLP-1 is preserved whereas the effect of GIP is severely impaired. |
| 2279 | 14968296 | The preserved effect of GLP-1 has inspired attempts to treat Type 2 diabetes with GLP-1 or analogues thereof, and intravenous GLP-1 administration has been shown to be able to near-normalize both fasting and postprandial glycaemic concentrations in the patients, perhaps because the treatment compensates for both the impaired secretion of GLP-1 and the impaired action of GIP. |
| 2280 | 14968296 | This effect, which is called the incretin effect and is estimated to be responsible for 50 to 70% of the insulin response to glucose, is caused mainly by the two intestinal insulin-stimulating hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 2281 | 14968296 | In studies of the mechanism of the impaired incretin effect in Type 2 diabetic patients, it has been found that the secretion of GIP is generally normal, whereas the secretion of GLP-1 is reduced, presumably as a consequence of the diabetic state. |
| 2282 | 14968296 | It might be of even greater importance that the effect of GLP-1 is preserved whereas the effect of GIP is severely impaired. |
| 2283 | 14968296 | The preserved effect of GLP-1 has inspired attempts to treat Type 2 diabetes with GLP-1 or analogues thereof, and intravenous GLP-1 administration has been shown to be able to near-normalize both fasting and postprandial glycaemic concentrations in the patients, perhaps because the treatment compensates for both the impaired secretion of GLP-1 and the impaired action of GIP. |
| 2284 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2285 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2286 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2287 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2288 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2289 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2290 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2291 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2292 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2293 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2294 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2295 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2296 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2297 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2298 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2299 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2300 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2301 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2302 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2303 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2304 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2305 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2306 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2307 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2308 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2309 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2310 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2311 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2312 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2313 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2314 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2315 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2316 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2317 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2318 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2319 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2320 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2321 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2322 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2323 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2324 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2325 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2326 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2327 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2328 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2329 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2330 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2331 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2332 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2333 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2334 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2335 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2336 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2337 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2338 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2339 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2340 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2341 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2342 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2343 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2344 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2345 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2346 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2347 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2348 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2349 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2350 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2351 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2352 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2353 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2354 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2355 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2356 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2357 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2358 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2359 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2360 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2361 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2362 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2363 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2364 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2365 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2366 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2367 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2368 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2369 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2370 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2371 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2372 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2373 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2374 | 14988249 | Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects. |
| 2375 | 14988249 | Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. |
| 2376 | 14988249 | On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. |
| 2377 | 14988249 | Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). |
| 2378 | 14988249 | Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. |
| 2379 | 14988249 | After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). |
| 2380 | 14988249 | The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). |
| 2381 | 14988249 | During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). |
| 2382 | 14988249 | These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. |
| 2383 | 14988249 | Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes. |
| 2384 | 15013938 | Extensive research during the past three decades has identified two gut hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, also known as gastric inhibitory polypeptide) that are important in postprandial glucose metabolism. |
| 2385 | 15013938 | Since they are potent insulin secretagogues, GIP and GLP-1 have received considerable attention as potential diabetes therapeutics. |
| 2386 | 15013938 | Both GLP-1 and GIP are rapidly inactivated in the circulation by the enzyme dipeptidyl peptidase IV (DPP-IV). |
| 2387 | 15013938 | Two approaches have been taken to utilise the insulinotropic and glucose-lowering actions of GLP-1 as an antidiabetic agent: the development of DPP-IV-resistant analogues and the inhibition of DPP-IV. |
| 2388 | 15013938 | This review focuses on the physiology of GLP-1 and GIP and the advances that have been made thus far in developing treatments based on these physiological incretins for Type 2 diabetes. |
| 2389 | 15013938 | Extensive research during the past three decades has identified two gut hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, also known as gastric inhibitory polypeptide) that are important in postprandial glucose metabolism. |
| 2390 | 15013938 | Since they are potent insulin secretagogues, GIP and GLP-1 have received considerable attention as potential diabetes therapeutics. |
| 2391 | 15013938 | Both GLP-1 and GIP are rapidly inactivated in the circulation by the enzyme dipeptidyl peptidase IV (DPP-IV). |
| 2392 | 15013938 | Two approaches have been taken to utilise the insulinotropic and glucose-lowering actions of GLP-1 as an antidiabetic agent: the development of DPP-IV-resistant analogues and the inhibition of DPP-IV. |
| 2393 | 15013938 | This review focuses on the physiology of GLP-1 and GIP and the advances that have been made thus far in developing treatments based on these physiological incretins for Type 2 diabetes. |
| 2394 | 15013938 | Extensive research during the past three decades has identified two gut hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, also known as gastric inhibitory polypeptide) that are important in postprandial glucose metabolism. |
| 2395 | 15013938 | Since they are potent insulin secretagogues, GIP and GLP-1 have received considerable attention as potential diabetes therapeutics. |
| 2396 | 15013938 | Both GLP-1 and GIP are rapidly inactivated in the circulation by the enzyme dipeptidyl peptidase IV (DPP-IV). |
| 2397 | 15013938 | Two approaches have been taken to utilise the insulinotropic and glucose-lowering actions of GLP-1 as an antidiabetic agent: the development of DPP-IV-resistant analogues and the inhibition of DPP-IV. |
| 2398 | 15013938 | This review focuses on the physiology of GLP-1 and GIP and the advances that have been made thus far in developing treatments based on these physiological incretins for Type 2 diabetes. |
| 2399 | 15013938 | Extensive research during the past three decades has identified two gut hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, also known as gastric inhibitory polypeptide) that are important in postprandial glucose metabolism. |
| 2400 | 15013938 | Since they are potent insulin secretagogues, GIP and GLP-1 have received considerable attention as potential diabetes therapeutics. |
| 2401 | 15013938 | Both GLP-1 and GIP are rapidly inactivated in the circulation by the enzyme dipeptidyl peptidase IV (DPP-IV). |
| 2402 | 15013938 | Two approaches have been taken to utilise the insulinotropic and glucose-lowering actions of GLP-1 as an antidiabetic agent: the development of DPP-IV-resistant analogues and the inhibition of DPP-IV. |
| 2403 | 15013938 | This review focuses on the physiology of GLP-1 and GIP and the advances that have been made thus far in developing treatments based on these physiological incretins for Type 2 diabetes. |
| 2404 | 15056941 | PACAP belongs to the vasoactive intestinal polypeptide (VIP)/secretin/glucagon superfamily, which also includes glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). |
| 2405 | 15111503 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are gut-derived incretins that potentiate glucose clearance following nutrient ingestion. |
| 2406 | 15111503 | Elimination of incretin receptor action in GIPR(-/-) or GLP-1R(-/-) mice produces only modest impairment in glucose homeostasis, perhaps due to compensatory upregulation of the remaining incretin. |
| 2407 | 15111503 | DIRKO mice exhibit normal body weight and fail to exhibit an improved glycemic response after exogenous administration of GIP or the GLP-1R agonist exendin-4. |
| 2408 | 15111503 | Glycemic excursion was abnormally increased and levels of glucose-stimulated insulin secretion were decreased following oral but not intraperitoneal glucose challenge in DIRKO compared with GIPR(-/-) or GLP-1R(-/-) mice. |
| 2409 | 15111503 | Although the dipeptidyl peptidase-IV (DPP-IV) inhibitors valine pyrrolidide (Val-Pyr) and SYR106124 lowered glucose and increased plasma insulin in wild-type and single incretin receptor knockout mice, the glucose-lowering actions of DPP-IV inhibitors were eliminated in DIRKO mice. |
| 2410 | 15111503 | These findings demonstrate that glucose-stimulated insulin secretion is maintained despite complete absence of both incretin receptors, and they delineate a critical role for incretin receptors as essential downstream targets for the acute glucoregulatory actions of DPP-IV inhibitors. |
| 2411 | 15111503 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are gut-derived incretins that potentiate glucose clearance following nutrient ingestion. |
| 2412 | 15111503 | Elimination of incretin receptor action in GIPR(-/-) or GLP-1R(-/-) mice produces only modest impairment in glucose homeostasis, perhaps due to compensatory upregulation of the remaining incretin. |
| 2413 | 15111503 | DIRKO mice exhibit normal body weight and fail to exhibit an improved glycemic response after exogenous administration of GIP or the GLP-1R agonist exendin-4. |
| 2414 | 15111503 | Glycemic excursion was abnormally increased and levels of glucose-stimulated insulin secretion were decreased following oral but not intraperitoneal glucose challenge in DIRKO compared with GIPR(-/-) or GLP-1R(-/-) mice. |
| 2415 | 15111503 | Although the dipeptidyl peptidase-IV (DPP-IV) inhibitors valine pyrrolidide (Val-Pyr) and SYR106124 lowered glucose and increased plasma insulin in wild-type and single incretin receptor knockout mice, the glucose-lowering actions of DPP-IV inhibitors were eliminated in DIRKO mice. |
| 2416 | 15111503 | These findings demonstrate that glucose-stimulated insulin secretion is maintained despite complete absence of both incretin receptors, and they delineate a critical role for incretin receptors as essential downstream targets for the acute glucoregulatory actions of DPP-IV inhibitors. |
| 2417 | 15120474 | Typical Danish Caucasian type 2 diabetic patients do not commonly carry genetic variants in GIP and GLP-1 encoding regions of the proGIP and proglucagon genes. |
| 2418 | 15122087 | Gastro-intestinal hormones GIP and GLP-1. |
| 2419 | 15183115 | Glucagon-like peptide-1 (7-36) amide (GLP-1) and glucose-dependent insulinotropic peptide (GIP) potentiate glucose-induced insulin release when present at the time of nutrient stimulation. |
| 2420 | 15183115 | However, when both GLP-1 and GIP, each at 0.5 nM, were added to the one hour pulses, they not only amplified insulin release during the pulses, as was the case with their single addition, but also increased the secretory response to a subsequent stimulation by glucose and GLP-1. |
| 2421 | 15183115 | These data distinguish between a desensitization effect of a prolonged exposure to GLP-1 and a positive priming effect of a discontinuous exposure to a combination of GLP-1 plus GIP. |
| 2422 | 15183115 | Glucagon-like peptide-1 (7-36) amide (GLP-1) and glucose-dependent insulinotropic peptide (GIP) potentiate glucose-induced insulin release when present at the time of nutrient stimulation. |
| 2423 | 15183115 | However, when both GLP-1 and GIP, each at 0.5 nM, were added to the one hour pulses, they not only amplified insulin release during the pulses, as was the case with their single addition, but also increased the secretory response to a subsequent stimulation by glucose and GLP-1. |
| 2424 | 15183115 | These data distinguish between a desensitization effect of a prolonged exposure to GLP-1 and a positive priming effect of a discontinuous exposure to a combination of GLP-1 plus GIP. |
| 2425 | 15206144 | [GIP receptor knockout mice]. |
| 2426 | 15206144 | Gastric inhibitory polypeptide(GIP) is a gastrointestinal peptide hormone, which is secreted from duodenal endocrine K cells after absorption of glucose or fat. |
| 2427 | 15206144 | To determine the further role of GIP in vivo, we generated GIP receptor-knockout mice. |
| 2428 | 15206144 | [GIP receptor knockout mice]. |
| 2429 | 15206144 | Gastric inhibitory polypeptide(GIP) is a gastrointestinal peptide hormone, which is secreted from duodenal endocrine K cells after absorption of glucose or fat. |
| 2430 | 15206144 | To determine the further role of GIP in vivo, we generated GIP receptor-knockout mice. |
| 2431 | 15206144 | [GIP receptor knockout mice]. |
| 2432 | 15206144 | Gastric inhibitory polypeptide(GIP) is a gastrointestinal peptide hormone, which is secreted from duodenal endocrine K cells after absorption of glucose or fat. |
| 2433 | 15206144 | To determine the further role of GIP in vivo, we generated GIP receptor-knockout mice. |
| 2434 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2435 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2436 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2437 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2438 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2439 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2440 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2441 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2442 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2443 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2444 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2445 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2446 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2447 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2448 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2449 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2450 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2451 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2452 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2453 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2454 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2455 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2456 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2457 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2458 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2459 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2460 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2461 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2462 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2463 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2464 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2465 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2466 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2467 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2468 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2469 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2470 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2471 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2472 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2473 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2474 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2475 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2476 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2477 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2478 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2479 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2480 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2481 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2482 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2483 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2484 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2485 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2486 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2487 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2488 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2489 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2490 | 15246869 | Comparative effects of GLP-1 and GIP on cAMP production, insulin secretion, and in vivo antidiabetic actions following substitution of Ala8/Ala2 with 2-aminobutyric acid. |
| 2491 | 15246869 | The two major incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), are currently being considered as prospective drug candidates for treatment of type 2 diabetes. |
| 2492 | 15246869 | One of the foremost barriers in progressing GLP-1 and GIP to the clinic concerns their rapid degradation and inactivation by the ubiquitous enzyme, dipeptidyl peptidase IV (DPP IV). |
| 2493 | 15246869 | Here, we compare the DPP IV resistance and biological properties of Abu8/Abu2 (2-aminobutyric acid) substituted analogues of GLP-1 and GIP engineered to impart DPP IV resistance. |
| 2494 | 15246869 | Whereas (Abu8)GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2)GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively). |
| 2495 | 15246869 | Native GIP, GLP-1, and particularly (Abu8)GLP-1 elicited significant adenylate cyclase and insulinotropic activity, while (Abu2)GIP was less effective. |
| 2496 | 15246869 | Similarly, in obese diabetic (ob/ob) mice, GIP, GLP-1, and (Abu8)GLP-1 displayed substantial glucose-lowering and insulin-releasing activities, whereas (Abu2)GIP was only weakly active. |
| 2497 | 15246869 | These studies illustrate divergent effects of penultimate amino acid Ala8/Ala2 substitution with Abu on the biological properties of GLP-1 and GIP, suggesting that (Abu8)GLP-1 represents a potential candidate for future therapeutic development. |
| 2498 | 15259310 | [GIP and GLP-1: multiplicity of regulator mechanisms for insulin secretion]. |
| 2499 | 15271645 | The strongest candidates for the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 2500 | 15271645 | Further analysis of the incretin effects in patients has revealed that the secretion of GIP is near normal, whereas the secretion of GLP-1 is decreased. |
| 2501 | 15271645 | On the other hand, the insulintropic effect of GLP-1 is preserved, whereas the effect of GIP is greatly reduced, mainly because of a complete loss of the normal GIP-induced potentiation of second-phase insulin secretion. |
| 2502 | 15271645 | Strong support for the hypothesis that the defect plays an important role in the insulin deficiency of patients is provided by the finding that administration of excess GLP-1 to patients may completely restore the glucose-induced insulin secretion as well as the beta-cells' sensitivity to glucose. |
| 2503 | 15271645 | The strongest candidates for the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 2504 | 15271645 | Further analysis of the incretin effects in patients has revealed that the secretion of GIP is near normal, whereas the secretion of GLP-1 is decreased. |
| 2505 | 15271645 | On the other hand, the insulintropic effect of GLP-1 is preserved, whereas the effect of GIP is greatly reduced, mainly because of a complete loss of the normal GIP-induced potentiation of second-phase insulin secretion. |
| 2506 | 15271645 | Strong support for the hypothesis that the defect plays an important role in the insulin deficiency of patients is provided by the finding that administration of excess GLP-1 to patients may completely restore the glucose-induced insulin secretion as well as the beta-cells' sensitivity to glucose. |
| 2507 | 15271645 | The strongest candidates for the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 2508 | 15271645 | Further analysis of the incretin effects in patients has revealed that the secretion of GIP is near normal, whereas the secretion of GLP-1 is decreased. |
| 2509 | 15271645 | On the other hand, the insulintropic effect of GLP-1 is preserved, whereas the effect of GIP is greatly reduced, mainly because of a complete loss of the normal GIP-induced potentiation of second-phase insulin secretion. |
| 2510 | 15271645 | Strong support for the hypothesis that the defect plays an important role in the insulin deficiency of patients is provided by the finding that administration of excess GLP-1 to patients may completely restore the glucose-induced insulin secretion as well as the beta-cells' sensitivity to glucose. |
| 2511 | 15302229 | Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP) is an important gastrointestinal regulator of insulin release and glucose homeostasis following a meal. |
| 2512 | 15302229 | The molecular cloning of receptors for GIP and the related hormone GLP-1 (glucagon-like peptide-1) has allowed examination of the characteristics of incretin analogs in transfected cell models. |
| 2513 | 15302229 | Further studies examined peptide chimeras of GIP and GLP-1 designed to localize bioactive determinants of the two hormones. |
| 2514 | 15302229 | Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP) is an important gastrointestinal regulator of insulin release and glucose homeostasis following a meal. |
| 2515 | 15302229 | The molecular cloning of receptors for GIP and the related hormone GLP-1 (glucagon-like peptide-1) has allowed examination of the characteristics of incretin analogs in transfected cell models. |
| 2516 | 15302229 | Further studies examined peptide chimeras of GIP and GLP-1 designed to localize bioactive determinants of the two hormones. |
| 2517 | 15302229 | Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP) is an important gastrointestinal regulator of insulin release and glucose homeostasis following a meal. |
| 2518 | 15302229 | The molecular cloning of receptors for GIP and the related hormone GLP-1 (glucagon-like peptide-1) has allowed examination of the characteristics of incretin analogs in transfected cell models. |
| 2519 | 15302229 | Further studies examined peptide chimeras of GIP and GLP-1 designed to localize bioactive determinants of the two hormones. |
| 2520 | 15318993 | Both GLP-1 and GIP have an impaired secretin effect in type 2 diabetics, and surgery can restore this function. |
| 2521 | 15318993 | The secretion of GLP-1 influences glucose metabolism by inhibiting glucagon secretion, stimulating insulin secretion, delaying gastric emptying and stimulating glycogenogenesis. |
| 2522 | 15330741 | At the molecular level, DPP IV cleaves two amino acids from the N-terminus of the intact, biologically active forms of both so-called incretin hormones, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide (formerly known as gastric inhibitory polypeptide), resulting in truncated metabolites, which are largely inactive. |
| 2523 | 15331546 | Reduced hepatic insulin extraction in response to gastric inhibitory polypeptide compensates for reduced insulin secretion in normal-weight and normal glucose tolerant first-degree relatives of type 2 diabetic patients. |
| 2524 | 15331546 | Our objective was to study whether young first-degree relatives of patients with type 2 diabetes (FDRs) have altered insulin secretion and insulin clearance in response to gastric inhibitory polypeptide (GIP) in combination with glucose and arginine. |
| 2525 | 15331546 | Insulin clearance was significantly reduced in the group of FDRs under basal conditions and in response to GIP, but there was no general defect in insulin clearance in response to glucose and arginine. |
| 2526 | 15331546 | The HOMA(IR) correlated negatively (P < 0.01) with insulin clearance under basal conditions (r = -0.96) and under GIP infusion (r = -0.56). |
| 2527 | 15331546 | We propose that impairment in insulin secretion capacity and decreased insulin sensitivity is compensated for several mechanisms, one of which includes a GIP-dependent reduction of the insulin clearance that will increase peripheral insulin levels to maintain normoglycemia. |
| 2528 | 15331546 | Reduced hepatic insulin extraction in response to gastric inhibitory polypeptide compensates for reduced insulin secretion in normal-weight and normal glucose tolerant first-degree relatives of type 2 diabetic patients. |
| 2529 | 15331546 | Our objective was to study whether young first-degree relatives of patients with type 2 diabetes (FDRs) have altered insulin secretion and insulin clearance in response to gastric inhibitory polypeptide (GIP) in combination with glucose and arginine. |
| 2530 | 15331546 | Insulin clearance was significantly reduced in the group of FDRs under basal conditions and in response to GIP, but there was no general defect in insulin clearance in response to glucose and arginine. |
| 2531 | 15331546 | The HOMA(IR) correlated negatively (P < 0.01) with insulin clearance under basal conditions (r = -0.96) and under GIP infusion (r = -0.56). |
| 2532 | 15331546 | We propose that impairment in insulin secretion capacity and decreased insulin sensitivity is compensated for several mechanisms, one of which includes a GIP-dependent reduction of the insulin clearance that will increase peripheral insulin levels to maintain normoglycemia. |
| 2533 | 15331546 | Reduced hepatic insulin extraction in response to gastric inhibitory polypeptide compensates for reduced insulin secretion in normal-weight and normal glucose tolerant first-degree relatives of type 2 diabetic patients. |
| 2534 | 15331546 | Our objective was to study whether young first-degree relatives of patients with type 2 diabetes (FDRs) have altered insulin secretion and insulin clearance in response to gastric inhibitory polypeptide (GIP) in combination with glucose and arginine. |
| 2535 | 15331546 | Insulin clearance was significantly reduced in the group of FDRs under basal conditions and in response to GIP, but there was no general defect in insulin clearance in response to glucose and arginine. |
| 2536 | 15331546 | The HOMA(IR) correlated negatively (P < 0.01) with insulin clearance under basal conditions (r = -0.96) and under GIP infusion (r = -0.56). |
| 2537 | 15331546 | We propose that impairment in insulin secretion capacity and decreased insulin sensitivity is compensated for several mechanisms, one of which includes a GIP-dependent reduction of the insulin clearance that will increase peripheral insulin levels to maintain normoglycemia. |
| 2538 | 15331546 | Reduced hepatic insulin extraction in response to gastric inhibitory polypeptide compensates for reduced insulin secretion in normal-weight and normal glucose tolerant first-degree relatives of type 2 diabetic patients. |
| 2539 | 15331546 | Our objective was to study whether young first-degree relatives of patients with type 2 diabetes (FDRs) have altered insulin secretion and insulin clearance in response to gastric inhibitory polypeptide (GIP) in combination with glucose and arginine. |
| 2540 | 15331546 | Insulin clearance was significantly reduced in the group of FDRs under basal conditions and in response to GIP, but there was no general defect in insulin clearance in response to glucose and arginine. |
| 2541 | 15331546 | The HOMA(IR) correlated negatively (P < 0.01) with insulin clearance under basal conditions (r = -0.96) and under GIP infusion (r = -0.56). |
| 2542 | 15331546 | We propose that impairment in insulin secretion capacity and decreased insulin sensitivity is compensated for several mechanisms, one of which includes a GIP-dependent reduction of the insulin clearance that will increase peripheral insulin levels to maintain normoglycemia. |
| 2543 | 15331546 | Reduced hepatic insulin extraction in response to gastric inhibitory polypeptide compensates for reduced insulin secretion in normal-weight and normal glucose tolerant first-degree relatives of type 2 diabetic patients. |
| 2544 | 15331546 | Our objective was to study whether young first-degree relatives of patients with type 2 diabetes (FDRs) have altered insulin secretion and insulin clearance in response to gastric inhibitory polypeptide (GIP) in combination with glucose and arginine. |
| 2545 | 15331546 | Insulin clearance was significantly reduced in the group of FDRs under basal conditions and in response to GIP, but there was no general defect in insulin clearance in response to glucose and arginine. |
| 2546 | 15331546 | The HOMA(IR) correlated negatively (P < 0.01) with insulin clearance under basal conditions (r = -0.96) and under GIP infusion (r = -0.56). |
| 2547 | 15331546 | We propose that impairment in insulin secretion capacity and decreased insulin sensitivity is compensated for several mechanisms, one of which includes a GIP-dependent reduction of the insulin clearance that will increase peripheral insulin levels to maintain normoglycemia. |
| 2548 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2549 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2550 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2551 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2552 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2553 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2554 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2555 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2556 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2557 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2558 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2559 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2560 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2561 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2562 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2563 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2564 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2565 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2566 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2567 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2568 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2569 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2570 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2571 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2572 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2573 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2574 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2575 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2576 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2577 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2578 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2579 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2580 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2581 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2582 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2583 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2584 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2585 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2586 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2587 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2588 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2589 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2590 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2591 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2592 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2593 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2594 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2595 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2596 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2597 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2598 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2599 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2600 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2601 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2602 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2603 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2604 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2605 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2606 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2607 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2608 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2609 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2610 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2611 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2612 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2613 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2614 | 15383372 | Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. |
| 2615 | 15383372 | Glucose-dependent insulinotropic polypeptide (GIP) regulates glucose homeostasis and high-fat diet-induced obesity and insulin resistance. |
| 2616 | 15383372 | Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. |
| 2617 | 15383372 | We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). |
| 2618 | 15383372 | Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. |
| 2619 | 15383372 | In various cell systems, bombesin and PMA regulate cell physiology by activating PKD signaling in a PKC-dependent fashion, whereas nutrients regulate cell physiology by inhibiting AMPK signaling. |
| 2620 | 15383372 | Western blot analyses of GIP/Ins cells using antibodies specific for activated and/or phosphorylated forms of PKD and AMPK and one substrate for each kinase revealed that bombesin and PMA, but not nutrients, activated PKC, but not PKD. |
| 2621 | 15383372 | Conversely, nutrients, but not bombesin or PMA, inhibited AMPK activity. |
| 2622 | 15383372 | Pharmacological studies showed that PKC inhibition blocked bombesin- and PMA-stimulated hormone release, but AMPK activation failed to suppress nutrient-stimulated hormone secretion. |
| 2623 | 15383372 | Forced expression of constitutively active vs. dominant negative PKDs or AMPKs failed to perturb bombesin- or nutrient-stimulated hormone release. |
| 2624 | 15383372 | Thus, in GIP/Ins cells, PKC regulates bombesin-stimulated hormone release, whereas nutrients may control hormone release by regulating the activity of AMPK-related kinases, rather than AMPK itself. |
| 2625 | 15491793 | Secretion of incretin hormones (GIP and GLP-1) and incretin effect after oral glucose in first-degree relatives of patients with type 2 diabetes. |
| 2626 | 15493880 | Effects of short-term chemical ablation of the GIP receptor on insulin secretion, islet morphology and glucose homeostasis in mice. |
| 2627 | 15493880 | In this study we have utilized a specific and enzymatically stable GIP receptor antagonist, (Pro3)GIP, to evaluate the contribution of endogenous GIP to insulin secretion and glucose homeostasis in mice. |
| 2628 | 15493880 | Insulin sensitivity of 11-day (Pro3)GIP treated mice was slightly impaired 60 min post injection compared with controls. |
| 2629 | 15493880 | Postprandial insulin secretion was not significantly different and no changes in pancreatic insulin content or islet morphology were observed in (Pro3)GIP treated mice. |
| 2630 | 15493880 | These data indicate that ablation of GIP signaling causes a readily reversible glucose intolerance without appreciable change of insulin secretion. |
| 2631 | 15493880 | Effects of short-term chemical ablation of the GIP receptor on insulin secretion, islet morphology and glucose homeostasis in mice. |
| 2632 | 15493880 | In this study we have utilized a specific and enzymatically stable GIP receptor antagonist, (Pro3)GIP, to evaluate the contribution of endogenous GIP to insulin secretion and glucose homeostasis in mice. |
| 2633 | 15493880 | Insulin sensitivity of 11-day (Pro3)GIP treated mice was slightly impaired 60 min post injection compared with controls. |
| 2634 | 15493880 | Postprandial insulin secretion was not significantly different and no changes in pancreatic insulin content or islet morphology were observed in (Pro3)GIP treated mice. |
| 2635 | 15493880 | These data indicate that ablation of GIP signaling causes a readily reversible glucose intolerance without appreciable change of insulin secretion. |
| 2636 | 15493880 | Effects of short-term chemical ablation of the GIP receptor on insulin secretion, islet morphology and glucose homeostasis in mice. |
| 2637 | 15493880 | In this study we have utilized a specific and enzymatically stable GIP receptor antagonist, (Pro3)GIP, to evaluate the contribution of endogenous GIP to insulin secretion and glucose homeostasis in mice. |
| 2638 | 15493880 | Insulin sensitivity of 11-day (Pro3)GIP treated mice was slightly impaired 60 min post injection compared with controls. |
| 2639 | 15493880 | Postprandial insulin secretion was not significantly different and no changes in pancreatic insulin content or islet morphology were observed in (Pro3)GIP treated mice. |
| 2640 | 15493880 | These data indicate that ablation of GIP signaling causes a readily reversible glucose intolerance without appreciable change of insulin secretion. |
| 2641 | 15493880 | Effects of short-term chemical ablation of the GIP receptor on insulin secretion, islet morphology and glucose homeostasis in mice. |
| 2642 | 15493880 | In this study we have utilized a specific and enzymatically stable GIP receptor antagonist, (Pro3)GIP, to evaluate the contribution of endogenous GIP to insulin secretion and glucose homeostasis in mice. |
| 2643 | 15493880 | Insulin sensitivity of 11-day (Pro3)GIP treated mice was slightly impaired 60 min post injection compared with controls. |
| 2644 | 15493880 | Postprandial insulin secretion was not significantly different and no changes in pancreatic insulin content or islet morphology were observed in (Pro3)GIP treated mice. |
| 2645 | 15493880 | These data indicate that ablation of GIP signaling causes a readily reversible glucose intolerance without appreciable change of insulin secretion. |
| 2646 | 15493880 | Effects of short-term chemical ablation of the GIP receptor on insulin secretion, islet morphology and glucose homeostasis in mice. |
| 2647 | 15493880 | In this study we have utilized a specific and enzymatically stable GIP receptor antagonist, (Pro3)GIP, to evaluate the contribution of endogenous GIP to insulin secretion and glucose homeostasis in mice. |
| 2648 | 15493880 | Insulin sensitivity of 11-day (Pro3)GIP treated mice was slightly impaired 60 min post injection compared with controls. |
| 2649 | 15493880 | Postprandial insulin secretion was not significantly different and no changes in pancreatic insulin content or islet morphology were observed in (Pro3)GIP treated mice. |
| 2650 | 15493880 | These data indicate that ablation of GIP signaling causes a readily reversible glucose intolerance without appreciable change of insulin secretion. |
| 2651 | 15495988 | Upon ingestion of food, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are synthesised and secreted by specialised gut cells. |
| 2652 | 15495988 | GLP-1 and GIP stimulate beta-cell proliferation and differentiation, whereas GLP-1 only inhibits gastric emptying and glucagon secretion, reduces food intake and improves insulin sensitivity. |
| 2653 | 15495988 | However, the insulinotropic action of exogenous GLP-1, but not that of GIP, is preserved in these subjects. |
| 2654 | 15495988 | After parenteral administration, GLP-1 has an extremely short duration of action because it is rapidly degraded by the ubiquitous enzyme dipeptidyl peptidase IV (DPPIV). |
| 2655 | 15495988 | To prolong GLP-1 bioactivity, DPPIV-resistant GLP-1 analogues, DPPIV inhibitors and exenatide, a long-acting synthetic GLP-1 receptor agonist derived from the Gila monster hormone exendin-4, have been developed. |
| 2656 | 15495988 | Upon ingestion of food, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are synthesised and secreted by specialised gut cells. |
| 2657 | 15495988 | GLP-1 and GIP stimulate beta-cell proliferation and differentiation, whereas GLP-1 only inhibits gastric emptying and glucagon secretion, reduces food intake and improves insulin sensitivity. |
| 2658 | 15495988 | However, the insulinotropic action of exogenous GLP-1, but not that of GIP, is preserved in these subjects. |
| 2659 | 15495988 | After parenteral administration, GLP-1 has an extremely short duration of action because it is rapidly degraded by the ubiquitous enzyme dipeptidyl peptidase IV (DPPIV). |
| 2660 | 15495988 | To prolong GLP-1 bioactivity, DPPIV-resistant GLP-1 analogues, DPPIV inhibitors and exenatide, a long-acting synthetic GLP-1 receptor agonist derived from the Gila monster hormone exendin-4, have been developed. |
| 2661 | 15495988 | Upon ingestion of food, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are synthesised and secreted by specialised gut cells. |
| 2662 | 15495988 | GLP-1 and GIP stimulate beta-cell proliferation and differentiation, whereas GLP-1 only inhibits gastric emptying and glucagon secretion, reduces food intake and improves insulin sensitivity. |
| 2663 | 15495988 | However, the insulinotropic action of exogenous GLP-1, but not that of GIP, is preserved in these subjects. |
| 2664 | 15495988 | After parenteral administration, GLP-1 has an extremely short duration of action because it is rapidly degraded by the ubiquitous enzyme dipeptidyl peptidase IV (DPPIV). |
| 2665 | 15495988 | To prolong GLP-1 bioactivity, DPPIV-resistant GLP-1 analogues, DPPIV inhibitors and exenatide, a long-acting synthetic GLP-1 receptor agonist derived from the Gila monster hormone exendin-4, have been developed. |
| 2666 | 15522230 | Glucose-dependent insulinotropic polypeptide is an incretin hormone that stimulates insulin secretion and reduces postprandial glycaemic excursions. |
| 2667 | 15522230 | This structural information could play an important role in the design of therapeutic agents based upon GIP receptor agonists. |
| 2668 | 15522230 | Glucose-dependent insulinotropic polypeptide is an incretin hormone that stimulates insulin secretion and reduces postprandial glycaemic excursions. |
| 2669 | 15522230 | This structural information could play an important role in the design of therapeutic agents based upon GIP receptor agonists. |
| 2670 | 15522997 | Moreover, the potentiation time course was related to glucose-dependent insulin-releasing polypeptide (GIP) concentrations in both groups, and the sensitivity of potentiation to GIP derived from this relationship tended to be impaired in FDR. |
| 2671 | 15522997 | In conclusion, although in absolute terms ISR is increased in insulin-resistant FDR, beta-cell function shows a cluster of interrelated abnormalities involving compensation for insulin resistance, potentiation, and sensitivity to GIP, suggesting a beta-cell defect in the amplifying pathway of insulin secretion. |
| 2672 | 15522997 | Moreover, the potentiation time course was related to glucose-dependent insulin-releasing polypeptide (GIP) concentrations in both groups, and the sensitivity of potentiation to GIP derived from this relationship tended to be impaired in FDR. |
| 2673 | 15522997 | In conclusion, although in absolute terms ISR is increased in insulin-resistant FDR, beta-cell function shows a cluster of interrelated abnormalities involving compensation for insulin resistance, potentiation, and sensitivity to GIP, suggesting a beta-cell defect in the amplifying pathway of insulin secretion. |
| 2674 | 15533777 | Later it was found that GIP is capable of augmenting glucose-stimulated insulin secretion, and subsequent studies provided evidence that, in humans, the peptide predominantly acts as an incretin hormone. |
| 2675 | 15533777 | While GIP strongly stimulates insulin release in healthy humans, the peptide has almost completely lost its insulinotropic effect in patients with type 2 diabetes. |
| 2676 | 15533777 | This is different from the actions of glucagon-like peptide 1, which stimulates insulin secretion even in the later stages of type 2 diabetes. |
| 2677 | 15533777 | Later it was found that GIP is capable of augmenting glucose-stimulated insulin secretion, and subsequent studies provided evidence that, in humans, the peptide predominantly acts as an incretin hormone. |
| 2678 | 15533777 | While GIP strongly stimulates insulin release in healthy humans, the peptide has almost completely lost its insulinotropic effect in patients with type 2 diabetes. |
| 2679 | 15533777 | This is different from the actions of glucagon-like peptide 1, which stimulates insulin secretion even in the later stages of type 2 diabetes. |
| 2680 | 15561910 | Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes. |
| 2681 | 15561910 | The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. |
| 2682 | 15561910 | In approximately 50% of first-degree relatives of patients with type 2 diabetes, similarly reduced insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. |
| 2683 | 15561910 | On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes. |
| 2684 | 15561910 | Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes. |
| 2685 | 15561910 | The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. |
| 2686 | 15561910 | In approximately 50% of first-degree relatives of patients with type 2 diabetes, similarly reduced insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. |
| 2687 | 15561910 | On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes. |
| 2688 | 15561910 | Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes. |
| 2689 | 15561910 | The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. |
| 2690 | 15561910 | In approximately 50% of first-degree relatives of patients with type 2 diabetes, similarly reduced insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. |
| 2691 | 15561910 | On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes. |
| 2692 | 15561911 | Together with the related hormone glucose-dependent insulinotropic polypeptide (GIP), it is responsible for the incretin effect, the augmentation of insulin secretion after oral as opposed to intravenous administration of glucose. |
| 2693 | 15561911 | This is due to decreased secretion of GLP-1 and loss of the insulinotropic effects of GIP. |
| 2694 | 15561911 | Together with the related hormone glucose-dependent insulinotropic polypeptide (GIP), it is responsible for the incretin effect, the augmentation of insulin secretion after oral as opposed to intravenous administration of glucose. |
| 2695 | 15561911 | This is due to decreased secretion of GLP-1 and loss of the insulinotropic effects of GIP. |
| 2696 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2697 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2698 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2699 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2700 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2701 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2702 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2703 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2704 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2705 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2706 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2707 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2708 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2709 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2710 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2711 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2712 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2713 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2714 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2715 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2716 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2717 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2718 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2719 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2720 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2721 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2722 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2723 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2724 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2725 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2726 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2727 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2728 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2729 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2730 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2731 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2732 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2733 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2734 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2735 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2736 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2737 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2738 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2739 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2740 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2741 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2742 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2743 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2744 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2745 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2746 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2747 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2748 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2749 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2750 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2751 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2752 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2753 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2754 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2755 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2756 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2757 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2758 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2759 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2760 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2761 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2762 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2763 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2764 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2765 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2766 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2767 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2768 | 15561915 | Stimulation of insulin secretion by intravenous bolus injection and continuous infusion of gastric inhibitory polypeptide in patients with type 2 diabetes and healthy control subjects. |
| 2769 | 15561915 | It was the aim of this study to determine the response of insulin secretion to different GIP doses administered by intravenous bolus injection and via continuous infusion in both healthy subjects and patients with type 2 diabetes. |
| 2770 | 15561915 | Capillary and venous blood was drawn for glucose, insulin, C-peptide, and GIP. |
| 2771 | 15561915 | GIP bolus administration evoked a significant increase in plasma insulin levels in both patients with type 2 diabetes and healthy subjects. |
| 2772 | 15561915 | In contrast, the continuous GIP infusion led to a weak increase in insulin secretion in both healthy subjects and type 2 diabetic patients. |
| 2773 | 15561915 | The dose-response relationship for the increase in insulin secretion after GIP bolus administration was similar in both groups, although at different degrees of beta-cell function. |
| 2774 | 15561915 | The stimulation of insulin secretion by GIP is stronger after its bolus administration than during continuous infusion. |
| 2775 | 15561915 | Even though the insulin secretory capacity is generally impaired in patients with type 2 diabetes, the relative sensitivity of insulin secretion to a bolus administration of GIP is almost preserved. |
| 2776 | 15561915 | Therefore, the existence of a specific GIP receptor defect in type 2 diabetes appears unlikely. |
| 2777 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2778 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2779 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2780 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2781 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2782 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2783 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2784 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2785 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2786 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2787 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2788 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2789 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2790 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2791 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2792 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2793 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2794 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2795 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2796 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2797 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2798 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2799 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2800 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2801 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2802 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2803 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2804 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2805 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2806 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2807 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2808 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2809 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2810 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2811 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2812 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2813 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2814 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2815 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2816 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2817 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2818 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2819 | 15579061 | Structurally modified analogues of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) as future antidiabetic agents. |
| 2820 | 15579061 | Glucagon-like peptide-1(7-36)amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis. |
| 2821 | 15579061 | Such actions of GLP-1 and GIP have generated considerable interest in their possible exploitation as novel agents for the treatment of type 2 diabetes. |
| 2822 | 15579061 | Despite the many attributes of GLP-1 and GIP as possible future antidiabetic agents, their rapid degradation in the circulation by dipeptidyl peptidase IV (DPP IV) to inactive truncated forms GLP-1(9-36)amide and GIP(3-42), severely limits their therapeutic usefulness. |
| 2823 | 15579061 | This review will consider recent developments in the design and effectiveness of synthetic DPP IV-resistant analogues of GLP-1 and GIP. |
| 2824 | 15579061 | Consideration will be given to the effects of N-terminal modification and amino acid substitution of GLP-1 and GIP either side of the DPP IV cleavage site on (i) susceptibility to enzymatic degradation, (ii) binding to native hormone receptor, (iii) ability to elevate intracellular cyclic AMP, (iv) potency as insulin secretagogues, and (v) antihyperglycaemic activity in type 2 diabetes. |
| 2825 | 15579061 | The antidiabetic properties of the best GLP-1 and GIP analogues indeed promise to provide the basis for novel, effective and long-acting drugs for type 2 diabetes therapy. |
| 2826 | 15582721 | Overexpression of a dominant negative GIP receptor in transgenic mice results in disturbed postnatal pancreatic islet and beta-cell development. |
| 2827 | 15582721 | The expression of a dominant negative glucose-dependent insulinotropic polypeptide receptor (GIPRdn) under the control of the rat pro-insulin gene promoter induces severe diabetes mellitus in transgenic mice. |
| 2828 | 15582721 | Overexpression of a dominant negative GIP receptor in transgenic mice results in disturbed postnatal pancreatic islet and beta-cell development. |
| 2829 | 15582721 | The expression of a dominant negative glucose-dependent insulinotropic polypeptide receptor (GIPRdn) under the control of the rat pro-insulin gene promoter induces severe diabetes mellitus in transgenic mice. |
| 2830 | 15604213 | Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice. |
| 2831 | 15604213 | In this study, we explored whether DPP-4 inhibition by valine-pyrrolidide (val-pyr; 100 micromol/kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose (1 g/kg) together with GLP-1 (10 nmol/kg), glucose-dependent insulinotropic polypeptide (GIP; 10 nmol/kg), pituitary adenylate cyclase-activating polypeptide 38 (PACAP38; 1.3 nmol/kg), or gastrin-releasing peptide (GRP; 20 nmol/kg) given at t = 0 in anesthetized C57BL/6J mice. |
| 2832 | 15604213 | It was found that the acute (1-5 min) insulin response to GLP-1 was augmented by val-pyr by 80% (4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/liter), that to GIP by 40% (2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/liter), that to PACAP38 by 75% (4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/liter), and that to GRP by 25% (1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/liter; all P < 0.05 or less). |
| 2833 | 15604213 | This was associated with enhanced glucose elimination rate after GLP-1 [glucose elimination constant (K(G)) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/min] and PACAP38 (2.1 +/- 0.3 vs. 3.2 +/- 0.3%/min; both P < 0.01), but not after GIP or GRP. |
| 2834 | 15604213 | The augmented insulin response to GRP by val-pyr was prevented by the GLP-1 receptor antagonist, exendin(3) (9-39), raising the possibility that GRP effects may occur secondary to stimulation of GLP-1 secretion. |
| 2835 | 15604213 | We conclude that DPP-4 inhibition augments the insulin response not only to GLP-1 but also to GIP, PACAP38, and GRP. |
| 2836 | 15604213 | Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice. |
| 2837 | 15604213 | In this study, we explored whether DPP-4 inhibition by valine-pyrrolidide (val-pyr; 100 micromol/kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose (1 g/kg) together with GLP-1 (10 nmol/kg), glucose-dependent insulinotropic polypeptide (GIP; 10 nmol/kg), pituitary adenylate cyclase-activating polypeptide 38 (PACAP38; 1.3 nmol/kg), or gastrin-releasing peptide (GRP; 20 nmol/kg) given at t = 0 in anesthetized C57BL/6J mice. |
| 2838 | 15604213 | It was found that the acute (1-5 min) insulin response to GLP-1 was augmented by val-pyr by 80% (4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/liter), that to GIP by 40% (2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/liter), that to PACAP38 by 75% (4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/liter), and that to GRP by 25% (1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/liter; all P < 0.05 or less). |
| 2839 | 15604213 | This was associated with enhanced glucose elimination rate after GLP-1 [glucose elimination constant (K(G)) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/min] and PACAP38 (2.1 +/- 0.3 vs. 3.2 +/- 0.3%/min; both P < 0.01), but not after GIP or GRP. |
| 2840 | 15604213 | The augmented insulin response to GRP by val-pyr was prevented by the GLP-1 receptor antagonist, exendin(3) (9-39), raising the possibility that GRP effects may occur secondary to stimulation of GLP-1 secretion. |
| 2841 | 15604213 | We conclude that DPP-4 inhibition augments the insulin response not only to GLP-1 but also to GIP, PACAP38, and GRP. |
| 2842 | 15604213 | Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice. |
| 2843 | 15604213 | In this study, we explored whether DPP-4 inhibition by valine-pyrrolidide (val-pyr; 100 micromol/kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose (1 g/kg) together with GLP-1 (10 nmol/kg), glucose-dependent insulinotropic polypeptide (GIP; 10 nmol/kg), pituitary adenylate cyclase-activating polypeptide 38 (PACAP38; 1.3 nmol/kg), or gastrin-releasing peptide (GRP; 20 nmol/kg) given at t = 0 in anesthetized C57BL/6J mice. |
| 2844 | 15604213 | It was found that the acute (1-5 min) insulin response to GLP-1 was augmented by val-pyr by 80% (4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/liter), that to GIP by 40% (2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/liter), that to PACAP38 by 75% (4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/liter), and that to GRP by 25% (1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/liter; all P < 0.05 or less). |
| 2845 | 15604213 | This was associated with enhanced glucose elimination rate after GLP-1 [glucose elimination constant (K(G)) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/min] and PACAP38 (2.1 +/- 0.3 vs. 3.2 +/- 0.3%/min; both P < 0.01), but not after GIP or GRP. |
| 2846 | 15604213 | The augmented insulin response to GRP by val-pyr was prevented by the GLP-1 receptor antagonist, exendin(3) (9-39), raising the possibility that GRP effects may occur secondary to stimulation of GLP-1 secretion. |
| 2847 | 15604213 | We conclude that DPP-4 inhibition augments the insulin response not only to GLP-1 but also to GIP, PACAP38, and GRP. |
| 2848 | 15604213 | Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice. |
| 2849 | 15604213 | In this study, we explored whether DPP-4 inhibition by valine-pyrrolidide (val-pyr; 100 micromol/kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose (1 g/kg) together with GLP-1 (10 nmol/kg), glucose-dependent insulinotropic polypeptide (GIP; 10 nmol/kg), pituitary adenylate cyclase-activating polypeptide 38 (PACAP38; 1.3 nmol/kg), or gastrin-releasing peptide (GRP; 20 nmol/kg) given at t = 0 in anesthetized C57BL/6J mice. |
| 2850 | 15604213 | It was found that the acute (1-5 min) insulin response to GLP-1 was augmented by val-pyr by 80% (4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/liter), that to GIP by 40% (2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/liter), that to PACAP38 by 75% (4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/liter), and that to GRP by 25% (1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/liter; all P < 0.05 or less). |
| 2851 | 15604213 | This was associated with enhanced glucose elimination rate after GLP-1 [glucose elimination constant (K(G)) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/min] and PACAP38 (2.1 +/- 0.3 vs. 3.2 +/- 0.3%/min; both P < 0.01), but not after GIP or GRP. |
| 2852 | 15604213 | The augmented insulin response to GRP by val-pyr was prevented by the GLP-1 receptor antagonist, exendin(3) (9-39), raising the possibility that GRP effects may occur secondary to stimulation of GLP-1 secretion. |
| 2853 | 15604213 | We conclude that DPP-4 inhibition augments the insulin response not only to GLP-1 but also to GIP, PACAP38, and GRP. |
| 2854 | 15604213 | Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice. |
| 2855 | 15604213 | In this study, we explored whether DPP-4 inhibition by valine-pyrrolidide (val-pyr; 100 micromol/kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose (1 g/kg) together with GLP-1 (10 nmol/kg), glucose-dependent insulinotropic polypeptide (GIP; 10 nmol/kg), pituitary adenylate cyclase-activating polypeptide 38 (PACAP38; 1.3 nmol/kg), or gastrin-releasing peptide (GRP; 20 nmol/kg) given at t = 0 in anesthetized C57BL/6J mice. |
| 2856 | 15604213 | It was found that the acute (1-5 min) insulin response to GLP-1 was augmented by val-pyr by 80% (4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/liter), that to GIP by 40% (2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/liter), that to PACAP38 by 75% (4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/liter), and that to GRP by 25% (1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/liter; all P < 0.05 or less). |
| 2857 | 15604213 | This was associated with enhanced glucose elimination rate after GLP-1 [glucose elimination constant (K(G)) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/min] and PACAP38 (2.1 +/- 0.3 vs. 3.2 +/- 0.3%/min; both P < 0.01), but not after GIP or GRP. |
| 2858 | 15604213 | The augmented insulin response to GRP by val-pyr was prevented by the GLP-1 receptor antagonist, exendin(3) (9-39), raising the possibility that GRP effects may occur secondary to stimulation of GLP-1 secretion. |
| 2859 | 15604213 | We conclude that DPP-4 inhibition augments the insulin response not only to GLP-1 but also to GIP, PACAP38, and GRP. |
| 2860 | 15655702 | The two most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 2861 | 15655702 | In patients with type 2 diabetes, the incretin effect is decreased, mainly due to loss of the GIP-regulated second phase of insulin secretion, and because of a decreased secretion of GLP-1. |
| 2862 | 15655702 | The two most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 2863 | 15655702 | In patients with type 2 diabetes, the incretin effect is decreased, mainly due to loss of the GIP-regulated second phase of insulin secretion, and because of a decreased secretion of GLP-1. |
| 2864 | 15655707 | Physiology of GIP--a lesson from GIP receptor knockout mice. |
| 2865 | 15655707 | GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. |
| 2866 | 15655707 | However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. |
| 2867 | 15655707 | We have bred and characterized mice with a targeted mutation of the GIP receptor gene. |
| 2868 | 15655707 | From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. |
| 2869 | 15655707 | Physiology of GIP--a lesson from GIP receptor knockout mice. |
| 2870 | 15655707 | GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. |
| 2871 | 15655707 | However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. |
| 2872 | 15655707 | We have bred and characterized mice with a targeted mutation of the GIP receptor gene. |
| 2873 | 15655707 | From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. |
| 2874 | 15655707 | Physiology of GIP--a lesson from GIP receptor knockout mice. |
| 2875 | 15655707 | GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. |
| 2876 | 15655707 | However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. |
| 2877 | 15655707 | We have bred and characterized mice with a targeted mutation of the GIP receptor gene. |
| 2878 | 15655707 | From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. |
| 2879 | 15655707 | Physiology of GIP--a lesson from GIP receptor knockout mice. |
| 2880 | 15655707 | GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. |
| 2881 | 15655707 | However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. |
| 2882 | 15655707 | We have bred and characterized mice with a targeted mutation of the GIP receptor gene. |
| 2883 | 15655707 | From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. |
| 2884 | 15655707 | Physiology of GIP--a lesson from GIP receptor knockout mice. |
| 2885 | 15655707 | GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. |
| 2886 | 15655707 | However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. |
| 2887 | 15655707 | We have bred and characterized mice with a targeted mutation of the GIP receptor gene. |
| 2888 | 15655707 | From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. |
| 2889 | 15655709 | Perhaps the most important effect of GIP is its potentiation of insulin secretion. |
| 2890 | 15655709 | There is emerging evidence that like the related hormone glucagon-like peptide-1, GIP may function as a beta cell growth factor and anti-apoptotic agent, further supporting a role for this hormone in balancing beta cell function to changing metabolic conditions. |
| 2891 | 15655709 | Perhaps the most important effect of GIP is its potentiation of insulin secretion. |
| 2892 | 15655709 | There is emerging evidence that like the related hormone glucagon-like peptide-1, GIP may function as a beta cell growth factor and anti-apoptotic agent, further supporting a role for this hormone in balancing beta cell function to changing metabolic conditions. |
| 2893 | 15655715 | Extrapancreatic effects of GIP and GLP-1. |
| 2894 | 15655715 | Glucagon-like peptide-1 (GLP1) and, to a lesser extent, glucose-dependent insulinotropic polypeptide (GIP) are potent stimulators of insulin secretion, and consequently have significant effects on the regulation of the glucose metabolism. |
| 2895 | 15655715 | Extrapancreatic effects of GIP and GLP-1. |
| 2896 | 15655715 | Glucagon-like peptide-1 (GLP1) and, to a lesser extent, glucose-dependent insulinotropic polypeptide (GIP) are potent stimulators of insulin secretion, and consequently have significant effects on the regulation of the glucose metabolism. |
| 2897 | 15655720 | Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. |
| 2898 | 15655720 | While derivatives of GLP-1 are under active investigation for the treatment of type 2 diabetes, the case is different for GIP. |
| 2899 | 15655720 | However, glucose-normalisation, as is typically observed during the intravenous administration of GLP-1 in patients with type 2 diabetes, has not yet been achieved with GIP or its derivatives. |
| 2900 | 15655720 | This concept has recently been reinforced by the observation that GIP receptor knock-out mice are protected from high-fat diet-induced obesity. |
| 2901 | 15655720 | However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. |
| 2902 | 15655720 | Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. |
| 2903 | 15655720 | While derivatives of GLP-1 are under active investigation for the treatment of type 2 diabetes, the case is different for GIP. |
| 2904 | 15655720 | However, glucose-normalisation, as is typically observed during the intravenous administration of GLP-1 in patients with type 2 diabetes, has not yet been achieved with GIP or its derivatives. |
| 2905 | 15655720 | This concept has recently been reinforced by the observation that GIP receptor knock-out mice are protected from high-fat diet-induced obesity. |
| 2906 | 15655720 | However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. |
| 2907 | 15655720 | Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. |
| 2908 | 15655720 | While derivatives of GLP-1 are under active investigation for the treatment of type 2 diabetes, the case is different for GIP. |
| 2909 | 15655720 | However, glucose-normalisation, as is typically observed during the intravenous administration of GLP-1 in patients with type 2 diabetes, has not yet been achieved with GIP or its derivatives. |
| 2910 | 15655720 | This concept has recently been reinforced by the observation that GIP receptor knock-out mice are protected from high-fat diet-induced obesity. |
| 2911 | 15655720 | However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. |
| 2912 | 15655720 | Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. |
| 2913 | 15655720 | While derivatives of GLP-1 are under active investigation for the treatment of type 2 diabetes, the case is different for GIP. |
| 2914 | 15655720 | However, glucose-normalisation, as is typically observed during the intravenous administration of GLP-1 in patients with type 2 diabetes, has not yet been achieved with GIP or its derivatives. |
| 2915 | 15655720 | This concept has recently been reinforced by the observation that GIP receptor knock-out mice are protected from high-fat diet-induced obesity. |
| 2916 | 15655720 | However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. |
| 2917 | 15655720 | Glucose-dependent insulinotropic polypeptide (GIP) is released from K-cells in the gut after meal ingestion, and acts in concert with glucagon-like peptide 1 (GLP-1) to augment glucose-stimulated insulin secretion. |
| 2918 | 15655720 | While derivatives of GLP-1 are under active investigation for the treatment of type 2 diabetes, the case is different for GIP. |
| 2919 | 15655720 | However, glucose-normalisation, as is typically observed during the intravenous administration of GLP-1 in patients with type 2 diabetes, has not yet been achieved with GIP or its derivatives. |
| 2920 | 15655720 | This concept has recently been reinforced by the observation that GIP receptor knock-out mice are protected from high-fat diet-induced obesity. |
| 2921 | 15655720 | However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. |
| 2922 | 15657373 | Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. |
| 2923 | 15657373 | To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). |
| 2924 | 15657373 | PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. |
| 2925 | 15657373 | There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). |
| 2926 | 15657373 | The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. |
| 2927 | 15657373 | Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. |
| 2928 | 15657373 | To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). |
| 2929 | 15657373 | PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. |
| 2930 | 15657373 | There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). |
| 2931 | 15657373 | The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. |
| 2932 | 15657373 | Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. |
| 2933 | 15657373 | To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). |
| 2934 | 15657373 | PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. |
| 2935 | 15657373 | There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). |
| 2936 | 15657373 | The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. |
| 2937 | 15657373 | Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. |
| 2938 | 15657373 | To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). |
| 2939 | 15657373 | PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. |
| 2940 | 15657373 | There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). |
| 2941 | 15657373 | The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. |
| 2942 | 15657373 | Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. |
| 2943 | 15657373 | To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). |
| 2944 | 15657373 | PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. |
| 2945 | 15657373 | There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). |
| 2946 | 15657373 | The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. |
| 2947 | 15715491 | Degradation, insulin secretion, and antihyperglycemic actions of two palmitate-derivitized N-terminal pyroglutamyl analogues of glucose-dependent insulinotropic polypeptide. |
| 2948 | 15715491 | In GIP-receptor transfected fibroblasts, N-pGluGIP(LysPAL(16)) and N-pGluGIP(LysPAL(37)) exhibited enhanced stimulation of cAMP production. |
| 2949 | 15715491 | When administered together with glucose to ob/ob mice, the glycemic excursions were significantly less for both analogues and insulin responses were greater than native GIP. |
| 2950 | 15715491 | Degradation, insulin secretion, and antihyperglycemic actions of two palmitate-derivitized N-terminal pyroglutamyl analogues of glucose-dependent insulinotropic polypeptide. |
| 2951 | 15715491 | In GIP-receptor transfected fibroblasts, N-pGluGIP(LysPAL(16)) and N-pGluGIP(LysPAL(37)) exhibited enhanced stimulation of cAMP production. |
| 2952 | 15715491 | When administered together with glucose to ob/ob mice, the glycemic excursions were significantly less for both analogues and insulin responses were greater than native GIP. |
| 2953 | 15715491 | Degradation, insulin secretion, and antihyperglycemic actions of two palmitate-derivitized N-terminal pyroglutamyl analogues of glucose-dependent insulinotropic polypeptide. |
| 2954 | 15715491 | In GIP-receptor transfected fibroblasts, N-pGluGIP(LysPAL(16)) and N-pGluGIP(LysPAL(37)) exhibited enhanced stimulation of cAMP production. |
| 2955 | 15715491 | When administered together with glucose to ob/ob mice, the glycemic excursions were significantly less for both analogues and insulin responses were greater than native GIP. |
| 2956 | 15780427 | In 1970, glucose dependent insulinotropic polypeptide (GIP), and finally, in 1985 glucagon-like peptide 1 (GLP-1) and its truncated form GLP-1(7-36) were recognized as true incretins. |
| 2957 | 15780432 | GIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice. |
| 2958 | 15780432 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut-derived incretins secreted in response to nutrient ingestion. |
| 2959 | 15780432 | In contrast, GLP-1, but not GIP, inhibits gastric emptying, glucagon secretion, and food intake. |
| 2960 | 15780432 | Furthermore, human subjects with Type 2 diabetes exhibit relative resistance to the actions of GIP, but not GLP-1R agonists. |
| 2961 | 15780432 | However, glucose-stimulated insulin secretion is significantly decreased following oral but not intraperitoneal glucose challenge in DIRKO mice and the glucose lowering actions of dipeptidyl peptidase-IV (DPP-IV) inhibitors are extinguished in DIRKO mice. |
| 2962 | 15780432 | GIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice. |
| 2963 | 15780432 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut-derived incretins secreted in response to nutrient ingestion. |
| 2964 | 15780432 | In contrast, GLP-1, but not GIP, inhibits gastric emptying, glucagon secretion, and food intake. |
| 2965 | 15780432 | Furthermore, human subjects with Type 2 diabetes exhibit relative resistance to the actions of GIP, but not GLP-1R agonists. |
| 2966 | 15780432 | However, glucose-stimulated insulin secretion is significantly decreased following oral but not intraperitoneal glucose challenge in DIRKO mice and the glucose lowering actions of dipeptidyl peptidase-IV (DPP-IV) inhibitors are extinguished in DIRKO mice. |
| 2967 | 15780432 | GIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice. |
| 2968 | 15780432 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut-derived incretins secreted in response to nutrient ingestion. |
| 2969 | 15780432 | In contrast, GLP-1, but not GIP, inhibits gastric emptying, glucagon secretion, and food intake. |
| 2970 | 15780432 | Furthermore, human subjects with Type 2 diabetes exhibit relative resistance to the actions of GIP, but not GLP-1R agonists. |
| 2971 | 15780432 | However, glucose-stimulated insulin secretion is significantly decreased following oral but not intraperitoneal glucose challenge in DIRKO mice and the glucose lowering actions of dipeptidyl peptidase-IV (DPP-IV) inhibitors are extinguished in DIRKO mice. |
| 2972 | 15780432 | GIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice. |
| 2973 | 15780432 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are gut-derived incretins secreted in response to nutrient ingestion. |
| 2974 | 15780432 | In contrast, GLP-1, but not GIP, inhibits gastric emptying, glucagon secretion, and food intake. |
| 2975 | 15780432 | Furthermore, human subjects with Type 2 diabetes exhibit relative resistance to the actions of GIP, but not GLP-1R agonists. |
| 2976 | 15780432 | However, glucose-stimulated insulin secretion is significantly decreased following oral but not intraperitoneal glucose challenge in DIRKO mice and the glucose lowering actions of dipeptidyl peptidase-IV (DPP-IV) inhibitors are extinguished in DIRKO mice. |
| 2977 | 15780434 | Preservation of the insulin response to parenteral glucagon-like peptide-1 (GLP-1), contrasting with lack of stimulation of insulin secretion by the other known incretin gastric inhibitory polypeptide (GIP), prompted studies with exogenous GLP-1 in recent-onset Type 1 diabetes. |
| 2978 | 15780434 | These studies showed substantial reduction of glycaemic excursions after ingestion of mixed nutrients during intravenous infusion of GLP-1 without administration of insulin, in subjects with a range of endogenous secretion of insulin in response to meals as demonstrated by blood levels of the insulin-connecting peptide (CP). |
| 2979 | 15780434 | The glycaemic effects were associated with inhibition of abnormal rises of blood levels of glucagon, and with suppression of endogenous release of human pancreatic polypeptide (HPP), by GLP-1. |
| 2980 | 15780434 | Studies of the effects of GLP-1 agonists (GLP-1 and exendin-4) given together with established insulin doses before a meal supported the hypothesis. |
| 2981 | 15780434 | It is suggested that further and more prolonged studies of the use of long-acting GLP-1 agonists as congeners with insulin in Type 1 diabetes mellitus are indicated. |
| 2982 | 15780435 | A number of new approaches to diabetes therapy are currently undergoing clinical trials, including those involving stimulation of the pancreatic beta-cell with the gut-derived insulinotropic hormones (incretins), GIP and GLP-1. |
| 2983 | 15780435 | It is now clear that both GIP and GLP-1 also have powerful effects on beta-cell differentation, mitogenesis and survival. |
| 2984 | 15780435 | A number of new approaches to diabetes therapy are currently undergoing clinical trials, including those involving stimulation of the pancreatic beta-cell with the gut-derived insulinotropic hormones (incretins), GIP and GLP-1. |
| 2985 | 15780435 | It is now clear that both GIP and GLP-1 also have powerful effects on beta-cell differentation, mitogenesis and survival. |
| 2986 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 2987 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 2988 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 2989 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 2990 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 2991 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 2992 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 2993 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 2994 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 2995 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 2996 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 2997 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 2998 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 2999 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3000 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3001 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3002 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 3003 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 3004 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 3005 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 3006 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 3007 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3008 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3009 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3010 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 3011 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 3012 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 3013 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 3014 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 3015 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3016 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3017 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3018 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 3019 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 3020 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 3021 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 3022 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 3023 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3024 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3025 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3026 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 3027 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 3028 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 3029 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 3030 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 3031 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3032 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3033 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3034 | 15793244 | Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility. |
| 3035 | 15793244 | Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). |
| 3036 | 15793244 | In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. |
| 3037 | 15793244 | In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. |
| 3038 | 15793244 | In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. |
| 3039 | 15793244 | We also found that GLP-1 inhibited gut motility whereas GIP did not. |
| 3040 | 15793244 | Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. |
| 3041 | 15793244 | Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently. |
| 3042 | 15803750 | Measured basal and stimulated plasma GIP levels of those diabetic rats during acid stimulation remained higher, regardless of insulin treatment (P < 0.05). |
| 3043 | 15803750 | Our results suggest that insulin has the ability to attenuate pentagastrin-stimulated acid output in rats, whereas GIP is not involved in this attenuation. |
| 3044 | 15803750 | Measured basal and stimulated plasma GIP levels of those diabetic rats during acid stimulation remained higher, regardless of insulin treatment (P < 0.05). |
| 3045 | 15803750 | Our results suggest that insulin has the ability to attenuate pentagastrin-stimulated acid output in rats, whereas GIP is not involved in this attenuation. |
| 3046 | 15886226 | Initially more rapid small intestinal glucose delivery increases plasma insulin, GIP, and GLP-1 but does not improve overall glycemia in healthy subjects. |
| 3047 | 15886226 | The latter is also dependent on stimulation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3048 | 15886226 | Between t = 0 and 75 min, plasma insulin, GIP, and GLP-1 were higher with the variable infusion. |
| 3049 | 15886226 | Initially more rapid small intestinal glucose delivery increases plasma insulin, GIP, and GLP-1 but does not improve overall glycemia in healthy subjects. |
| 3050 | 15886226 | The latter is also dependent on stimulation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3051 | 15886226 | Between t = 0 and 75 min, plasma insulin, GIP, and GLP-1 were higher with the variable infusion. |
| 3052 | 15886226 | Initially more rapid small intestinal glucose delivery increases plasma insulin, GIP, and GLP-1 but does not improve overall glycemia in healthy subjects. |
| 3053 | 15886226 | The latter is also dependent on stimulation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3054 | 15886226 | Between t = 0 and 75 min, plasma insulin, GIP, and GLP-1 were higher with the variable infusion. |
| 3055 | 15899957 | Normal secretion and action of the gut incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in young men with low birth weight. |
| 3056 | 15907807 | In this paper, we report on (1) the kinetics of binding, (2) the type of inhibition, (3) the selectivity with respect to other peptidases, and (4) the inhibitory potency on the DPP IV catalyzed degradation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and substance P. |
| 3057 | 15907807 | It is a micromolar inhibitor for dipeptidyl-peptidase 8 and does not significantly inhibit dipeptidyl-peptidase II (EC 3.4.11.2), prolyl oligopeptidase (EC 3.4.21.26), aminopeptidase P (EC 3.4.11.9) or aminopeptidase M (EC 3.4.11.2). |
| 3058 | 15907807 | There was no evidence for substrate specific inhibition of DPP IV by Vildagliptin or for important allosteric factors affecting the inhibition constant in presence of GIP and GLP-1. |
| 3059 | 15907807 | In this paper, we report on (1) the kinetics of binding, (2) the type of inhibition, (3) the selectivity with respect to other peptidases, and (4) the inhibitory potency on the DPP IV catalyzed degradation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and substance P. |
| 3060 | 15907807 | It is a micromolar inhibitor for dipeptidyl-peptidase 8 and does not significantly inhibit dipeptidyl-peptidase II (EC 3.4.11.2), prolyl oligopeptidase (EC 3.4.21.26), aminopeptidase P (EC 3.4.11.9) or aminopeptidase M (EC 3.4.11.2). |
| 3061 | 15907807 | There was no evidence for substrate specific inhibition of DPP IV by Vildagliptin or for important allosteric factors affecting the inhibition constant in presence of GIP and GLP-1. |
| 3062 | 15923344 | Once-daily injections of N-AcGIP(LysPAL(37)) over a 14-day period significantly decreased plasma glucose, glycated hemoglobin, and improved glucose tolerance compared with ob/ob mice treated with saline or native GIP. |
| 3063 | 15923344 | No evidence was found for GIP receptor desensitization and the metabolic effects of N-AcGIP(LysPAL(37)) were independent of any change in feeding or body weight. |
| 3064 | 15923344 | Once-daily injections of N-AcGIP(LysPAL(37)) over a 14-day period significantly decreased plasma glucose, glycated hemoglobin, and improved glucose tolerance compared with ob/ob mice treated with saline or native GIP. |
| 3065 | 15923344 | No evidence was found for GIP receptor desensitization and the metabolic effects of N-AcGIP(LysPAL(37)) were independent of any change in feeding or body weight. |
| 3066 | 15983224 | Glucagon-like peptide 1 (GLP-1) has been proposed to act as an incretin hormone due to its ability to enhance glucose-stimulated insulin secretion. |
| 3067 | 15983224 | Because GLP-1 also decelerates gastric emptying, it physiologically reduces rather than augments postprandial insulin secretory responses. |
| 3068 | 15983224 | Therefore, we aimed to antagonize the deceleration of gastric emptying by GLP-1 to study its effects on insulin secretion after a meal. |
| 3069 | 15983224 | Capillary and venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1, glucagon, gastric inhibitory polypeptide (GIP), and pancreatic polypeptide (specific immunoassays). |
| 3070 | 15983224 | Insulin secretory responses to the meal were lower during GLP-1 administration (P < 0.05 vs. placebo). |
| 3071 | 15983224 | However, when erythromycin was added to GLP-1, insulin concentrations were similar to those in placebo experiments. |
| 3072 | 15983224 | The time course of GIP secretion was delayed during GLP-1 administration (P < 0.05), but when erythromycin was added, the pattern was similar to placebo experiments. |
| 3073 | 15983224 | GLP-1 administration led to a reduction in pancreatic polypeptide plasma concentrations (P < 0.05). |
| 3074 | 15983224 | Intravenous erythromycin counteracts the deceleration of gastric emptying caused by GLP-1, probably by interacting with the parasympathetic nervous system (pancreatic polypeptide responses). |
| 3075 | 15983224 | Despite augmented rises in insulin secretion, the glucose-lowering effect of GLP-1 is markedly reduced when the deceleration of gastric emptying is antagonized, illustrating the importance of this facet of the multiple antidiabetic actions of GLP-1. |
| 3076 | 15983224 | Glucagon-like peptide 1 (GLP-1) has been proposed to act as an incretin hormone due to its ability to enhance glucose-stimulated insulin secretion. |
| 3077 | 15983224 | Because GLP-1 also decelerates gastric emptying, it physiologically reduces rather than augments postprandial insulin secretory responses. |
| 3078 | 15983224 | Therefore, we aimed to antagonize the deceleration of gastric emptying by GLP-1 to study its effects on insulin secretion after a meal. |
| 3079 | 15983224 | Capillary and venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1, glucagon, gastric inhibitory polypeptide (GIP), and pancreatic polypeptide (specific immunoassays). |
| 3080 | 15983224 | Insulin secretory responses to the meal were lower during GLP-1 administration (P < 0.05 vs. placebo). |
| 3081 | 15983224 | However, when erythromycin was added to GLP-1, insulin concentrations were similar to those in placebo experiments. |
| 3082 | 15983224 | The time course of GIP secretion was delayed during GLP-1 administration (P < 0.05), but when erythromycin was added, the pattern was similar to placebo experiments. |
| 3083 | 15983224 | GLP-1 administration led to a reduction in pancreatic polypeptide plasma concentrations (P < 0.05). |
| 3084 | 15983224 | Intravenous erythromycin counteracts the deceleration of gastric emptying caused by GLP-1, probably by interacting with the parasympathetic nervous system (pancreatic polypeptide responses). |
| 3085 | 15983224 | Despite augmented rises in insulin secretion, the glucose-lowering effect of GLP-1 is markedly reduced when the deceleration of gastric emptying is antagonized, illustrating the importance of this facet of the multiple antidiabetic actions of GLP-1. |
| 3086 | 16009062 | On the role of the incretin hormones GIP and GLP-1 in the pathogenesis of Type 2 diabetes mellitus. |
| 3087 | 16046120 | Dipeptidyl peptidase IV (DPP4) is a multifunctional type II transmembrane serine peptidase which regulates various physiological processes, most notably plasma glucose homeostasis by cleaving peptide hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. |
| 3088 | 16046312 | Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. |
| 3089 | 16046312 | In this study, we investigated the effects of chemical ablation of GIP receptor (GIP-R) action on aspects of obesity-related diabetes using a stable and specific GIP-R antagonist, (Pro3)GIP. |
| 3090 | 16046312 | GIP-R ablation also significantly lowered overall plasma glucose (1.4-fold; P < 0.05) and insulin (1.5-fold; P < 0.05) responses to feeding. |
| 3091 | 16046312 | These changes were associated with significantly enhanced (1.6-fold; P < 0.05) insulin sensitivity in the (Pro3)GIP-treated group. |
| 3092 | 16046312 | Daily injection of (Pro3)GIP reduced pancreatic insulin content (1.3-fold; P < 0.05) and partially corrected the obesity-related islet hypertrophy and beta-cell hyperplasia of ob/ob mice. |
| 3093 | 16046312 | These studies highlight a role for GIP in obesity-related glucose intolerance and emphasize the potential of specific GIP-R antagonists as a new class of drugs for the alleviation of insulin resistance and treatment of type 2 diabetes. |
| 3094 | 16046312 | Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. |
| 3095 | 16046312 | In this study, we investigated the effects of chemical ablation of GIP receptor (GIP-R) action on aspects of obesity-related diabetes using a stable and specific GIP-R antagonist, (Pro3)GIP. |
| 3096 | 16046312 | GIP-R ablation also significantly lowered overall plasma glucose (1.4-fold; P < 0.05) and insulin (1.5-fold; P < 0.05) responses to feeding. |
| 3097 | 16046312 | These changes were associated with significantly enhanced (1.6-fold; P < 0.05) insulin sensitivity in the (Pro3)GIP-treated group. |
| 3098 | 16046312 | Daily injection of (Pro3)GIP reduced pancreatic insulin content (1.3-fold; P < 0.05) and partially corrected the obesity-related islet hypertrophy and beta-cell hyperplasia of ob/ob mice. |
| 3099 | 16046312 | These studies highlight a role for GIP in obesity-related glucose intolerance and emphasize the potential of specific GIP-R antagonists as a new class of drugs for the alleviation of insulin resistance and treatment of type 2 diabetes. |
| 3100 | 16046312 | Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. |
| 3101 | 16046312 | In this study, we investigated the effects of chemical ablation of GIP receptor (GIP-R) action on aspects of obesity-related diabetes using a stable and specific GIP-R antagonist, (Pro3)GIP. |
| 3102 | 16046312 | GIP-R ablation also significantly lowered overall plasma glucose (1.4-fold; P < 0.05) and insulin (1.5-fold; P < 0.05) responses to feeding. |
| 3103 | 16046312 | These changes were associated with significantly enhanced (1.6-fold; P < 0.05) insulin sensitivity in the (Pro3)GIP-treated group. |
| 3104 | 16046312 | Daily injection of (Pro3)GIP reduced pancreatic insulin content (1.3-fold; P < 0.05) and partially corrected the obesity-related islet hypertrophy and beta-cell hyperplasia of ob/ob mice. |
| 3105 | 16046312 | These studies highlight a role for GIP in obesity-related glucose intolerance and emphasize the potential of specific GIP-R antagonists as a new class of drugs for the alleviation of insulin resistance and treatment of type 2 diabetes. |
| 3106 | 16046312 | Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. |
| 3107 | 16046312 | In this study, we investigated the effects of chemical ablation of GIP receptor (GIP-R) action on aspects of obesity-related diabetes using a stable and specific GIP-R antagonist, (Pro3)GIP. |
| 3108 | 16046312 | GIP-R ablation also significantly lowered overall plasma glucose (1.4-fold; P < 0.05) and insulin (1.5-fold; P < 0.05) responses to feeding. |
| 3109 | 16046312 | These changes were associated with significantly enhanced (1.6-fold; P < 0.05) insulin sensitivity in the (Pro3)GIP-treated group. |
| 3110 | 16046312 | Daily injection of (Pro3)GIP reduced pancreatic insulin content (1.3-fold; P < 0.05) and partially corrected the obesity-related islet hypertrophy and beta-cell hyperplasia of ob/ob mice. |
| 3111 | 16046312 | These studies highlight a role for GIP in obesity-related glucose intolerance and emphasize the potential of specific GIP-R antagonists as a new class of drugs for the alleviation of insulin resistance and treatment of type 2 diabetes. |
| 3112 | 16046312 | Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. |
| 3113 | 16046312 | In this study, we investigated the effects of chemical ablation of GIP receptor (GIP-R) action on aspects of obesity-related diabetes using a stable and specific GIP-R antagonist, (Pro3)GIP. |
| 3114 | 16046312 | GIP-R ablation also significantly lowered overall plasma glucose (1.4-fold; P < 0.05) and insulin (1.5-fold; P < 0.05) responses to feeding. |
| 3115 | 16046312 | These changes were associated with significantly enhanced (1.6-fold; P < 0.05) insulin sensitivity in the (Pro3)GIP-treated group. |
| 3116 | 16046312 | Daily injection of (Pro3)GIP reduced pancreatic insulin content (1.3-fold; P < 0.05) and partially corrected the obesity-related islet hypertrophy and beta-cell hyperplasia of ob/ob mice. |
| 3117 | 16046312 | These studies highlight a role for GIP in obesity-related glucose intolerance and emphasize the potential of specific GIP-R antagonists as a new class of drugs for the alleviation of insulin resistance and treatment of type 2 diabetes. |
| 3118 | 16050953 | A comparison of the cellular and biological properties of DPP-IV-resistant N-glucitol analogues of glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. |
| 3119 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 3120 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 3121 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 3122 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 3123 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 3124 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 3125 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 3126 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 3127 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 3128 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 3129 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 3130 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 3131 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 3132 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 3133 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 3134 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 3135 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 3136 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 3137 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 3138 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 3139 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 3140 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 3141 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 3142 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 3143 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 3144 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 3145 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 3146 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 3147 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 3148 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 3149 | 16142014 | Biological actions of the incretins GIP and GLP-1 and therapeutic perspectives in patients with type 2 diabetes. |
| 3150 | 16142014 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide GIP, and glucagon-like peptide-1 GLP-1. |
| 3151 | 16142014 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 3152 | 16142014 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 3153 | 16142014 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 3154 | 16142014 | A number of pharmacological strategies have been developed to provide continuous delivery of GLP-1 and to prevent degradation of GLP-1, including continuous administration of GLP-1, DPP-IV inhibitors and DPP-IV resistant GLP-1 analogues. |
| 3155 | 16142014 | Biological actions of the incretins GIP and GLP-1 and therapeutic perspectives in patients with type 2 diabetes. |
| 3156 | 16142014 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide GIP, and glucagon-like peptide-1 GLP-1. |
| 3157 | 16142014 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 3158 | 16142014 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 3159 | 16142014 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 3160 | 16142014 | A number of pharmacological strategies have been developed to provide continuous delivery of GLP-1 and to prevent degradation of GLP-1, including continuous administration of GLP-1, DPP-IV inhibitors and DPP-IV resistant GLP-1 analogues. |
| 3161 | 16142014 | Biological actions of the incretins GIP and GLP-1 and therapeutic perspectives in patients with type 2 diabetes. |
| 3162 | 16142014 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide GIP, and glucagon-like peptide-1 GLP-1. |
| 3163 | 16142014 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 3164 | 16142014 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 3165 | 16142014 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 3166 | 16142014 | A number of pharmacological strategies have been developed to provide continuous delivery of GLP-1 and to prevent degradation of GLP-1, including continuous administration of GLP-1, DPP-IV inhibitors and DPP-IV resistant GLP-1 analogues. |
| 3167 | 16142014 | Biological actions of the incretins GIP and GLP-1 and therapeutic perspectives in patients with type 2 diabetes. |
| 3168 | 16142014 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide GIP, and glucagon-like peptide-1 GLP-1. |
| 3169 | 16142014 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 3170 | 16142014 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 3171 | 16142014 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 3172 | 16142014 | A number of pharmacological strategies have been developed to provide continuous delivery of GLP-1 and to prevent degradation of GLP-1, including continuous administration of GLP-1, DPP-IV inhibitors and DPP-IV resistant GLP-1 analogues. |
| 3173 | 16181707 | Effects on glucose homeostasis and insulin secretion of long term activation of the glucose-dependent insulinotropic polypeptide (GIP) receptor by N-AcGIP(LysPAL37) in normal mice. |
| 3174 | 16181707 | The present study was designed to assess the metabolic effects in healthy mice of long term activation of the GIP receptor by N-AcGIP(LysPAL37), a potent long-acting GIP receptor agonist. |
| 3175 | 16181707 | Daily injection of N-AcGIP(LysPAL37) (25 nmol/kg body weight) for 14 days had no significant effect on food intake, body weight, glycated hemoglobin levels, non-fasting plasma glucose and insulin concentrations compared to saline treated controls. |
| 3176 | 16181707 | These data indicate that long term activation of the GIP receptor by daily treatment with N-AcGIP(LysPAL37) improved glucose tolerance due to enhancement of pancreatic beta cell glucose responsiveness and insulin secretion. |
| 3177 | 16181707 | Effects on glucose homeostasis and insulin secretion of long term activation of the glucose-dependent insulinotropic polypeptide (GIP) receptor by N-AcGIP(LysPAL37) in normal mice. |
| 3178 | 16181707 | The present study was designed to assess the metabolic effects in healthy mice of long term activation of the GIP receptor by N-AcGIP(LysPAL37), a potent long-acting GIP receptor agonist. |
| 3179 | 16181707 | Daily injection of N-AcGIP(LysPAL37) (25 nmol/kg body weight) for 14 days had no significant effect on food intake, body weight, glycated hemoglobin levels, non-fasting plasma glucose and insulin concentrations compared to saline treated controls. |
| 3180 | 16181707 | These data indicate that long term activation of the GIP receptor by daily treatment with N-AcGIP(LysPAL37) improved glucose tolerance due to enhancement of pancreatic beta cell glucose responsiveness and insulin secretion. |
| 3181 | 16181707 | Effects on glucose homeostasis and insulin secretion of long term activation of the glucose-dependent insulinotropic polypeptide (GIP) receptor by N-AcGIP(LysPAL37) in normal mice. |
| 3182 | 16181707 | The present study was designed to assess the metabolic effects in healthy mice of long term activation of the GIP receptor by N-AcGIP(LysPAL37), a potent long-acting GIP receptor agonist. |
| 3183 | 16181707 | Daily injection of N-AcGIP(LysPAL37) (25 nmol/kg body weight) for 14 days had no significant effect on food intake, body weight, glycated hemoglobin levels, non-fasting plasma glucose and insulin concentrations compared to saline treated controls. |
| 3184 | 16181707 | These data indicate that long term activation of the GIP receptor by daily treatment with N-AcGIP(LysPAL37) improved glucose tolerance due to enhancement of pancreatic beta cell glucose responsiveness and insulin secretion. |
| 3185 | 16219666 | Human duodenal enteroendocrine cells: source of both incretin peptides, GLP-1 and GIP. |
| 3186 | 16219666 | Among the products of enteroendocrine cells are the incretins glucagon-like peptide-1 (GLP-1, secreted by L cells) and glucose-dependent insulinotropic peptide (GIP, secreted by K cells). |
| 3187 | 16219666 | Newly diagnosed type 2 diabetic subjects had increased plasma GLP-1 levels between 20 and 80 min, concurrently with rising plasma insulin levels. |
| 3188 | 16219666 | Human duodenal enteroendocrine cells: source of both incretin peptides, GLP-1 and GIP. |
| 3189 | 16219666 | Among the products of enteroendocrine cells are the incretins glucagon-like peptide-1 (GLP-1, secreted by L cells) and glucose-dependent insulinotropic peptide (GIP, secreted by K cells). |
| 3190 | 16219666 | Newly diagnosed type 2 diabetic subjects had increased plasma GLP-1 levels between 20 and 80 min, concurrently with rising plasma insulin levels. |
| 3191 | 16378704 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-induced insulin secretion. |
| 3192 | 16378704 | The present study was designed to assess the insulinotropic effects of a potent long-acting GIP receptor agonist, N-AcGIP(LysPAL37), in aging mice. |
| 3193 | 16378704 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-induced insulin secretion. |
| 3194 | 16378704 | The present study was designed to assess the insulinotropic effects of a potent long-acting GIP receptor agonist, N-AcGIP(LysPAL37), in aging mice. |
| 3195 | 16402076 | GIP is an insulinotropic agent with stimulatory effects on insulin synthesis and release from the pancreas. |
| 3196 | 16402076 | Furthermore, as observed in humans, chronic clozapine treatment also caused weight gain, and increased levels of insulin, triglycerides and leptin in the plasma. |
| 3197 | 16403775 | Sp1/Sp3 binding is associated with cell-specific expression of the glucose-dependent insulinotropic polypeptide receptor gene. |
| 3198 | 16403775 | Because aberrant GIP receptor (GIPR) expression has been implicated in abnormal GIP responses associated with type 2 diabetes mellitus and food-induced Cushing's syndrome, we sought to identify factors that regulate the GIPR. |
| 3199 | 16403775 | Within this region, we identified three putative Sp1 binding motifs, located at positions -77, -60, and -50, that can specifically bind both Sp1 and Sp3. |
| 3200 | 16403775 | Cotransfection of S2 Schneider cells with GIPR-luciferase chimeric constructs and either Sp1 or Sp3 expression vectors indicated that both Sp1 and the long form of Sp3 activate transcription through binding to the Sp1 sites located between -100 and -40. |
| 3201 | 16403775 | Lastly, chromatin immunoprecipitation analyses revealed that both Sp1 and Sp3 bind to the GIPR promoter region in RIN38 cells. |
| 3202 | 16403775 | These results indicate that cell-specific expression of GIPR is associated with the binding of the transcription factors Sp1 and Sp3 to the GIPR promoter. |
| 3203 | 16403775 | Sp1/Sp3 binding is associated with cell-specific expression of the glucose-dependent insulinotropic polypeptide receptor gene. |
| 3204 | 16403775 | Because aberrant GIP receptor (GIPR) expression has been implicated in abnormal GIP responses associated with type 2 diabetes mellitus and food-induced Cushing's syndrome, we sought to identify factors that regulate the GIPR. |
| 3205 | 16403775 | Within this region, we identified three putative Sp1 binding motifs, located at positions -77, -60, and -50, that can specifically bind both Sp1 and Sp3. |
| 3206 | 16403775 | Cotransfection of S2 Schneider cells with GIPR-luciferase chimeric constructs and either Sp1 or Sp3 expression vectors indicated that both Sp1 and the long form of Sp3 activate transcription through binding to the Sp1 sites located between -100 and -40. |
| 3207 | 16403775 | Lastly, chromatin immunoprecipitation analyses revealed that both Sp1 and Sp3 bind to the GIPR promoter region in RIN38 cells. |
| 3208 | 16403775 | These results indicate that cell-specific expression of GIPR is associated with the binding of the transcription factors Sp1 and Sp3 to the GIPR promoter. |
| 3209 | 16407790 | [New therapeutic approach in patients with type 2 diabetes based on glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP)]. |
| 3210 | 16407790 | A number of recent studies have highlighted the role of the so-called incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) in beta-cell function and development. |
| 3211 | 16407790 | Two strategies have been applied: the first is treatment with GLP-1, either with chronic infusions or with analogues with diminished clearance, and the second is inhibiting dipeptidyl peptidase IV, the enzyme that inactivates both GLP-1 and GIP in vivo. |
| 3212 | 16407790 | Apart from their glucose-dependent manner of stimulating insulin secretion, GLP-1, its analogues, and GIP have been demonstrated to stimulate beta-cell growth, differentiation, proliferation, and survival. |
| 3213 | 16407790 | [New therapeutic approach in patients with type 2 diabetes based on glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP)]. |
| 3214 | 16407790 | A number of recent studies have highlighted the role of the so-called incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) in beta-cell function and development. |
| 3215 | 16407790 | Two strategies have been applied: the first is treatment with GLP-1, either with chronic infusions or with analogues with diminished clearance, and the second is inhibiting dipeptidyl peptidase IV, the enzyme that inactivates both GLP-1 and GIP in vivo. |
| 3216 | 16407790 | Apart from their glucose-dependent manner of stimulating insulin secretion, GLP-1, its analogues, and GIP have been demonstrated to stimulate beta-cell growth, differentiation, proliferation, and survival. |
| 3217 | 16407790 | [New therapeutic approach in patients with type 2 diabetes based on glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP)]. |
| 3218 | 16407790 | A number of recent studies have highlighted the role of the so-called incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) in beta-cell function and development. |
| 3219 | 16407790 | Two strategies have been applied: the first is treatment with GLP-1, either with chronic infusions or with analogues with diminished clearance, and the second is inhibiting dipeptidyl peptidase IV, the enzyme that inactivates both GLP-1 and GIP in vivo. |
| 3220 | 16407790 | Apart from their glucose-dependent manner of stimulating insulin secretion, GLP-1, its analogues, and GIP have been demonstrated to stimulate beta-cell growth, differentiation, proliferation, and survival. |
| 3221 | 16407790 | [New therapeutic approach in patients with type 2 diabetes based on glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP)]. |
| 3222 | 16407790 | A number of recent studies have highlighted the role of the so-called incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) in beta-cell function and development. |
| 3223 | 16407790 | Two strategies have been applied: the first is treatment with GLP-1, either with chronic infusions or with analogues with diminished clearance, and the second is inhibiting dipeptidyl peptidase IV, the enzyme that inactivates both GLP-1 and GIP in vivo. |
| 3224 | 16407790 | Apart from their glucose-dependent manner of stimulating insulin secretion, GLP-1, its analogues, and GIP have been demonstrated to stimulate beta-cell growth, differentiation, proliferation, and survival. |
| 3225 | 16409149 | Similarly, glucose-dependent insulinotropic polypeptide (GIP) receptor activation stimulates insulin secretion, enhances beta-cell proliferation, and reduces apoptosis. |
| 3226 | 16409149 | Moreover, potentiation of the endogenous postprandial levels of GLP-1 and GIP via inhibition of dipeptidyl peptidase-IV (DPP-IV) also expands beta-cell mass via related mechanisms. |
| 3227 | 16409149 | Complementary approaches to regeneration of beta-cell mass involve combinations of factors, exemplified by epidermal growth factor and gastrin, which promote islet neogenesis and ameliorate diabetes in rodent studies. |
| 3228 | 16409149 | Similarly, glucose-dependent insulinotropic polypeptide (GIP) receptor activation stimulates insulin secretion, enhances beta-cell proliferation, and reduces apoptosis. |
| 3229 | 16409149 | Moreover, potentiation of the endogenous postprandial levels of GLP-1 and GIP via inhibition of dipeptidyl peptidase-IV (DPP-IV) also expands beta-cell mass via related mechanisms. |
| 3230 | 16409149 | Complementary approaches to regeneration of beta-cell mass involve combinations of factors, exemplified by epidermal growth factor and gastrin, which promote islet neogenesis and ameliorate diabetes in rodent studies. |
| 3231 | 16416146 | Gastric inhibitory polypeptide (GIP) was initially thought to regulate gastric acid secretion, whereas glucagon-like peptide-1 (GLP-1) was discovered as a result of a systematic search for intestinal insulinotropic products of proglucagon gene expression. |
| 3232 | 16416146 | The incretin effect is markedly impaired or absent in patients with type 2 diabetes because of decreased secretion of GLP-1 and a loss of the insulinotropic effects of GIP. |
| 3233 | 16416146 | Metabolic control can be restored or greatly improved by administration of exogenous GLP-1, but this peptide is almost immediately degraded by dipeptidyl peptidase IV (DPP-IV), and therefore has little clinical value. |
| 3234 | 16416146 | DPP-IV-resistant analogues (incretin mimetics) have been identified or developed, and inhibitors of DPP-IV have also proved effective in protecting endogenous GLP-1 (and GIP) from degradation. |
| 3235 | 16416146 | Gastric inhibitory polypeptide (GIP) was initially thought to regulate gastric acid secretion, whereas glucagon-like peptide-1 (GLP-1) was discovered as a result of a systematic search for intestinal insulinotropic products of proglucagon gene expression. |
| 3236 | 16416146 | The incretin effect is markedly impaired or absent in patients with type 2 diabetes because of decreased secretion of GLP-1 and a loss of the insulinotropic effects of GIP. |
| 3237 | 16416146 | Metabolic control can be restored or greatly improved by administration of exogenous GLP-1, but this peptide is almost immediately degraded by dipeptidyl peptidase IV (DPP-IV), and therefore has little clinical value. |
| 3238 | 16416146 | DPP-IV-resistant analogues (incretin mimetics) have been identified or developed, and inhibitors of DPP-IV have also proved effective in protecting endogenous GLP-1 (and GIP) from degradation. |
| 3239 | 16416146 | Gastric inhibitory polypeptide (GIP) was initially thought to regulate gastric acid secretion, whereas glucagon-like peptide-1 (GLP-1) was discovered as a result of a systematic search for intestinal insulinotropic products of proglucagon gene expression. |
| 3240 | 16416146 | The incretin effect is markedly impaired or absent in patients with type 2 diabetes because of decreased secretion of GLP-1 and a loss of the insulinotropic effects of GIP. |
| 3241 | 16416146 | Metabolic control can be restored or greatly improved by administration of exogenous GLP-1, but this peptide is almost immediately degraded by dipeptidyl peptidase IV (DPP-IV), and therefore has little clinical value. |
| 3242 | 16416146 | DPP-IV-resistant analogues (incretin mimetics) have been identified or developed, and inhibitors of DPP-IV have also proved effective in protecting endogenous GLP-1 (and GIP) from degradation. |
| 3243 | 16442340 | A number of alternative therapies for type 2 diabetes are currently under development that take advantage of the actions of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide on the pancreatic beta-cell. |
| 3244 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3245 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3246 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3247 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3248 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3249 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3250 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3251 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3252 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3253 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3254 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3255 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3256 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3257 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3258 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3259 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3260 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3261 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3262 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3263 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3264 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3265 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3266 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3267 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3268 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3269 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3270 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3271 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3272 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3273 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3274 | 16451070 | Glucose-dependent insulinotropic polypeptide (GIP) is a physiological insulin releasing peptide. |
| 3275 | 16451070 | We have developed two novel fatty acid derivatized GIP analogues, which bind to serum albumin and demonstrate enhanced duration of action in vivo. |
| 3276 | 16451070 | GIP(Lys(16)PAL) and GIP(Lys(37)PAL) were resistant to dipeptidyl peptidase IV (DPP IV) degradation. |
| 3277 | 16451070 | In vitro studies demonstrated that GIP analogues retained their ability to activate the GIP receptor through production of cAMP and to stimulate insulin secretion. |
| 3278 | 16451070 | Intraperitoneal administration of GIP analogues to obese diabetic (ob/ob) mice significantly decreased the glycemic excursion and elicited increased and prolonged insulin responses compared to native GIP. |
| 3279 | 16451070 | A protracted glucose-lowering effect was observed 24 h following GIP(Lys(37)PAL) administration. |
| 3280 | 16469773 | Bone histomorphometrical analyses revealed that bone formation parameters in the mice lacking GIP receptor (GIPR(-/-)) were significantly lower than those of wild-type (GIPR(+/+)) mice, and that the number of osteoclasts, especially multinuclear osteoclasts, was significantly increased in GIPR(-/-) mice, indicating that GIPR(-/-) mice have high-turnover osteoporosis. |
| 3281 | 16469773 | Because GIPR(-/-) mice exhibited an increased plasma calcium concentration after meal ingestion, GIP directly links calcium contained in meal to calcium deposition on bone. |
| 3282 | 16469773 | Bone histomorphometrical analyses revealed that bone formation parameters in the mice lacking GIP receptor (GIPR(-/-)) were significantly lower than those of wild-type (GIPR(+/+)) mice, and that the number of osteoclasts, especially multinuclear osteoclasts, was significantly increased in GIPR(-/-) mice, indicating that GIPR(-/-) mice have high-turnover osteoporosis. |
| 3283 | 16469773 | Because GIPR(-/-) mice exhibited an increased plasma calcium concentration after meal ingestion, GIP directly links calcium contained in meal to calcium deposition on bone. |
| 3284 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3285 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3286 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3287 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3288 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3289 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3290 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3291 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3292 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3293 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3294 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3295 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3296 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3297 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3298 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3299 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3300 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3301 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3302 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3303 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3304 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3305 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3306 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3307 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3308 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3309 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3310 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3311 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3312 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3313 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3314 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3315 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3316 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3317 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3318 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3319 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3320 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3321 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3322 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3323 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3324 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3325 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3326 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3327 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3328 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3329 | 16476726 | Prohormone convertase 1/3 is essential for processing of the glucose-dependent insulinotropic polypeptide precursor. |
| 3330 | 16476726 | The physiology of the incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and their role in type 2 diabetes currently attract great interest. |
| 3331 | 16476726 | Recently we reported an essential role for prohormone convertase (PC) 1/3 in the cleavage of intestinal proglucagon, resulting in formation of GLP-1, as demonstrated in PC1/3-deficient mice. |
| 3332 | 16476726 | This study investigates the processing of proGIP in PC1/3 and PC2 null mice and in cell lines using adenovirus-mediated overexpression. |
| 3333 | 16476726 | Supporting a role for PC1/3 in proGIP processing, we found co-localization of GIP and PC1/3 but not PC2 in intestinal sections by immunohistochemistry, and analysis of intestinal extracts from PC1/3-deficient animals demonstrated severely impaired processing to GIP, whereas processing to GIP was unaltered in PC2-deficient mice. |
| 3334 | 16476726 | Accordingly, overexpression of preproGIP in the neuroendocrine AtT-20 cell line that expresses high levels of endogenous PC1/3 and negligible levels of PC2 resulted in production of GIP. |
| 3335 | 16476726 | Similar results were obtained after co-expression of preproGIP and PC1/3 in GH4 cells that express no PC2 and only low levels of PC1/3. |
| 3336 | 16476726 | In addition, studies in GH4 cells and the alpha-TC1.9 cell line, expressing PC2 but not PC1/3, indicate that PC2 can mediate processing to GIP but also to other fragments not found in intestinal extracts. |
| 3337 | 16476726 | Taken together, our data indicate that PC1/3 is essential and sufficient for the production of the intestinal incretin hormone GIP, whereas PC2, although capable of cleaving proGIP, does not participate in intestinal proGIP processing and is not found in intestinal GIP-expressing cells. |
| 3338 | 16492545 | At the same time, insulin obligatorily recruits GLUT4 glucose transporters in muscle and fat. |
| 3339 | 16492545 | Amylin and insulin secreted in response to nutrients already absorbed act as a feedback switch for glucose sourcing. |
| 3340 | 16492545 | The insulinotropic (incretin) gut peptides, GLP-1 and GIP, secreted in response to yet-to-be-absorbed intraluminal nutrients, amplify beta-cell secretion and thereby activate the glucose sourcing switch in a feedforward manner. |
| 3341 | 16503716 | The emergence of the glucoregulatory hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide has expanded our understanding of glucose homeostasis. |
| 3342 | 16503716 | In particular, the glucoregulatory actions of the incretin hormone GLP-1 include enhancement of glucosedependent insulin secretion, suppression of inappropriately elevated glucagon secretion, slowing of gastric emptying, and reduction of food intake. |
| 3343 | 16503716 | One is the use of agents that mimic the enhancement of glucose-dependent insulin secretion, and potentially other antihyperglycemic actions of incretins, and the other is the use of dipeptidyl peptidase-IV inhibitors, which reduce the inactivation of GLP-1, increasing the concentration of endogenous GLP-1. |
| 3344 | 16517403 | Gut peptides, exemplified by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted in a nutrient-dependent manner and stimulate glucose-dependent insulin secretion. |
| 3345 | 16517403 | Both GIP and GLP-1 also promote beta cell proliferation and inhibit apoptosis, leading to expansion of beta cell mass. |
| 3346 | 16517403 | GLP-1, but not GIP, controls glycemia via additional actions on glucose sensors, inhibition of gastric emptying, food intake and glucagon secretion. |
| 3347 | 16517403 | Furthermore, GLP-1, unlike GIP, potently stimulates insulin secretion and reduces blood glucose in human subjects with type 2 diabetes. |
| 3348 | 16517403 | This article summarizes current concepts of incretin action and highlights the potential therapeutic utility of GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors for the treatment of type 2 diabetes. |
| 3349 | 16517403 | Gut peptides, exemplified by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted in a nutrient-dependent manner and stimulate glucose-dependent insulin secretion. |
| 3350 | 16517403 | Both GIP and GLP-1 also promote beta cell proliferation and inhibit apoptosis, leading to expansion of beta cell mass. |
| 3351 | 16517403 | GLP-1, but not GIP, controls glycemia via additional actions on glucose sensors, inhibition of gastric emptying, food intake and glucagon secretion. |
| 3352 | 16517403 | Furthermore, GLP-1, unlike GIP, potently stimulates insulin secretion and reduces blood glucose in human subjects with type 2 diabetes. |
| 3353 | 16517403 | This article summarizes current concepts of incretin action and highlights the potential therapeutic utility of GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors for the treatment of type 2 diabetes. |
| 3354 | 16517403 | Gut peptides, exemplified by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted in a nutrient-dependent manner and stimulate glucose-dependent insulin secretion. |
| 3355 | 16517403 | Both GIP and GLP-1 also promote beta cell proliferation and inhibit apoptosis, leading to expansion of beta cell mass. |
| 3356 | 16517403 | GLP-1, but not GIP, controls glycemia via additional actions on glucose sensors, inhibition of gastric emptying, food intake and glucagon secretion. |
| 3357 | 16517403 | Furthermore, GLP-1, unlike GIP, potently stimulates insulin secretion and reduces blood glucose in human subjects with type 2 diabetes. |
| 3358 | 16517403 | This article summarizes current concepts of incretin action and highlights the potential therapeutic utility of GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors for the treatment of type 2 diabetes. |
| 3359 | 16517403 | Gut peptides, exemplified by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted in a nutrient-dependent manner and stimulate glucose-dependent insulin secretion. |
| 3360 | 16517403 | Both GIP and GLP-1 also promote beta cell proliferation and inhibit apoptosis, leading to expansion of beta cell mass. |
| 3361 | 16517403 | GLP-1, but not GIP, controls glycemia via additional actions on glucose sensors, inhibition of gastric emptying, food intake and glucagon secretion. |
| 3362 | 16517403 | Furthermore, GLP-1, unlike GIP, potently stimulates insulin secretion and reduces blood glucose in human subjects with type 2 diabetes. |
| 3363 | 16517403 | This article summarizes current concepts of incretin action and highlights the potential therapeutic utility of GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors for the treatment of type 2 diabetes. |
| 3364 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3365 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3366 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3367 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3368 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3369 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3370 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3371 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3372 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3373 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3374 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3375 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3376 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3377 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3378 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3379 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3380 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3381 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3382 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3383 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3384 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3385 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3386 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3387 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3388 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3389 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3390 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3391 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3392 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3393 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3394 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3395 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3396 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3397 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3398 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3399 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3400 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3401 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3402 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3403 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3404 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3405 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3406 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3407 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3408 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3409 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3410 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3411 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3412 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3413 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3414 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3415 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3416 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3417 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3418 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3419 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3420 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3421 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3422 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3423 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3424 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3425 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3426 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3427 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3428 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3429 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3430 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3431 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3432 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3433 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3434 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3435 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3436 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3437 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3438 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3439 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3440 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3441 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3442 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3443 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3444 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3445 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3446 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3447 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3448 | 16522728 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), have been suggested to act as beta-cell growth factors and may therefore be of critical importance for the maintenance of a proper beta-cell mass. |
| 3449 | 16522728 | GLP-1, GIP and the long-acting GLP-1 derivative, liraglutide, increased beta-cell replication 50-80% at 10-100 nM upon a 24 h stimulus, whereas glucagon at a similar concentration had no significant effect. |
| 3450 | 16522728 | The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. |
| 3451 | 16522728 | The response to both GLP-1 and GIP was completely blocked by the protein kinase A (PKA) inhibitor, H89. |
| 3452 | 16522728 | In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. |
| 3453 | 16522728 | The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, had no inhibitory effect on either GLP-1 or GIP stimulated proliferation. |
| 3454 | 16522728 | GLP-1 time-dependently induced the cyclin D1 mRNA and protein levels in INS-1E, whereas the cyclin D2 levels were unaffected. |
| 3455 | 16522728 | However, minor effect of GLP-1 stimulation was observed on the cyclin D3 mRNA levels. |
| 3456 | 16522728 | Transient transfection of a cyclin D1 promoter-luciferase reporter construct into islet monolayer cells or INS-1 cells revealed approximately a 2-3 fold increase of transcriptional activity in response to GLP-1 and GIP, and a 4-7 fold increase in response to forskolin. |
| 3457 | 16522728 | The stimulation of the cyclin D1 promoter by GLP-1 was inhibited by H89, wortmannin, and PD98059. |
| 3458 | 16522728 | We conclude that incretin-induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1. |
| 3459 | 16522728 | GLP-1, GIP and liraglutide may have the potential to increase beta-cell replication in humans which would have significant impact on long-term diabetes treatment. |
| 3460 | 16551338 | Effect of glucagon-like peptide-1 on the beta cell response to glucose-dependent insulinotropic polypeptide in elderly patients with diabetes mellitus. |
| 3461 | 16598904 | These gluco-incretin hormones are GLP-1 (glucagon-like peptide-1) and GIP (gluco-dependent insulinotropic polypeptide). |
| 3462 | 16621806 | Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that stimulates the secretion of insulin after ingestion of food. |
| 3463 | 16621806 | Alanine scan studies of these N-terminal residues showed that the GIP-(1-42)Ala(6) was the only analogue to show insulin-secreting activity similar to that of the native GIP. |
| 3464 | 16621806 | Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that stimulates the secretion of insulin after ingestion of food. |
| 3465 | 16621806 | Alanine scan studies of these N-terminal residues showed that the GIP-(1-42)Ala(6) was the only analogue to show insulin-secreting activity similar to that of the native GIP. |
| 3466 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3467 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3468 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3469 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3470 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3471 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3472 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3473 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3474 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3475 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3476 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3477 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3478 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3479 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3480 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3481 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3482 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3483 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3484 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3485 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3486 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3487 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3488 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3489 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3490 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3491 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3492 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3493 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3494 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3495 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3496 | 16675042 | Glucose-dependent insulinotropic polypeptide (GIP) is a key physiological insulin releasing peptide and potential antidiabetic agent. |
| 3497 | 16675042 | The bioactivity of two modified C-terminally truncated fragment GIP peptides, GIP(1-16) and (Pro3)GIP(1-16), was examined in terms of insulin secretion and glucose homeostasis using BRIN-BD11 cells and type 2 diabetic mice. |
| 3498 | 16675042 | In vitro insulin release studies demonstrated that GIP(1-16) and (Pro3)GIP(1-16) possessed weak GIP-receptor agonist and antagonistic properties, respectively. |
| 3499 | 16675042 | Intraperitoneal administration of GIP(1-16) in combination with glucose to obese diabetic (ob/ob) mice did not effect the glycaemic excursion and had a marginal effect on insulin release. |
| 3500 | 16675042 | Based on the established concept of a therapeutic benefit of GIP receptor antagonism in obesity-diabetes, ob/ob mice received once daily injection of (Pro3)GIP(1-16) for 14 days. |
| 3501 | 16675042 | No significant effects were observed on food intake, body weight, HbA1c, glucose tolerance, metabolic response to feeding and either insulin secretion or insulin sensitivity following prolonged (Pro3)GIP(1-16) treatment. |
| 3502 | 16682937 | The gastrointestinal hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) promote the incretin effect. |
| 3503 | 16682937 | Type 2 diabetes is characterized by an incretin defect: while GIP does not stimulate insulin secretion, GLP-1 action is still preserved under supraphysiological concentrations. |
| 3504 | 16682937 | GLP-1 stimulates insulin secretion only under hyperglycaemic conditions, therefore it does not cause hypoglycaemia. |
| 3505 | 16682937 | The improvement of beta cell function can be indirectly observed from the increased insulin secretory capacity of humans receiving GLP-1. |
| 3506 | 16682937 | In contrast to GIP, GLP-1 may represent an attractive therapeutic method for type 2 diabetes due to its multiple effects also including the simulation of satiety in the central nervous system by acting as transmitter or by crossing the blood brain barrier. |
| 3507 | 16682937 | The gastrointestinal hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) promote the incretin effect. |
| 3508 | 16682937 | Type 2 diabetes is characterized by an incretin defect: while GIP does not stimulate insulin secretion, GLP-1 action is still preserved under supraphysiological concentrations. |
| 3509 | 16682937 | GLP-1 stimulates insulin secretion only under hyperglycaemic conditions, therefore it does not cause hypoglycaemia. |
| 3510 | 16682937 | The improvement of beta cell function can be indirectly observed from the increased insulin secretory capacity of humans receiving GLP-1. |
| 3511 | 16682937 | In contrast to GIP, GLP-1 may represent an attractive therapeutic method for type 2 diabetes due to its multiple effects also including the simulation of satiety in the central nervous system by acting as transmitter or by crossing the blood brain barrier. |
| 3512 | 16682937 | The gastrointestinal hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) promote the incretin effect. |
| 3513 | 16682937 | Type 2 diabetes is characterized by an incretin defect: while GIP does not stimulate insulin secretion, GLP-1 action is still preserved under supraphysiological concentrations. |
| 3514 | 16682937 | GLP-1 stimulates insulin secretion only under hyperglycaemic conditions, therefore it does not cause hypoglycaemia. |
| 3515 | 16682937 | The improvement of beta cell function can be indirectly observed from the increased insulin secretory capacity of humans receiving GLP-1. |
| 3516 | 16682937 | In contrast to GIP, GLP-1 may represent an attractive therapeutic method for type 2 diabetes due to its multiple effects also including the simulation of satiety in the central nervous system by acting as transmitter or by crossing the blood brain barrier. |
| 3517 | 16751350 | But more recent characterization and understanding of the role of incretin hormones from the gut--notably, glucagon-like peptide 1 and gastric inhibitory polypeptide--and amylin from pancreatic beta cells has led to a more complete model of glucose homeostasis. |
| 3518 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3519 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3520 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3521 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3522 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3523 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3524 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3525 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3526 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3527 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3528 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3529 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3530 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3531 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3532 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3533 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3534 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3535 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3536 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3537 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3538 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3539 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3540 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3541 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3542 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3543 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3544 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3545 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3546 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3547 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3548 | 16859646 | Evaluation of the antidiabetic activity of DPP IV resistant N-terminally modified versus mid-chain acylated analogues of glucose-dependent insulinotropic polypeptide. |
| 3549 | 16859646 | Glucose dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with therapeutic potential for type 2 diabetes due to its insulin-releasing and antihyperglycaemic actions. |
| 3550 | 16859646 | Numerous GIP analogues have now been generated exhibiting DPP IV resistance and extended bioactivity profiles. |
| 3551 | 16859646 | In this study, we report a direct comparison of the long-term antidiabetic actions of three such GIP molecules, N-AcGIP, GIP(Lys(37)PAL) and N-AcGIP(Lys(37)PAL) in obese diabetic (ob/ob) mice. |
| 3552 | 16859646 | Administration of either N-AcGIP, GIP(Lys(37)PAL) or N-AcGIP(Lys(37)PAL) significantly decreased non-fasting plasma glucose and improved glucose tolerance compared to saline treated controls. |
| 3553 | 16859646 | The metabolic and insulin secretory responses to native GIP were also enhanced in 14-day analogue treated mice, revealing no evidence of GIP-receptor desensitization. |
| 3554 | 16898571 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. |
| 3555 | 16898571 | This is due to 1) an approximate 15% reduction in postprandial GLP-1 secretion and 2) a near total loss of insulinotropic activity of GIP. |
| 3556 | 16898571 | This review article summarizes clinical studies on abnormalities in the secretion and insulinotropic effects of GIP and GLP-1 in patients with type 2 diabetes as well as in individuals at high risk. |
| 3557 | 16898571 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. |
| 3558 | 16898571 | This is due to 1) an approximate 15% reduction in postprandial GLP-1 secretion and 2) a near total loss of insulinotropic activity of GIP. |
| 3559 | 16898571 | This review article summarizes clinical studies on abnormalities in the secretion and insulinotropic effects of GIP and GLP-1 in patients with type 2 diabetes as well as in individuals at high risk. |
| 3560 | 16898571 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. |
| 3561 | 16898571 | This is due to 1) an approximate 15% reduction in postprandial GLP-1 secretion and 2) a near total loss of insulinotropic activity of GIP. |
| 3562 | 16898571 | This review article summarizes clinical studies on abnormalities in the secretion and insulinotropic effects of GIP and GLP-1 in patients with type 2 diabetes as well as in individuals at high risk. |
| 3563 | 16899793 | Glucose-dependent insulinotropic polypeptide modulates adipocyte lipolysis and reesterification. |
| 3564 | 16919548 | After a meal, the rise in postprandial glucose (PPG) is controlled by the rapid pancreatic release of insulin, stimulated by both glucose and the intestinal production of the incretins glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1. |
| 3565 | 16929363 | GLP-1 controls blood glucose through regulation of glucose-dependent insulin secretion, inhibition of glucagon secretion and gastric emptying, and reduction of food intake. |
| 3566 | 16929363 | Dipeptidyl-peptidase-IV inhibitors, currently in phase III clinical trials, stabilize the postprandial levels of GLP-1 and gastric inhibitory polypeptide and lower blood glucose in diabetic patients via inhibition of glucagon secretion and enhancement of glucose-stimulated insulin secretion. |
| 3567 | 16939389 | As an enzyme, DPP IV cleaves the N-terminal dipeptide from the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. |
| 3568 | 16945366 | GLP-1 and GIP are insulin-releasing 'incretin' hormones inactivated following degradation by dipeptidyl peptidase IV. |
| 3569 | 16945366 | In vivo metformin lowered plasma DPP IV activity in ob/ob mice, and improved glucose-lowering and insulin-releasing effects of exogenous GLP-1 administration. |
| 3570 | 16949016 | Several enteroendocrine cells produce numerous peptides codifying either orexigenic (ghrelin, orexins) or anorexigenic signals (pancreatic polypeptide, peptide YY, cholecystokinin, amylin, bombesin homologs, apolipoprotein A-IV, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, oxyntomodulin), which interact in a complex network with other peripheral signals of energy balance and with different neuropeptides involved in the central control of appetite and energy homeostasis. |
| 3571 | 16995414 | Endocrine pancreas producing insulin, glucagon, somatostatin and pancreatic polypeptide is under the influence of different types of regulation; among them the regulatory role of enteropancreatic axis plays an important role. |
| 3572 | 16995414 | Incretin effect of glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is significantly involved in the insulin secretion which is modulated by many other hormones. |
| 3573 | 17052195 | Recent studies highlight diverse beta-cell actions of GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). |
| 3574 | 17052195 | These intestinal hormones target the beta-cell to stimulate glucose-dependent insulin secretion through activation of protein kinase A and associated pathways. |
| 3575 | 17064063 | Dipeptidyl peptidase IV (DPP4) deactivates glucose-regulating hormones such as GLP-1 and GIP, thus, DPP4 inhibition has become a useful therapy for type 2 diabetes. |
| 3576 | 17065392 | Effects of sub-chronic exposure to naturally occurring N-terminally truncated metabolites of glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), GIP(3-42) and GLP-1(9-36)amide, on insulin secretion and glucose homeostasis in ob/ob mice. |
| 3577 | 17065392 | Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important enteroendocrine hormones that are rapidly degraded by an ubiquitous enzyme dipeptidyl peptidase IV to yield truncated metabolites GIP(3-42) and GLP-1(9-36)amide. |
| 3578 | 17065392 | In this study, we investigated the effects of sub-chronic exposure to these major circulating forms of GIP and GLP-1 on blood glucose control and endocrine pancreatic function in obese diabetic (ob/ob) mice. |
| 3579 | 17065392 | GLP-1(9-36)amide also had no effect on plasma glucose homeostasis or insulin secretion. |
| 3580 | 17065392 | These data indicate that sub-chronic exposure to GIP and GLP-1 metabolites does not result in physiological impairment of insulin secretion or blood glucose control. |
| 3581 | 17065392 | GIP(3-42) might exert an overall beneficial effect by improving insulin sensitivity through extrapancreatic action. |
| 3582 | 17065392 | Effects of sub-chronic exposure to naturally occurring N-terminally truncated metabolites of glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), GIP(3-42) and GLP-1(9-36)amide, on insulin secretion and glucose homeostasis in ob/ob mice. |
| 3583 | 17065392 | Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important enteroendocrine hormones that are rapidly degraded by an ubiquitous enzyme dipeptidyl peptidase IV to yield truncated metabolites GIP(3-42) and GLP-1(9-36)amide. |
| 3584 | 17065392 | In this study, we investigated the effects of sub-chronic exposure to these major circulating forms of GIP and GLP-1 on blood glucose control and endocrine pancreatic function in obese diabetic (ob/ob) mice. |
| 3585 | 17065392 | GLP-1(9-36)amide also had no effect on plasma glucose homeostasis or insulin secretion. |
| 3586 | 17065392 | These data indicate that sub-chronic exposure to GIP and GLP-1 metabolites does not result in physiological impairment of insulin secretion or blood glucose control. |
| 3587 | 17065392 | GIP(3-42) might exert an overall beneficial effect by improving insulin sensitivity through extrapancreatic action. |
| 3588 | 17065392 | Effects of sub-chronic exposure to naturally occurring N-terminally truncated metabolites of glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), GIP(3-42) and GLP-1(9-36)amide, on insulin secretion and glucose homeostasis in ob/ob mice. |
| 3589 | 17065392 | Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important enteroendocrine hormones that are rapidly degraded by an ubiquitous enzyme dipeptidyl peptidase IV to yield truncated metabolites GIP(3-42) and GLP-1(9-36)amide. |
| 3590 | 17065392 | In this study, we investigated the effects of sub-chronic exposure to these major circulating forms of GIP and GLP-1 on blood glucose control and endocrine pancreatic function in obese diabetic (ob/ob) mice. |
| 3591 | 17065392 | GLP-1(9-36)amide also had no effect on plasma glucose homeostasis or insulin secretion. |
| 3592 | 17065392 | These data indicate that sub-chronic exposure to GIP and GLP-1 metabolites does not result in physiological impairment of insulin secretion or blood glucose control. |
| 3593 | 17065392 | GIP(3-42) might exert an overall beneficial effect by improving insulin sensitivity through extrapancreatic action. |
| 3594 | 17065392 | Effects of sub-chronic exposure to naturally occurring N-terminally truncated metabolites of glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), GIP(3-42) and GLP-1(9-36)amide, on insulin secretion and glucose homeostasis in ob/ob mice. |
| 3595 | 17065392 | Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important enteroendocrine hormones that are rapidly degraded by an ubiquitous enzyme dipeptidyl peptidase IV to yield truncated metabolites GIP(3-42) and GLP-1(9-36)amide. |
| 3596 | 17065392 | In this study, we investigated the effects of sub-chronic exposure to these major circulating forms of GIP and GLP-1 on blood glucose control and endocrine pancreatic function in obese diabetic (ob/ob) mice. |
| 3597 | 17065392 | GLP-1(9-36)amide also had no effect on plasma glucose homeostasis or insulin secretion. |
| 3598 | 17065392 | These data indicate that sub-chronic exposure to GIP and GLP-1 metabolites does not result in physiological impairment of insulin secretion or blood glucose control. |
| 3599 | 17065392 | GIP(3-42) might exert an overall beneficial effect by improving insulin sensitivity through extrapancreatic action. |
| 3600 | 17065392 | Effects of sub-chronic exposure to naturally occurring N-terminally truncated metabolites of glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), GIP(3-42) and GLP-1(9-36)amide, on insulin secretion and glucose homeostasis in ob/ob mice. |
| 3601 | 17065392 | Glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are important enteroendocrine hormones that are rapidly degraded by an ubiquitous enzyme dipeptidyl peptidase IV to yield truncated metabolites GIP(3-42) and GLP-1(9-36)amide. |
| 3602 | 17065392 | In this study, we investigated the effects of sub-chronic exposure to these major circulating forms of GIP and GLP-1 on blood glucose control and endocrine pancreatic function in obese diabetic (ob/ob) mice. |
| 3603 | 17065392 | GLP-1(9-36)amide also had no effect on plasma glucose homeostasis or insulin secretion. |
| 3604 | 17065392 | These data indicate that sub-chronic exposure to GIP and GLP-1 metabolites does not result in physiological impairment of insulin secretion or blood glucose control. |
| 3605 | 17065392 | GIP(3-42) might exert an overall beneficial effect by improving insulin sensitivity through extrapancreatic action. |
| 3606 | 17076764 | In this review, the effects of the gastrointestinal hormones ghrelin, cholecystokinin, peptide YY, glucagon-like peptide, oxyntomodulin and gastric inhibitory polypeptide on glucose and energy metabolism are reviewed. |
| 3607 | 17100408 | It improves glycaemic control by inhibiting DPP-4 from inactivating the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, prolonging incretin activity in response to ingestion of nutrients. |
| 3608 | 17160910 | DPP IV rapidly inactivates the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 3609 | 17160910 | Inhibition of DPP IV prolongs and enhances the activity of endogenous GLP-1 and GIP, which serve as important prandial stimulators of insulin secretion and regulators of blood glucose control. |
| 3610 | 17160910 | DPP IV rapidly inactivates the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 3611 | 17160910 | Inhibition of DPP IV prolongs and enhances the activity of endogenous GLP-1 and GIP, which serve as important prandial stimulators of insulin secretion and regulators of blood glucose control. |
| 3612 | 17187081 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) control glucose homeostasis through well-defined actions on the islet beta cell via stimulation of insulin secretion and preservation and expansion of beta cell mass. |
| 3613 | 17187081 | We examined the importance of endogenous incretin receptors for control of glucose homeostasis through analysis of Glp1r(-/-), Gipr(-/-), and double incretin receptor knockout (DIRKO) mice fed a high-fat (HF) diet. |
| 3614 | 17187081 | Moreover, plasma levels of plasminogen activator inhibitor-1 and resistin failed to increase significantly in DIRKO mice after HF feeding, and the GIP receptor agonist [D-Ala(2)]GIP, but not the GLP-1 receptor agonist exendin-4, increased the levels of plasma resistin in studies of both acute and chronic administration. |
| 3615 | 17187081 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) control glucose homeostasis through well-defined actions on the islet beta cell via stimulation of insulin secretion and preservation and expansion of beta cell mass. |
| 3616 | 17187081 | We examined the importance of endogenous incretin receptors for control of glucose homeostasis through analysis of Glp1r(-/-), Gipr(-/-), and double incretin receptor knockout (DIRKO) mice fed a high-fat (HF) diet. |
| 3617 | 17187081 | Moreover, plasma levels of plasminogen activator inhibitor-1 and resistin failed to increase significantly in DIRKO mice after HF feeding, and the GIP receptor agonist [D-Ala(2)]GIP, but not the GLP-1 receptor agonist exendin-4, increased the levels of plasma resistin in studies of both acute and chronic administration. |
| 3618 | 17244606 | Activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes. |
| 3619 | 17244606 | A role for a protein kinase B, LKB1, and AMP-activated protein kinase cascade. |
| 3620 | 17244606 | Considerably less is known about the effects of GIP on fat metabolism, and the present study was directed at identifying the mechanisms underlying its stimulatory action on lipoprotein lipase (LPL). |
| 3621 | 17244606 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B (PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). |
| 3622 | 17244606 | In contrast, the other major incretin hormone, glucagon-like peptide-1, exhibited no significant effects on LPL activity or PKB, LKB1, or AMPK phosphorylation. |
| 3623 | 17244606 | Chronic elevation of circulating GIP levels in the Vancouver diabetic fatty Zucker rat in vivo resulted in increased LPL activity and elevated triglyceride accumulation in epididymal fat tissue, combined with a modulation of PKB, LKB1, and AMPK phosphorylation similar to that observed in vitro. |
| 3624 | 17244606 | Activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes. |
| 3625 | 17244606 | A role for a protein kinase B, LKB1, and AMP-activated protein kinase cascade. |
| 3626 | 17244606 | Considerably less is known about the effects of GIP on fat metabolism, and the present study was directed at identifying the mechanisms underlying its stimulatory action on lipoprotein lipase (LPL). |
| 3627 | 17244606 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B (PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). |
| 3628 | 17244606 | In contrast, the other major incretin hormone, glucagon-like peptide-1, exhibited no significant effects on LPL activity or PKB, LKB1, or AMPK phosphorylation. |
| 3629 | 17244606 | Chronic elevation of circulating GIP levels in the Vancouver diabetic fatty Zucker rat in vivo resulted in increased LPL activity and elevated triglyceride accumulation in epididymal fat tissue, combined with a modulation of PKB, LKB1, and AMPK phosphorylation similar to that observed in vitro. |
| 3630 | 17244606 | Activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes. |
| 3631 | 17244606 | A role for a protein kinase B, LKB1, and AMP-activated protein kinase cascade. |
| 3632 | 17244606 | Considerably less is known about the effects of GIP on fat metabolism, and the present study was directed at identifying the mechanisms underlying its stimulatory action on lipoprotein lipase (LPL). |
| 3633 | 17244606 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B (PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). |
| 3634 | 17244606 | In contrast, the other major incretin hormone, glucagon-like peptide-1, exhibited no significant effects on LPL activity or PKB, LKB1, or AMPK phosphorylation. |
| 3635 | 17244606 | Chronic elevation of circulating GIP levels in the Vancouver diabetic fatty Zucker rat in vivo resulted in increased LPL activity and elevated triglyceride accumulation in epididymal fat tissue, combined with a modulation of PKB, LKB1, and AMPK phosphorylation similar to that observed in vitro. |
| 3636 | 17244606 | Activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes. |
| 3637 | 17244606 | A role for a protein kinase B, LKB1, and AMP-activated protein kinase cascade. |
| 3638 | 17244606 | Considerably less is known about the effects of GIP on fat metabolism, and the present study was directed at identifying the mechanisms underlying its stimulatory action on lipoprotein lipase (LPL). |
| 3639 | 17244606 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B (PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). |
| 3640 | 17244606 | In contrast, the other major incretin hormone, glucagon-like peptide-1, exhibited no significant effects on LPL activity or PKB, LKB1, or AMPK phosphorylation. |
| 3641 | 17244606 | Chronic elevation of circulating GIP levels in the Vancouver diabetic fatty Zucker rat in vivo resulted in increased LPL activity and elevated triglyceride accumulation in epididymal fat tissue, combined with a modulation of PKB, LKB1, and AMPK phosphorylation similar to that observed in vitro. |
| 3642 | 17261085 | Effects of chemical ablation of the GIP and GLP-1 receptors on metabolic aspects of obesity-diabetes were investigated using the stable receptor antagonists (Pro3)GIP and exendin(9-39)amide. |
| 3643 | 17263764 | Glucagon-like peptide-1 (7-36) amide (GLP-1) is a gut hormone, released postprandially,which stimulates insulin secretion and insulin gene expression as well as pancreatic B-cell growth. |
| 3644 | 17263764 | Together with glucose-dependent insulinotropic polypeptide (GIP), it is responsible for the incretin effect which is the augmentation of insulin secretion following oral administration of glucose. |
| 3645 | 17263764 | Patients with Type 2 diabetes have greatly impaired or absent incretin-mediated insulin secretion which is mainly as a result of decreased secretion of GLP-1. |
| 3646 | 17263764 | In addition to stimulating insulin secretion and promoting pancreatic B-cell mass, GLP-1 suppresses glucagon secretion,delays gastric emptying and inhibits food intake. |
| 3647 | 17263764 | However, GLP-1 is metabolized extremely rapidly in the circulation by the enzyme dipeptidyl peptidase IV(DPP-IV). |
| 3648 | 17299398 | In this study, we genetically engineered an enteroendocrine cell line (STC-1) to express insulin under the control of the glucose-dependent insulinotropic polypeptide promoter. |
| 3649 | 17299398 | Gi-INS-7 cells expressed glucose transporter 2 (GLUT2) and glucokinase (GK) and secreted insulin in response to elevated glucose levels in vitro. |
| 3650 | 17315049 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are important incretin hormones contributing to 50-70% of the stimulation of insulin secretion after a meal. |
| 3651 | 17315049 | Dipeptidyl-peptidase IV (DPP-4) inhibitors inhibit the degradation of GLP-1 and GIP as well as that of other regulatory peptides. |
| 3652 | 17315049 | Like other DPP-4 inhibitors, sitagliptin reduces hemoglobin A1c (HbA1c), fasting and postprandial glucose by glucose-dependent stimulation of insulin secretion and inhibition of glucagon secretion. |
| 3653 | 17315241 | Comparison of the anti-diabetic effects of GIP- and GLP-1-receptor activation in obese diabetic (ob/ob) mice: studies with DPP IV resistant N-AcGIP and exendin(1-39)amide. |
| 3654 | 17352516 | Sitagliptin, an oral dipeptidyl peptidase-4 (DPP-4) inhibitor, improves glycaemic control by inhibiting DPP-4 inactivation of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. |
| 3655 | 17352676 | A number of alternative therapies for type 2 diabetes are currently under development that take advantage of the actions of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide on the pancreatic beta-cell. |
| 3656 | 17353295 | The major factors for progressive loss of beta-cell function and mass are glucotoxicity, lipotoxicity, proinflammatory cytokines, leptin, and islet cell amyloid. |
| 3657 | 17353295 | The TZDs improve insulin secretory capacity, decrease beta-cell apoptosis, and reduce islet cell amyloid with maintenance of neogenesis. |
| 3658 | 17353295 | From the two major incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), only the first one or its mimetics or enhancers can be used for treatment because the diabetic beta-cell is resistant to GIP action. |
| 3659 | 17353295 | The acute effect of GLP-1 and GLP-1 receptor agonists on beta-cells is stimulation of glucose-dependent insulin release, followed by enhancement of insulin biosynthesis and stimulation of insulin gene transcription. |
| 3660 | 17353295 | The inhibition of the activity of the DPP-IV enzyme enhances endogenous GLP-1 action in vivo, mediated not only by GLP-1 but also by other mediators. |
| 3661 | 17360984 | Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: possible contribution to impaired incretin effects in diabetes. |
| 3662 | 17360984 | Stimulation of insulin secretion by the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) has been found to be diminished in type 2 diabetes. |
| 3663 | 17360984 | Gene expression of incretin receptors, GLP-1R and GIPR, were significantly decreased in islets of 90% pancreatectomized (Px) hyperglycemic rats, with recovery when glucose levels were normalized by phlorizin. |
| 3664 | 17360984 | Perifused islets isolated from hyperglycemic Px rats showed reduced insulin responses to GLP-1 and GIP. |
| 3665 | 17360984 | To examine the acute effect of hyperglycemia on incretin receptor expression, a hyperglycemic clamp study was performed for 96 h with reduction of GLP-1 receptor expression but increase in GIP receptor expression. |
| 3666 | 17360984 | The reduction of GLP-1 receptor expression by high glucose was prevented by dominant-negative protein kinase C (PKC)alpha overexpression, whereas GLP-1 receptor expression was reduced with wild-type PKCalpha overexpression. |
| 3667 | 17360984 | Taken together, GLP-1 and GIP receptor expression is decreased with chronic hyperglycemia, and this decrease likely contributes to the impaired incretin effects found in diabetes. |
| 3668 | 17360984 | Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: possible contribution to impaired incretin effects in diabetes. |
| 3669 | 17360984 | Stimulation of insulin secretion by the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) has been found to be diminished in type 2 diabetes. |
| 3670 | 17360984 | Gene expression of incretin receptors, GLP-1R and GIPR, were significantly decreased in islets of 90% pancreatectomized (Px) hyperglycemic rats, with recovery when glucose levels were normalized by phlorizin. |
| 3671 | 17360984 | Perifused islets isolated from hyperglycemic Px rats showed reduced insulin responses to GLP-1 and GIP. |
| 3672 | 17360984 | To examine the acute effect of hyperglycemia on incretin receptor expression, a hyperglycemic clamp study was performed for 96 h with reduction of GLP-1 receptor expression but increase in GIP receptor expression. |
| 3673 | 17360984 | The reduction of GLP-1 receptor expression by high glucose was prevented by dominant-negative protein kinase C (PKC)alpha overexpression, whereas GLP-1 receptor expression was reduced with wild-type PKCalpha overexpression. |
| 3674 | 17360984 | Taken together, GLP-1 and GIP receptor expression is decreased with chronic hyperglycemia, and this decrease likely contributes to the impaired incretin effects found in diabetes. |
| 3675 | 17360984 | Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: possible contribution to impaired incretin effects in diabetes. |
| 3676 | 17360984 | Stimulation of insulin secretion by the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) has been found to be diminished in type 2 diabetes. |
| 3677 | 17360984 | Gene expression of incretin receptors, GLP-1R and GIPR, were significantly decreased in islets of 90% pancreatectomized (Px) hyperglycemic rats, with recovery when glucose levels were normalized by phlorizin. |
| 3678 | 17360984 | Perifused islets isolated from hyperglycemic Px rats showed reduced insulin responses to GLP-1 and GIP. |
| 3679 | 17360984 | To examine the acute effect of hyperglycemia on incretin receptor expression, a hyperglycemic clamp study was performed for 96 h with reduction of GLP-1 receptor expression but increase in GIP receptor expression. |
| 3680 | 17360984 | The reduction of GLP-1 receptor expression by high glucose was prevented by dominant-negative protein kinase C (PKC)alpha overexpression, whereas GLP-1 receptor expression was reduced with wild-type PKCalpha overexpression. |
| 3681 | 17360984 | Taken together, GLP-1 and GIP receptor expression is decreased with chronic hyperglycemia, and this decrease likely contributes to the impaired incretin effects found in diabetes. |
| 3682 | 17383951 | The article beside of summarizing the physiological aspects of the two most important incretins, the glucagon-like peptide (GLP)-1 and glucose-dependent insulinotrope polypeptide (GIP), gives a detailed overview of multifaceted effects of GLP-1 and their potential application in the therapy of type 2 diabetes mellitus. |
| 3683 | 17393464 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal incretin hormone, which modulates physiological insulin secretion. |
| 3684 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3685 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3686 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3687 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3688 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3689 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3690 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3691 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3692 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3693 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3694 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3695 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3696 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3697 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3698 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3699 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3700 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3701 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3702 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3703 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3704 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3705 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3706 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3707 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3708 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3709 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3710 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3711 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3712 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3713 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3714 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3715 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3716 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3717 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3718 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3719 | 17437246 | Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion. |
| 3720 | 17437246 | We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR). |
| 3721 | 17437246 | GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break. |
| 3722 | 17437246 | A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template. |
| 3723 | 17437246 | The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR. |
| 3724 | 17437246 | On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex. |
| 3725 | 17437246 | This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR. |
| 3726 | 17484514 | Normal secretion of the incretin hormones glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 during gestational diabetes mellitus. |
| 3727 | 17486662 | Comparison of the subchronic antidiabetic effects of DPP IV-resistant GIP and GLP-1 analogues in obese diabetic (ob/ob) mice. |
| 3728 | 17486662 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are the two key incretin hormones released from the gastrointestinal tract that regulate blood glucose homeostasis through potent insulin secretion. |
| 3729 | 17486662 | The rapid degradation of GIP and GLP-1 by the ubiquitous enzyme dipeptidyl peptidase IV (DPP IV) renders both peptides noninsulinotropic. |
| 3730 | 17486662 | Subchronic administration of N-AcGIP, (Val8)GLP-1 or combined peptide administration had no significant effects on the body weight, food intake and plasma insulin concentrations. |
| 3731 | 17486662 | These results provide evidence for an improvement of glucose homeostasis following treatment with enzyme-resistant GIP and GLP-1 analogues. |
| 3732 | 17486662 | Comparison of the subchronic antidiabetic effects of DPP IV-resistant GIP and GLP-1 analogues in obese diabetic (ob/ob) mice. |
| 3733 | 17486662 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are the two key incretin hormones released from the gastrointestinal tract that regulate blood glucose homeostasis through potent insulin secretion. |
| 3734 | 17486662 | The rapid degradation of GIP and GLP-1 by the ubiquitous enzyme dipeptidyl peptidase IV (DPP IV) renders both peptides noninsulinotropic. |
| 3735 | 17486662 | Subchronic administration of N-AcGIP, (Val8)GLP-1 or combined peptide administration had no significant effects on the body weight, food intake and plasma insulin concentrations. |
| 3736 | 17486662 | These results provide evidence for an improvement of glucose homeostasis following treatment with enzyme-resistant GIP and GLP-1 analogues. |
| 3737 | 17486662 | Comparison of the subchronic antidiabetic effects of DPP IV-resistant GIP and GLP-1 analogues in obese diabetic (ob/ob) mice. |
| 3738 | 17486662 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are the two key incretin hormones released from the gastrointestinal tract that regulate blood glucose homeostasis through potent insulin secretion. |
| 3739 | 17486662 | The rapid degradation of GIP and GLP-1 by the ubiquitous enzyme dipeptidyl peptidase IV (DPP IV) renders both peptides noninsulinotropic. |
| 3740 | 17486662 | Subchronic administration of N-AcGIP, (Val8)GLP-1 or combined peptide administration had no significant effects on the body weight, food intake and plasma insulin concentrations. |
| 3741 | 17486662 | These results provide evidence for an improvement of glucose homeostasis following treatment with enzyme-resistant GIP and GLP-1 analogues. |
| 3742 | 17486662 | Comparison of the subchronic antidiabetic effects of DPP IV-resistant GIP and GLP-1 analogues in obese diabetic (ob/ob) mice. |
| 3743 | 17486662 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are the two key incretin hormones released from the gastrointestinal tract that regulate blood glucose homeostasis through potent insulin secretion. |
| 3744 | 17486662 | The rapid degradation of GIP and GLP-1 by the ubiquitous enzyme dipeptidyl peptidase IV (DPP IV) renders both peptides noninsulinotropic. |
| 3745 | 17486662 | Subchronic administration of N-AcGIP, (Val8)GLP-1 or combined peptide administration had no significant effects on the body weight, food intake and plasma insulin concentrations. |
| 3746 | 17486662 | These results provide evidence for an improvement of glucose homeostasis following treatment with enzyme-resistant GIP and GLP-1 analogues. |
| 3747 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3748 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3749 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3750 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3751 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3752 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3753 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3754 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3755 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3756 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3757 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3758 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3759 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3760 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3761 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3762 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3763 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3764 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3765 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3766 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3767 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3768 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3769 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3770 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3771 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3772 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3773 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3774 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3775 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3776 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3777 | 17498508 | Biology of incretins: GLP-1 and GIP. |
| 3778 | 17498508 | This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 3779 | 17498508 | The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. |
| 3780 | 17498508 | GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. |
| 3781 | 17498508 | The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. |
| 3782 | 17498508 | GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. |
| 3783 | 17505054 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that has a potent stimulatory effect on insulin release under conditions of normal glucose tolerance. |
| 3784 | 17505054 | Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. |
| 3785 | 17505054 | These results suggest that the GIP-R is ubiquitated, resulting in downregulation of the actions of GIP. |
| 3786 | 17505054 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that has a potent stimulatory effect on insulin release under conditions of normal glucose tolerance. |
| 3787 | 17505054 | Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. |
| 3788 | 17505054 | These results suggest that the GIP-R is ubiquitated, resulting in downregulation of the actions of GIP. |
| 3789 | 17505054 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that has a potent stimulatory effect on insulin release under conditions of normal glucose tolerance. |
| 3790 | 17505054 | Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. |
| 3791 | 17505054 | These results suggest that the GIP-R is ubiquitated, resulting in downregulation of the actions of GIP. |
| 3792 | 17543192 | Dipeptidyl peptidase IV is a serine protease with an indirect role in antihyperglycaemia via degradation of the incretin hormones glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide. |
| 3793 | 17543192 | In this study, we have investigated upon selectivity of dipeptidyl peptidase IV compared to two other members of the S9b family, dipeptidyl peptidase 8 and 9, based on kinetic analyses of the pancreatic peptide hormones neuropeptide Y and peptide YY. |
| 3794 | 17543192 | We report a striking 250-fold preference for cleavage of neuropeptide Y compared to peptide YY observed for DPP-8/-9, but not for DPP-IV. |
| 3795 | 17553392 | [Effect of incretin hormones GIP and GLP-1 for the pathogenesis of type 2 diabetes mellitus]. |
| 3796 | 17553392 | This phenomenon is called the incretin effect and is caused by the two incretin hormones GIP and GLP-1. |
| 3797 | 17553392 | [Effect of incretin hormones GIP and GLP-1 for the pathogenesis of type 2 diabetes mellitus]. |
| 3798 | 17553392 | This phenomenon is called the incretin effect and is caused by the two incretin hormones GIP and GLP-1. |
| 3799 | 17573070 | Nateglinide also prevented the degradation of glucagon-like peptide-1 (GLP-1) by DPP IV in a time and concentration-dependent manner. |
| 3800 | 17573070 | In vitro nateglinide and GLP-1 effects on insulin release were additive. |
| 3801 | 17573070 | In vivo nateglinide improved the glucose-lowering and insulin-releasing activity of GLP-1 in obese-diabetic ob/ob mice. |
| 3802 | 17573070 | Nateglinide similarly benefited the glucose and insulin responses to feeding in ob/ob mice and such actions were abolished by co-administration of exendin(9-39) and (Pro(3))GIP to block incretin hormone action. |
| 3803 | 17573070 | These data indicate that the use of nateglinide as a prandial insulin-releasing agent may partly rely on inhibition of GLP-1 degradation as well as beta-cell K(ATP) channel inhibition. |
| 3804 | 17580730 | Like other DPP-4 inhibitors its action is mediated by increasing levels of the incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). |
| 3805 | 17590699 | The present study was undertaken to assess GIP responses in type 2 diabetes using three antibodies (S100, GP01 and GP24). |
| 3806 | 17590699 | Using S100, GIP responses in the diabetic group were significantly lower at 30' (P<0.025) and at 120' (P<0.01) and the integrated incremental GIP responses also were significantly lower in the diabetic group (P< 0.025). |
| 3807 | 17590699 | The present study was undertaken to assess GIP responses in type 2 diabetes using three antibodies (S100, GP01 and GP24). |
| 3808 | 17590699 | Using S100, GIP responses in the diabetic group were significantly lower at 30' (P<0.025) and at 120' (P<0.01) and the integrated incremental GIP responses also were significantly lower in the diabetic group (P< 0.025). |
| 3809 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3810 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3811 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3812 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3813 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3814 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3815 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3816 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3817 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3818 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3819 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3820 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3821 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3822 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3823 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3824 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3825 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3826 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3827 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3828 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3829 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3830 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3831 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3832 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3833 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3834 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3835 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3836 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3837 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3838 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3839 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3840 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3841 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3842 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3843 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3844 | 17609256 | Reduction of hepatic insulin clearance after oral glucose ingestion is not mediated by glucagon-like peptide 1 or gastric inhibitory polypeptide in humans. |
| 3845 | 17609256 | Therefore, we determined insulin clearance in response to endogenously secreted and exogenously administered GIP and GLP-1. |
| 3846 | 17609256 | Insulin clearance was estimated from the molar C-peptide-to-insulin ratio calculated at basal conditions and from the respective areas under the curve after glucose, GIP, or GLP-1 administration. |
| 3847 | 17609256 | The endogenous secretion of GIP or GLP-1 was unrelated to the changes in insulin clearance. |
| 3848 | 17609256 | The C-peptide-to-insulin ratio was unchanged after the intravenous administration of GIP or GLP-1 in the fasting state (P = 0.27 and P = 0.35, respectively). |
| 3849 | 17609256 | Likewise, infusing GLP-1 during a meal course did not alter insulin clearance (P = 0.87). |
| 3850 | 17609256 | Neither GIP nor GLP-1 has significant effects on insulin extraction. |
| 3851 | 17609258 | We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3852 | 17609258 | The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). |
| 3853 | 17609258 | In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3854 | 17609258 | We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3855 | 17609258 | The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). |
| 3856 | 17609258 | In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3857 | 17609258 | We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3858 | 17609258 | The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). |
| 3859 | 17609258 | In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. |
| 3860 | 17624916 | Association analyses of GIP and GIPR polymorphisms with traits of the metabolic syndrome. |
| 3861 | 17624916 | Glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin release via interaction with its pancreatic receptor (GIP receptor (GIPR)). |
| 3862 | 17624916 | To investigate whether variations in GIP and GIPR genes are associated with risk factors of the metabolic syndrome we sequenced gene regions and identified two coding SNPs (GIP Ser103Gly, GIPR Glu354Gln) and one splice site SNP (GIP rs2291726) in 47 subjects. |
| 3863 | 17624916 | In conclusion, we identified a common splice site mutation (rs2291726) of the GIP gene which results in a truncated protein and provide preliminary evidence for an association of the heterozygous GIPR Glu354Gln genotype with CVD. |
| 3864 | 17624916 | Association analyses of GIP and GIPR polymorphisms with traits of the metabolic syndrome. |
| 3865 | 17624916 | Glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin release via interaction with its pancreatic receptor (GIP receptor (GIPR)). |
| 3866 | 17624916 | To investigate whether variations in GIP and GIPR genes are associated with risk factors of the metabolic syndrome we sequenced gene regions and identified two coding SNPs (GIP Ser103Gly, GIPR Glu354Gln) and one splice site SNP (GIP rs2291726) in 47 subjects. |
| 3867 | 17624916 | In conclusion, we identified a common splice site mutation (rs2291726) of the GIP gene which results in a truncated protein and provide preliminary evidence for an association of the heterozygous GIPR Glu354Gln genotype with CVD. |
| 3868 | 17624916 | Association analyses of GIP and GIPR polymorphisms with traits of the metabolic syndrome. |
| 3869 | 17624916 | Glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin release via interaction with its pancreatic receptor (GIP receptor (GIPR)). |
| 3870 | 17624916 | To investigate whether variations in GIP and GIPR genes are associated with risk factors of the metabolic syndrome we sequenced gene regions and identified two coding SNPs (GIP Ser103Gly, GIPR Glu354Gln) and one splice site SNP (GIP rs2291726) in 47 subjects. |
| 3871 | 17624916 | In conclusion, we identified a common splice site mutation (rs2291726) of the GIP gene which results in a truncated protein and provide preliminary evidence for an association of the heterozygous GIPR Glu354Gln genotype with CVD. |
| 3872 | 17624916 | Association analyses of GIP and GIPR polymorphisms with traits of the metabolic syndrome. |
| 3873 | 17624916 | Glucose-dependent insulinotropic polypeptide (GIP) stimulates insulin release via interaction with its pancreatic receptor (GIP receptor (GIPR)). |
| 3874 | 17624916 | To investigate whether variations in GIP and GIPR genes are associated with risk factors of the metabolic syndrome we sequenced gene regions and identified two coding SNPs (GIP Ser103Gly, GIPR Glu354Gln) and one splice site SNP (GIP rs2291726) in 47 subjects. |
| 3875 | 17624916 | In conclusion, we identified a common splice site mutation (rs2291726) of the GIP gene which results in a truncated protein and provide preliminary evidence for an association of the heterozygous GIPR Glu354Gln genotype with CVD. |
| 3876 | 17629492 | The physiological incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), lower blood glucose levels through multiple mechanisms, including enhancement of glucose-stimulated insulin secretion. |
| 3877 | 17629492 | Here, we discuss recent approaches to incretin-based therapy, including the use of long-acting GLP-1 receptor agonists, degradation-resistant GLP-1 analogs, GLP-1 analogs conjugated to albumin, non-peptide small molecules that bind to the GLP-1 receptor, and inhibitors of dipeptidyl peptidase IV, the enzyme that degrades both GIP and GLP-1. |
| 3878 | 17629492 | The physiological incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), lower blood glucose levels through multiple mechanisms, including enhancement of glucose-stimulated insulin secretion. |
| 3879 | 17629492 | Here, we discuss recent approaches to incretin-based therapy, including the use of long-acting GLP-1 receptor agonists, degradation-resistant GLP-1 analogs, GLP-1 analogs conjugated to albumin, non-peptide small molecules that bind to the GLP-1 receptor, and inhibitors of dipeptidyl peptidase IV, the enzyme that degrades both GIP and GLP-1. |
| 3880 | 17654450 | These observations in animals and man suggest that GIP receptor antagonism may afford an alternative therapeutic option for treatment of obesity-diabetes. |
| 3881 | 17655515 | Unlike conventional oral antidiabetic agents, these agents promote glucose homeostasis through inhibition of DPP-IV, the enzyme responsible for degradation of two key glucoregulatory hormones: glucagon-like peptide-1 (GLP-1), which extends the action of insulin while also suppressing the release of glucagon, and glucose-dependent insulinotropic peptide (GIP). |
| 3882 | 17655515 | Other proposed mechanisms of action of GLP-1 and thus DPP-IV inhibitors include satiety, increased beta-cell production, and inhibition of apoptosis of beta cells. |
| 3883 | 17655515 | Clinical studies have evaluated the potential for DPP-IV inhibition to reduce glucagon levels, delay gastric emptying, and stimulate insulin release. |
| 3884 | 17717280 | Incretin receptors for glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide are essential for the sustained metabolic actions of vildagliptin in mice. |
| 3885 | 17724014 | Of the approximately 19 million individuals with T2DM in the United States, only about a third achieve the hemoglobin A(1c) (HbA(1c)0 goal set forth by the American Diabetes Association (HbA(1c) <7% [6% if it can be achieved safely]). |
| 3886 | 17724014 | Dipeptidyl peptidase IV inhibitors suppress the degradation of incretins, thus extending the activity of GLP-1 and GIP. |
| 3887 | 17848629 | GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. |
| 3888 | 17848629 | This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. |
| 3889 | 17848629 | Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. |
| 3890 | 17848629 | (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. |
| 3891 | 17848629 | These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. |
| 3892 | 17848629 | These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet. |
| 3893 | 17848629 | GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. |
| 3894 | 17848629 | This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. |
| 3895 | 17848629 | Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. |
| 3896 | 17848629 | (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. |
| 3897 | 17848629 | These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. |
| 3898 | 17848629 | These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet. |
| 3899 | 17848629 | GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. |
| 3900 | 17848629 | This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. |
| 3901 | 17848629 | Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. |
| 3902 | 17848629 | (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. |
| 3903 | 17848629 | These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. |
| 3904 | 17848629 | These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet. |
| 3905 | 17848629 | GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. |
| 3906 | 17848629 | This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. |
| 3907 | 17848629 | Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. |
| 3908 | 17848629 | (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. |
| 3909 | 17848629 | These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. |
| 3910 | 17848629 | These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet. |
| 3911 | 17848629 | GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. |
| 3912 | 17848629 | This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. |
| 3913 | 17848629 | Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. |
| 3914 | 17848629 | (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. |
| 3915 | 17848629 | These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. |
| 3916 | 17848629 | These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet. |
| 3917 | 17884459 | We measured plasma levels of glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), ghrelin, leptin, adiponectin, resistin, C-reactive protein, cytokines, and their soluble receptors, as well as nonesterified free fatty acids (NEFAs). |
| 3918 | 17884459 | Although there was a clear trend for differences in the insulinogenic index, the areas under the curves for insulin, systolic blood pressure, adiponectin, and C-reactive protein across the glucose tolerance categories revealed no statistical significance. |
| 3919 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3920 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3921 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3922 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3923 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3924 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3925 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3926 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3927 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3928 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3929 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3930 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3931 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3932 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3933 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3934 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3935 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3936 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3937 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3938 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3939 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3940 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3941 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3942 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3943 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3944 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3945 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3946 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3947 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3948 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3949 | 17890220 | Resistin is a key mediator of glucose-dependent insulinotropic polypeptide (GIP) stimulation of lipoprotein lipase (LPL) activity in adipocytes. |
| 3950 | 17890220 | In previous studies on the stimulatory effect of GIP on adipocyte lipoprotein lipase (LPL), a pathway was identified involving increased phosphorylation of protein kinase B (PKB) and reduced phosphorylation of LKB1 and AMP-activated protein kinase (AMPK). |
| 3951 | 17890220 | In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased resistin secretion through a pathway involving p38 mitogen-activated protein kinase (p38 MAPK) and the stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK). |
| 3952 | 17890220 | Chronic elevation of circulating GIP levels in the Vancouver Diabetic Fatty (VDF) Zucker rat resulted in increases in circulating resistin levels and activation of p38 MAPK or SAPK/JNK in epididymal fat tissue, suggesting the existence of identical pathways in vivo as well as in vitro. |
| 3953 | 17890220 | Administration of resistin to 3T3-L1 adipocytes mimicked the effects of GIP on the PKB/LKB1/AMPK/LPL pathway: increasing phosphorylation of PKB, reducing levels of phosphorylated LKB1 and AMPK, and increasing LPL activity. |
| 3954 | 17890220 | Knockdown of resistin using RNA interference attenuated the effect of GIP on the PKB/LKB1/AMPK/LPL pathway in 3T3-L1 adipocytes, supporting a role for resistin as a mediator. |
| 3955 | 17958029 | The two incretin hormones GLP-1 (Glucagon-Like Peptide-1) and GIP (Glucose-dependent Insulinotropic Peptide) are released by the gut in response to nutrient ingestion. |
| 3956 | 17958029 | In addition to its insulinotropic action, GLP-1 (but not GIP) suppresses glucagon secretion, delays gastric emptying and promotes satiety. |
| 3957 | 17958029 | Because GLP-1 is rapidly degraded by the ubiquitous enzyme, dipeptidyl peptidase-IV (DPP-IV) and has a very short-lived action, DPP-IV resistant mimetics have been designed. |
| 3958 | 17958029 | Several randomized placebo-controlled studies with DPP-IV resistant GLP-1 analogues confirmed their efficacy to improve glycemic control in type 2 diabetic patients. |
| 3959 | 17958029 | The two incretin hormones GLP-1 (Glucagon-Like Peptide-1) and GIP (Glucose-dependent Insulinotropic Peptide) are released by the gut in response to nutrient ingestion. |
| 3960 | 17958029 | In addition to its insulinotropic action, GLP-1 (but not GIP) suppresses glucagon secretion, delays gastric emptying and promotes satiety. |
| 3961 | 17958029 | Because GLP-1 is rapidly degraded by the ubiquitous enzyme, dipeptidyl peptidase-IV (DPP-IV) and has a very short-lived action, DPP-IV resistant mimetics have been designed. |
| 3962 | 17958029 | Several randomized placebo-controlled studies with DPP-IV resistant GLP-1 analogues confirmed their efficacy to improve glycemic control in type 2 diabetic patients. |
| 3963 | 17981665 | A number of alternative therapies are currently being developed to take advantage of the actions of the incretin hormones Glucagon-Like Peptide-1 (GLP-1) and Glucose-dependent Insulinotropic Polypeptide (GIP). |
| 3964 | 17981667 | One emerging area of interest is centred upon the actions of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which enhance meal-induced insulin secretion and have trophic effects on the beta-cell. |
| 3965 | 17981667 | Two new classes of agents have recently gained regulatory approval for therapy of type 2 diabetes; long-acting stable analogues of GLP-1, the so-called incretin mimetics, and inhibitors of dipeptidyl peptidase 4 (DPP-4, the enzyme responsible for the rapid degradation of the incretin hormones), the so-called incretin enhancers. |
| 3966 | 18019673 | DPPIV are enzymes widely present in the body which proteolytically degrade GLP-1 and GIP (as well as other active substances). |
| 3967 | 18020966 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. |
| 3968 | 18020966 | They have a number of important biological effects, which include release of insulin, inhibition of glucagon and somatostatin, maintenance of beta-cell mass, delay of gastric emptying, and inhibition of feeding. |
| 3969 | 18020966 | Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. |
| 3970 | 18020966 | GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. |
| 3971 | 18020966 | As GLP-1 has a very short half-life, due to rapid degradation by the enzyme dipeptidyl peptidase IV (DPPIV), analogues of GIP and GLP-1 that are resistant to the action of DPPIV have been developed and clinical trials have shown their effectiveness. |
| 3972 | 18020966 | Strategies to augment the biological actions of GIP and/or GLP-1 in T2D are expected to minimise weight gain, reduce hypoglycaemic episodes and prevent progressive beta-cell failure by increasing beta-cell mass. |
| 3973 | 18020966 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. |
| 3974 | 18020966 | They have a number of important biological effects, which include release of insulin, inhibition of glucagon and somatostatin, maintenance of beta-cell mass, delay of gastric emptying, and inhibition of feeding. |
| 3975 | 18020966 | Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. |
| 3976 | 18020966 | GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. |
| 3977 | 18020966 | As GLP-1 has a very short half-life, due to rapid degradation by the enzyme dipeptidyl peptidase IV (DPPIV), analogues of GIP and GLP-1 that are resistant to the action of DPPIV have been developed and clinical trials have shown their effectiveness. |
| 3978 | 18020966 | Strategies to augment the biological actions of GIP and/or GLP-1 in T2D are expected to minimise weight gain, reduce hypoglycaemic episodes and prevent progressive beta-cell failure by increasing beta-cell mass. |
| 3979 | 18020966 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. |
| 3980 | 18020966 | They have a number of important biological effects, which include release of insulin, inhibition of glucagon and somatostatin, maintenance of beta-cell mass, delay of gastric emptying, and inhibition of feeding. |
| 3981 | 18020966 | Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. |
| 3982 | 18020966 | GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. |
| 3983 | 18020966 | As GLP-1 has a very short half-life, due to rapid degradation by the enzyme dipeptidyl peptidase IV (DPPIV), analogues of GIP and GLP-1 that are resistant to the action of DPPIV have been developed and clinical trials have shown their effectiveness. |
| 3984 | 18020966 | Strategies to augment the biological actions of GIP and/or GLP-1 in T2D are expected to minimise weight gain, reduce hypoglycaemic episodes and prevent progressive beta-cell failure by increasing beta-cell mass. |
| 3985 | 18020966 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. |
| 3986 | 18020966 | They have a number of important biological effects, which include release of insulin, inhibition of glucagon and somatostatin, maintenance of beta-cell mass, delay of gastric emptying, and inhibition of feeding. |
| 3987 | 18020966 | Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. |
| 3988 | 18020966 | GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. |
| 3989 | 18020966 | As GLP-1 has a very short half-life, due to rapid degradation by the enzyme dipeptidyl peptidase IV (DPPIV), analogues of GIP and GLP-1 that are resistant to the action of DPPIV have been developed and clinical trials have shown their effectiveness. |
| 3990 | 18020966 | Strategies to augment the biological actions of GIP and/or GLP-1 in T2D are expected to minimise weight gain, reduce hypoglycaemic episodes and prevent progressive beta-cell failure by increasing beta-cell mass. |
| 3991 | 18039776 | Gastrointestinal hormones including gastric inhibitory polypeptide (GIP), glucagon-like peptide (GLP)-1, and GLP-2 are secreted immediately after meal ingestion, and GIP and GLP-2 have been shown to regulate bone turnover. |
| 3992 | 18039776 | We investigated the role of GLP-1 in the regulation of bone metabolism using GLP-1 receptor knockout (Glp-1r(-/-)) mice. |
| 3993 | 18039776 | Although GLP-1 had no direct effect on osteoclasts and osteoblasts, Glp-1r(-/-) mice exhibited higher levels of urinary deoxypyridinoline, a marker of bone resorption, and reduced levels of calcitonin mRNA transcripts in the thyroid. |
| 3994 | 18039776 | Moreover, calcitonin treatment effectively suppressed urinary levels of deoxypyridinoline in Glp-1r(-/-), mice and the GLP-1 receptor agonist exendin-4 increased calcitonin gene expression in the thyroid of wild-type mice. |
| 3995 | 18054732 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are physiological gut peptides with insulin-releasing and extrapancreatic glucoregulatory actions. |
| 3996 | 18054732 | Incretin analogues/mimetics activate GLP-1 or GIP receptors whilst avoiding physiological inactivation by dipeptidyl peptidase 4 (DPP-4), and they represent one of the newest classes of antidiabetic drug. |
| 3997 | 18054732 | This review discusses the various attributes of GLP-1 and GIP for diabetes treatment and summarises current clinical data. |
| 3998 | 18054732 | Additionally, it explores the therapeutic possibilities offered by preclinical agents, such as non-peptide GLP-1 mimetics, GLP-1/glucagon hybrid peptides, and specific GIP receptor antagonists. |
| 3999 | 18054732 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are physiological gut peptides with insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4000 | 18054732 | Incretin analogues/mimetics activate GLP-1 or GIP receptors whilst avoiding physiological inactivation by dipeptidyl peptidase 4 (DPP-4), and they represent one of the newest classes of antidiabetic drug. |
| 4001 | 18054732 | This review discusses the various attributes of GLP-1 and GIP for diabetes treatment and summarises current clinical data. |
| 4002 | 18054732 | Additionally, it explores the therapeutic possibilities offered by preclinical agents, such as non-peptide GLP-1 mimetics, GLP-1/glucagon hybrid peptides, and specific GIP receptor antagonists. |
| 4003 | 18054732 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are physiological gut peptides with insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4004 | 18054732 | Incretin analogues/mimetics activate GLP-1 or GIP receptors whilst avoiding physiological inactivation by dipeptidyl peptidase 4 (DPP-4), and they represent one of the newest classes of antidiabetic drug. |
| 4005 | 18054732 | This review discusses the various attributes of GLP-1 and GIP for diabetes treatment and summarises current clinical data. |
| 4006 | 18054732 | Additionally, it explores the therapeutic possibilities offered by preclinical agents, such as non-peptide GLP-1 mimetics, GLP-1/glucagon hybrid peptides, and specific GIP receptor antagonists. |
| 4007 | 18054732 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are physiological gut peptides with insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4008 | 18054732 | Incretin analogues/mimetics activate GLP-1 or GIP receptors whilst avoiding physiological inactivation by dipeptidyl peptidase 4 (DPP-4), and they represent one of the newest classes of antidiabetic drug. |
| 4009 | 18054732 | This review discusses the various attributes of GLP-1 and GIP for diabetes treatment and summarises current clinical data. |
| 4010 | 18054732 | Additionally, it explores the therapeutic possibilities offered by preclinical agents, such as non-peptide GLP-1 mimetics, GLP-1/glucagon hybrid peptides, and specific GIP receptor antagonists. |
| 4011 | 18063845 | In type 2 diabetes, there is a possibility that an important part of the impaired insulin secretion is due to the gastric inhibitory polypeptide (GIP) hormone. |
| 4012 | 18063845 | This study investigated changes that occur in the pancreatic GIP receptors' (GIP-Rs) expression and in GIP secretion in obese and type 2 diabetic rats and its relation to plasma glucose and insulin levels during oral glucose tolerance test (OGTT) compared to control rats. |
| 4013 | 18063845 | In conclusion, both obese and diabetic rats had an impaired early-phase insulinotropic effect of GIP due to impaired gene expression of GIP-Rs which could be a potential target to prevent transition of obesity to diabetes and to improve insulin secretion in the latter. |
| 4014 | 18063845 | In type 2 diabetes, there is a possibility that an important part of the impaired insulin secretion is due to the gastric inhibitory polypeptide (GIP) hormone. |
| 4015 | 18063845 | This study investigated changes that occur in the pancreatic GIP receptors' (GIP-Rs) expression and in GIP secretion in obese and type 2 diabetic rats and its relation to plasma glucose and insulin levels during oral glucose tolerance test (OGTT) compared to control rats. |
| 4016 | 18063845 | In conclusion, both obese and diabetic rats had an impaired early-phase insulinotropic effect of GIP due to impaired gene expression of GIP-Rs which could be a potential target to prevent transition of obesity to diabetes and to improve insulin secretion in the latter. |
| 4017 | 18063845 | In type 2 diabetes, there is a possibility that an important part of the impaired insulin secretion is due to the gastric inhibitory polypeptide (GIP) hormone. |
| 4018 | 18063845 | This study investigated changes that occur in the pancreatic GIP receptors' (GIP-Rs) expression and in GIP secretion in obese and type 2 diabetic rats and its relation to plasma glucose and insulin levels during oral glucose tolerance test (OGTT) compared to control rats. |
| 4019 | 18063845 | In conclusion, both obese and diabetic rats had an impaired early-phase insulinotropic effect of GIP due to impaired gene expression of GIP-Rs which could be a potential target to prevent transition of obesity to diabetes and to improve insulin secretion in the latter. |
| 4020 | 18068977 | Dipeptidyl peptidase-IV (DPP-IV) is an enzyme responsible for the inactivation of the glucoregulatory incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 4021 | 18174966 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are important incretin hormones contributing to 50-70% of the stimulation of insulin secretion after a meal. |
| 4022 | 18174966 | Dipeptidyl-peptidase IV (DPP-4) inhibitors inhibit the degradation of GLP-1 and GIP as well as that of other regulatory peptides. |
| 4023 | 18174966 | Like other DPP-4 inhibitors, sitagliptin reduces hemoglobin A1c (HbA1c), fasting and postprandial glucose by glucose-dependent stimulation of insulin secretion and inhibition of glucagon secretion. |
| 4024 | 18205109 | The main mediators of the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4025 | 18205109 | Detailed analysis of incretin defect proved that GIP secretion remains within physiological limits, whereas GLP-1 secretion is significantly decreased. |
| 4026 | 18205109 | Nevertheless, GLP-1 insulinotropic effect is preserved and GIP effect is significantly impaired. |
| 4027 | 18205109 | In consequence, substitutional GLP-1 administration aiming at the reduction of its deficiency, seems to be logical therapeutic management, because despite a physiologically retained quantity response from GIP, resistance to this peptide is frequently found. |
| 4028 | 18205109 | The main mediators of the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4029 | 18205109 | Detailed analysis of incretin defect proved that GIP secretion remains within physiological limits, whereas GLP-1 secretion is significantly decreased. |
| 4030 | 18205109 | Nevertheless, GLP-1 insulinotropic effect is preserved and GIP effect is significantly impaired. |
| 4031 | 18205109 | In consequence, substitutional GLP-1 administration aiming at the reduction of its deficiency, seems to be logical therapeutic management, because despite a physiologically retained quantity response from GIP, resistance to this peptide is frequently found. |
| 4032 | 18205109 | The main mediators of the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4033 | 18205109 | Detailed analysis of incretin defect proved that GIP secretion remains within physiological limits, whereas GLP-1 secretion is significantly decreased. |
| 4034 | 18205109 | Nevertheless, GLP-1 insulinotropic effect is preserved and GIP effect is significantly impaired. |
| 4035 | 18205109 | In consequence, substitutional GLP-1 administration aiming at the reduction of its deficiency, seems to be logical therapeutic management, because despite a physiologically retained quantity response from GIP, resistance to this peptide is frequently found. |
| 4036 | 18205109 | The main mediators of the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4037 | 18205109 | Detailed analysis of incretin defect proved that GIP secretion remains within physiological limits, whereas GLP-1 secretion is significantly decreased. |
| 4038 | 18205109 | Nevertheless, GLP-1 insulinotropic effect is preserved and GIP effect is significantly impaired. |
| 4039 | 18205109 | In consequence, substitutional GLP-1 administration aiming at the reduction of its deficiency, seems to be logical therapeutic management, because despite a physiologically retained quantity response from GIP, resistance to this peptide is frequently found. |
| 4040 | 18375745 | Incretins: pathophysiological and therapeutic implications of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. |
| 4041 | 18375745 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are intestinal postprandial hormones that stimulate insulin release from the pancreas as long as circulating glucose concentrations are raised. |
| 4042 | 18375745 | In addition to their effect on insulin secretion and consequent glucose lowering, GIP and GLP-1, especially the latter, have a number of physiological effects such as inhibition of glucagon release, gastric emptying and food intake, as well as a tropic action on pancreatic B-cell mass. |
| 4043 | 18375745 | Incretins: pathophysiological and therapeutic implications of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. |
| 4044 | 18375745 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are intestinal postprandial hormones that stimulate insulin release from the pancreas as long as circulating glucose concentrations are raised. |
| 4045 | 18375745 | In addition to their effect on insulin secretion and consequent glucose lowering, GIP and GLP-1, especially the latter, have a number of physiological effects such as inhibition of glucagon release, gastric emptying and food intake, as well as a tropic action on pancreatic B-cell mass. |
| 4046 | 18375745 | Incretins: pathophysiological and therapeutic implications of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. |
| 4047 | 18375745 | Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are intestinal postprandial hormones that stimulate insulin release from the pancreas as long as circulating glucose concentrations are raised. |
| 4048 | 18375745 | In addition to their effect on insulin secretion and consequent glucose lowering, GIP and GLP-1, especially the latter, have a number of physiological effects such as inhibition of glucagon release, gastric emptying and food intake, as well as a tropic action on pancreatic B-cell mass. |
| 4049 | 18375772 | Advancement in the knowledge surrounding the physiology of endogenous glucoregulatory peptide hormones, such as glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, has led to new therapeutic targets for the treatment of type 2 diabetes mellitus. |
| 4050 | 18375772 | This article, part 3 of a 3-part series, reviews the new class of medications known as DPP-4 inhibitors as well as discusses a future buccal insulin formulation, Oral-Lyn, on the horizon for the treatment of diabetes mellitus. |
| 4051 | 18505834 | To test this hypothesis, C57BL/6 mice and GIP-receptor knockout mice (Gipr(-/-)) were exposed to OVX or sham operation (n = 10 per group). |
| 4052 | 18505834 | Cumulative food intake in OVX Gipr(-/-) animals was significantly reduced and associated with significantly lower hypothalamic mRNA expression of the orexigenic neuropeptide Y (NPY) but not of cocaine-amphetamine-related transcript (CART), melanocortin receptors (MCR-3 and MCR-4), or thyrotropin-releasing hormone (TRH). |
| 4053 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4054 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4055 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4056 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4057 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4058 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4059 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4060 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4061 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4062 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4063 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4064 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4065 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4066 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4067 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4068 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4069 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4070 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4071 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4072 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4073 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4074 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4075 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4076 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4077 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4078 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4079 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4080 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4081 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4082 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4083 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4084 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4085 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4086 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4087 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4088 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4089 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4090 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4091 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4092 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4093 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4094 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4095 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4096 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4097 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4098 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4099 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4100 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4101 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4102 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4103 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4104 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4105 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4106 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4107 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4108 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4109 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4110 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4111 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4112 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4113 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4114 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4115 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4116 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4117 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4118 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4119 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4120 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4121 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4122 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4123 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4124 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4125 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4126 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4127 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4128 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4129 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4130 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4131 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4132 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4133 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4134 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4135 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4136 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4137 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4138 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4139 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4140 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4141 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4142 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4143 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4144 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4145 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4146 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4147 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4148 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4149 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4150 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4151 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4152 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4153 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4154 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4155 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4156 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4157 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4158 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4159 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4160 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4161 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4162 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4163 | 18593849 | Pax6 and Pdx1 are required for production of glucose-dependent insulinotropic polypeptide in proglucagon-expressing L cells. |
| 4164 | 18593849 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretin hormones that play important roles in maintaining glucose homeostasis and are being actively pursued as novel therapeutic agents for diabetes. |
| 4165 | 18593849 | GIP is produced by dispersed enteroendocrine cells and interestingly at times is coexpressed with GLP-1. |
| 4166 | 18593849 | We performed comparative immunostaining of Pax6 and Pdx1 in GIP- and GLP-1-secreting cells. |
| 4167 | 18593849 | We investigated whether Pax6 and Pdx1 activate the human GIP promoter in control IEC-6 cells and GIP-expressing STC-1 cells. |
| 4168 | 18593849 | Pax6 and Pdx1 consistently colocalized in GIP-immunoreactive cells. |
| 4169 | 18593849 | Cells that coexpress GIP and GLP-1 were Pax6 and Pdx1 positive, whereas cells expressing only GLP-1 were Pax6 positive but did not express Pdx1. |
| 4170 | 18593849 | GIP promoter activity was enhanced in IEC-6 cells by exogenous Pax6 or Pdx1 and diminished in STC-1 cells by inhibition of endogenous Pax6 or Pdx1 by dominant-negative forms. |
| 4171 | 18593849 | EMSA studies indicated that Pax6 and Pdx1 bind to this proximal sequence of the human GIP promoter. |
| 4172 | 18593849 | Our findings indicate that concomitant expression of Pax6 and Pdx1 is important for GIP expression. |
| 4173 | 18593849 | Our results also suggest that the presence of Pdx1 defines whether GLP-1-expressing gastrointestinal L cells also coexpress GIP. |
| 4174 | 18600568 | The two incretins glucagon-like peptide-1 (7-36) (GLP-1(7-36)) amide and glucose-dependent insulinotropic peptide (GIP) are released from the small intestine in response to the ingestion of nutrients and regulate glucose homeostasis in a glucose-dependent fashion; however, the action of both incretins is terminated by the rapid N-terminal cleavage of two amino acid residues of GLP-1 and GIP by dipeptidyl peptidase-IV (DPP-IV). |
| 4175 | 18600568 | The preservation of active GLP-1 and GIP by inhibiting DPP-IV activity is an attractive strategy for the treatment of diabetes in patients who exhibit a reduced incretin response. |
| 4176 | 18600568 | The two incretins glucagon-like peptide-1 (7-36) (GLP-1(7-36)) amide and glucose-dependent insulinotropic peptide (GIP) are released from the small intestine in response to the ingestion of nutrients and regulate glucose homeostasis in a glucose-dependent fashion; however, the action of both incretins is terminated by the rapid N-terminal cleavage of two amino acid residues of GLP-1 and GIP by dipeptidyl peptidase-IV (DPP-IV). |
| 4177 | 18600568 | The preservation of active GLP-1 and GIP by inhibiting DPP-IV activity is an attractive strategy for the treatment of diabetes in patients who exhibit a reduced incretin response. |
| 4178 | 18600596 | In contrast, the newly developed incretin-based therapies for T2DM employ the beta-cell-preserving properties of incretin hormones - glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 4179 | 18600596 | Furthermore, the insulinotropic effects of GLP-1 and GIP are glucose-dependent, reducing the risk of hypoglycemia. |
| 4180 | 18600596 | In contrast, the newly developed incretin-based therapies for T2DM employ the beta-cell-preserving properties of incretin hormones - glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 4181 | 18600596 | Furthermore, the insulinotropic effects of GLP-1 and GIP are glucose-dependent, reducing the risk of hypoglycemia. |
| 4182 | 18640588 | Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes. |
| 4183 | 18640588 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). |
| 4184 | 18640588 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 4185 | 18640588 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 4186 | 18640588 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 4187 | 18640588 | Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes. |
| 4188 | 18640588 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). |
| 4189 | 18640588 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 4190 | 18640588 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 4191 | 18640588 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 4192 | 18640588 | Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes. |
| 4193 | 18640588 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). |
| 4194 | 18640588 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 4195 | 18640588 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 4196 | 18640588 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 4197 | 18640588 | Physiology of incretins (GIP and GLP-1) and abnormalities in type 2 diabetes. |
| 4198 | 18640588 | In humans, the incretin effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). |
| 4199 | 18640588 | GIP is secreted by K cells from the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L cells located in the distal intestine. |
| 4200 | 18640588 | GIP and GLP-1 are both rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV (DPP-IV). |
| 4201 | 18640588 | In addition to its effects on insulin secretion, GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis, inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion, reduction of food intake, and trophic effects on the pancreas. |
| 4202 | 18641927 | DPP4 inhibition results in increased blood concentration of the incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). |
| 4203 | 18723001 | Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice. |
| 4204 | 18723001 | In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr(-/-)) mice. |
| 4205 | 18723001 | In HFD-fed Gipr(-/-) mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. |
| 4206 | 18723001 | In addition, the PPARalpha mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr(-/-) mice compared with those in HFD-fed WT mice. |
| 4207 | 18723001 | These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD. |
| 4208 | 18723001 | Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice. |
| 4209 | 18723001 | In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr(-/-)) mice. |
| 4210 | 18723001 | In HFD-fed Gipr(-/-) mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. |
| 4211 | 18723001 | In addition, the PPARalpha mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr(-/-) mice compared with those in HFD-fed WT mice. |
| 4212 | 18723001 | These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD. |
| 4213 | 18723001 | Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice. |
| 4214 | 18723001 | In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr(-/-)) mice. |
| 4215 | 18723001 | In HFD-fed Gipr(-/-) mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. |
| 4216 | 18723001 | In addition, the PPARalpha mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr(-/-) mice compared with those in HFD-fed WT mice. |
| 4217 | 18723001 | These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD. |
| 4218 | 18777503 | It is hypothesized that at the basis of this pathology lies an incretin defect of insulinotropic gut-derived hormones, relying on decreased secretion of GLP-1 (glucagon-like peptide 1), with preserved insulinotropic effect, whereas GIP (glucose-dependent insulinotropic polypeptide) secretion remains within physiological limits, but its action is mostly impaired due to total loss of possibility for stimulation of the second phase insulin secretion. |
| 4219 | 18777503 | In the presence of these findings there are many ongoing clinical studies with the use of GLP-1 analogues or GLP-1 receptors activators (GLP-1 agonists), as well as the inhibitors of dipeptidyl peptidase IV (DPP-IV), the enzyme responsible for incretin proteolysis, in the treatment of type 2 diabetes. |
| 4220 | 18795210 | Targeting Incretins in Type 2 Diabetes: Role of GLP-1 Receptor Agonists and DPP-4 Inhibitors. |
| 4221 | 18795210 | Strategies to leverage the beneficial effects of GLP-1 include GLP-1 receptor agonists or analogs or dipeptidyl peptidase-4 (DPP-4) inhibitors-agents that act by slowing the inactivation of endogenous GLP-1 and GIP. |
| 4222 | 18795210 | This review will provide an overview of current and emerging agents that augment the incretin system with a focus on the role of GLP-1 receptor agonists and DPP-4 inhibitors. |
| 4223 | 18806525 | Inhibition of the enzyme DPP-IV results in increased activity of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), the incretin hormones. |
| 4224 | 18806525 | Through the action of GLP-1 and GIP, DPP-IV inhibitors improve preprandial and postprandial glucose by enhancing insulin secretion and reducing postprandial concentrations of glucagon. |
| 4225 | 18930564 | The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have very similar properties in protecting neurons from toxic effects, and are capable of reversing the detrimental effects that beta-amyloid fragments have on synaptic plasticity. |
| 4226 | 19026698 | Prolonged GIP receptor activation using stable mini-PEGylated GIP improves glucose homeostasis and beta-cell function in age-related glucose intolerance. |
| 4227 | 19026698 | GIP[mPEG] decreased glucose and increased insulin concentrations when administered prior to a glucose challenge. |
| 4228 | 19026698 | Insulin sensitivity, circulating triglycerides and resistin levels were unchanged by the treatment regimen, but plasma adiponectin levels increased. |
| 4229 | 19026698 | These data indicate that prolonged activation of the GIP receptor with GIP[mPEG] counters aspects of impaired beta-cell function and age-related glucose intolerance. |
| 4230 | 19026698 | Prolonged GIP receptor activation using stable mini-PEGylated GIP improves glucose homeostasis and beta-cell function in age-related glucose intolerance. |
| 4231 | 19026698 | GIP[mPEG] decreased glucose and increased insulin concentrations when administered prior to a glucose challenge. |
| 4232 | 19026698 | Insulin sensitivity, circulating triglycerides and resistin levels were unchanged by the treatment regimen, but plasma adiponectin levels increased. |
| 4233 | 19026698 | These data indicate that prolonged activation of the GIP receptor with GIP[mPEG] counters aspects of impaired beta-cell function and age-related glucose intolerance. |
| 4234 | 19026698 | Prolonged GIP receptor activation using stable mini-PEGylated GIP improves glucose homeostasis and beta-cell function in age-related glucose intolerance. |
| 4235 | 19026698 | GIP[mPEG] decreased glucose and increased insulin concentrations when administered prior to a glucose challenge. |
| 4236 | 19026698 | Insulin sensitivity, circulating triglycerides and resistin levels were unchanged by the treatment regimen, but plasma adiponectin levels increased. |
| 4237 | 19026698 | These data indicate that prolonged activation of the GIP receptor with GIP[mPEG] counters aspects of impaired beta-cell function and age-related glucose intolerance. |
| 4238 | 19036624 | This paper briefly reviews the concept of incretins and describes the biological effects of the two incretins identified so far: the glucose-dependent insulinotropic polypeptide (GIP); and the glucagon-like peptide-1 (GLP-1). |
| 4239 | 19036624 | GIP is released by the Kcells of the duodenum, while GLP-1 is released by the Lcells of the distal ileum, in response to nutrient absorption. |
| 4240 | 19036624 | GIP and GLP-1 stimulate insulin biosynthesis and insulin secretion in a glucose-dependent manner. |
| 4241 | 19036624 | This paper briefly reviews the concept of incretins and describes the biological effects of the two incretins identified so far: the glucose-dependent insulinotropic polypeptide (GIP); and the glucagon-like peptide-1 (GLP-1). |
| 4242 | 19036624 | GIP is released by the Kcells of the duodenum, while GLP-1 is released by the Lcells of the distal ileum, in response to nutrient absorption. |
| 4243 | 19036624 | GIP and GLP-1 stimulate insulin biosynthesis and insulin secretion in a glucose-dependent manner. |
| 4244 | 19036624 | This paper briefly reviews the concept of incretins and describes the biological effects of the two incretins identified so far: the glucose-dependent insulinotropic polypeptide (GIP); and the glucagon-like peptide-1 (GLP-1). |
| 4245 | 19036624 | GIP is released by the Kcells of the duodenum, while GLP-1 is released by the Lcells of the distal ileum, in response to nutrient absorption. |
| 4246 | 19036624 | GIP and GLP-1 stimulate insulin biosynthesis and insulin secretion in a glucose-dependent manner. |
| 4247 | 19056762 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. |
| 4248 | 19056762 | Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. |
| 4249 | 19056762 | There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. |
| 4250 | 19056762 | Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). |
| 4251 | 19056762 | After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. |
| 4252 | 19056762 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. |
| 4253 | 19056762 | Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. |
| 4254 | 19056762 | There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. |
| 4255 | 19056762 | Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). |
| 4256 | 19056762 | After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. |
| 4257 | 19056762 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. |
| 4258 | 19056762 | Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. |
| 4259 | 19056762 | There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. |
| 4260 | 19056762 | Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). |
| 4261 | 19056762 | After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. |
| 4262 | 19056762 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. |
| 4263 | 19056762 | Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. |
| 4264 | 19056762 | There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. |
| 4265 | 19056762 | Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). |
| 4266 | 19056762 | After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. |
| 4267 | 19056762 | The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. |
| 4268 | 19056762 | Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. |
| 4269 | 19056762 | There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. |
| 4270 | 19056762 | Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). |
| 4271 | 19056762 | After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. |
| 4272 | 19065992 | Sitagliptin, the first commercially available dipeptidyl peptidase-4 inhibitor, inhibits the metabolism and inactivation of the incretin hormones GLP-1 and GIP. |
| 4273 | 19073224 | GLP-1 and GIP are the two key incretin hormones that regulate post-prandial glucose homeostasis. |
| 4274 | 19073224 | Furthermore, potent enzyme-resistant GIP and GLP-1 receptor agonists such as N-AcGIP and exendin-4 have now been developed. |
| 4275 | 19073224 | Adipose tissue mRNA levels of adiponectin, leptin, resistin, GIP-R, LPL and DGAT-1 were not significantly altered. |
| 4276 | 19073224 | These results illustrate efficacy of enzyme resistant GIP and GLP-1 analogues for treatment of glucose intolerance induced by high fat feeding. |
| 4277 | 19073224 | GLP-1 and GIP are the two key incretin hormones that regulate post-prandial glucose homeostasis. |
| 4278 | 19073224 | Furthermore, potent enzyme-resistant GIP and GLP-1 receptor agonists such as N-AcGIP and exendin-4 have now been developed. |
| 4279 | 19073224 | Adipose tissue mRNA levels of adiponectin, leptin, resistin, GIP-R, LPL and DGAT-1 were not significantly altered. |
| 4280 | 19073224 | These results illustrate efficacy of enzyme resistant GIP and GLP-1 analogues for treatment of glucose intolerance induced by high fat feeding. |
| 4281 | 19073224 | GLP-1 and GIP are the two key incretin hormones that regulate post-prandial glucose homeostasis. |
| 4282 | 19073224 | Furthermore, potent enzyme-resistant GIP and GLP-1 receptor agonists such as N-AcGIP and exendin-4 have now been developed. |
| 4283 | 19073224 | Adipose tissue mRNA levels of adiponectin, leptin, resistin, GIP-R, LPL and DGAT-1 were not significantly altered. |
| 4284 | 19073224 | These results illustrate efficacy of enzyme resistant GIP and GLP-1 analogues for treatment of glucose intolerance induced by high fat feeding. |
| 4285 | 19088791 | Coffee consumption may also mediate levels of gut peptides (glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1), hormones intimately involved in the regulation of satiety and insulin secretion. |
| 4286 | 19174495 | Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. |
| 4287 | 19179813 | Insulin, glucagon, amylin, the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and other hormones and enzymes interact to maintain glucose homeostasis and normal cellular metabolism. |
| 4288 | 19179813 | In addition to reducing HbA1c and fasting plasma glucose, the recently developed diabetes therapies GLP-1 receptor agonists (eg, exenatide, liraglutide) and dipeptidyl peptidase-4 (DPP-4) inhibitors (eg, sitagliptin, vildagliptin) appear to have beneficial effects on beta-cell dysfunction and, possibly, on alpha-cell dysregulation. |
| 4289 | 19217790 | DPP-4, a protease that specifically cleaves dipeptides from proteins and oligopeptides after a penultimate N-terminal proline or alanine, is involved in the degradation of a number of neuropeptides, peptide hormones and cytokines, including the incretins GLP-1 and GIP. |
| 4290 | 19217790 | As soon as released from the gut in response to food intake, GLP-1 and GIP exert a potent glucose-dependent insulinotropic action, thereby playing a key role in the maintenance of post-meal glycemic control. |
| 4291 | 19217790 | Consequently, inhibiting DPP-4 prolongs the action of GLP-1 and GIP, which in turn improves glucose homeostasis with a low risk of hypoglycemia and potential for disease modification. |
| 4292 | 19217790 | Achieving desired selectivity for DPP-4 over other related peptidases such as DPP-8 and DPP-9 (inhibition of which was linked to toxicity in animal studies) and long-acting potential for maximal efficacy (particularly in more severe diabetic patients) were the major challenges. |
| 4293 | 19217790 | DPP-4, a protease that specifically cleaves dipeptides from proteins and oligopeptides after a penultimate N-terminal proline or alanine, is involved in the degradation of a number of neuropeptides, peptide hormones and cytokines, including the incretins GLP-1 and GIP. |
| 4294 | 19217790 | As soon as released from the gut in response to food intake, GLP-1 and GIP exert a potent glucose-dependent insulinotropic action, thereby playing a key role in the maintenance of post-meal glycemic control. |
| 4295 | 19217790 | Consequently, inhibiting DPP-4 prolongs the action of GLP-1 and GIP, which in turn improves glucose homeostasis with a low risk of hypoglycemia and potential for disease modification. |
| 4296 | 19217790 | Achieving desired selectivity for DPP-4 over other related peptidases such as DPP-8 and DPP-9 (inhibition of which was linked to toxicity in animal studies) and long-acting potential for maximal efficacy (particularly in more severe diabetic patients) were the major challenges. |
| 4297 | 19217790 | DPP-4, a protease that specifically cleaves dipeptides from proteins and oligopeptides after a penultimate N-terminal proline or alanine, is involved in the degradation of a number of neuropeptides, peptide hormones and cytokines, including the incretins GLP-1 and GIP. |
| 4298 | 19217790 | As soon as released from the gut in response to food intake, GLP-1 and GIP exert a potent glucose-dependent insulinotropic action, thereby playing a key role in the maintenance of post-meal glycemic control. |
| 4299 | 19217790 | Consequently, inhibiting DPP-4 prolongs the action of GLP-1 and GIP, which in turn improves glucose homeostasis with a low risk of hypoglycemia and potential for disease modification. |
| 4300 | 19217790 | Achieving desired selectivity for DPP-4 over other related peptidases such as DPP-8 and DPP-9 (inhibition of which was linked to toxicity in animal studies) and long-acting potential for maximal efficacy (particularly in more severe diabetic patients) were the major challenges. |
| 4301 | 19221011 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. |
| 4302 | 19221011 | We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. |
| 4303 | 19221011 | GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. |
| 4304 | 19221011 | We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans. |
| 4305 | 19221011 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. |
| 4306 | 19221011 | We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. |
| 4307 | 19221011 | GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. |
| 4308 | 19221011 | We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans. |
| 4309 | 19221011 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. |
| 4310 | 19221011 | We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. |
| 4311 | 19221011 | GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. |
| 4312 | 19221011 | We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans. |
| 4313 | 19221011 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. |
| 4314 | 19221011 | We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. |
| 4315 | 19221011 | GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. |
| 4316 | 19221011 | We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans. |
| 4317 | 19229515 | Circadian rhythms of GIP and GLP1 in glucose-tolerant and in type 2 diabetic patients after biliopancreatic diversion. |
| 4318 | 19233842 | Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide. |
| 4319 | 19233842 | Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. |
| 4320 | 19233842 | The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). |
| 4321 | 19233842 | In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. |
| 4322 | 19233842 | Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. |
| 4323 | 19233842 | Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide. |
| 4324 | 19233842 | Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. |
| 4325 | 19233842 | The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). |
| 4326 | 19233842 | In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. |
| 4327 | 19233842 | Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. |
| 4328 | 19233842 | Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide. |
| 4329 | 19233842 | Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. |
| 4330 | 19233842 | The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). |
| 4331 | 19233842 | In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. |
| 4332 | 19233842 | Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. |
| 4333 | 19233842 | Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide. |
| 4334 | 19233842 | Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. |
| 4335 | 19233842 | The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). |
| 4336 | 19233842 | In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. |
| 4337 | 19233842 | Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. |
| 4338 | 19275548 | The two key hormones responsible are named glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 4339 | 19275548 | The other group comprises the gliptins (e.g. sitagliptin and vildagliptin) which boost endogenous incretin activity by inhibiting the enzyme dipeptidyl peptidase 4 (DPP 4) that degrades both GLP-1 and GIP. |
| 4340 | 19275548 | The two key hormones responsible are named glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 4341 | 19275548 | The other group comprises the gliptins (e.g. sitagliptin and vildagliptin) which boost endogenous incretin activity by inhibiting the enzyme dipeptidyl peptidase 4 (DPP 4) that degrades both GLP-1 and GIP. |
| 4342 | 19275672 | This review article focuses on the therapeutic potential of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in treating type 2 diabetes mellitus (T2DM). |
| 4343 | 19275672 | Therefore, the actions of GLP-1 and GIP, which include potentation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4344 | 19275672 | Two new drug classes based on the actions of the incretin hormones have recently been approved for therapy of T2DM; injectable long-acting stable analogues of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4345 | 19275672 | This review article focuses on the therapeutic potential of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in treating type 2 diabetes mellitus (T2DM). |
| 4346 | 19275672 | Therefore, the actions of GLP-1 and GIP, which include potentation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4347 | 19275672 | Two new drug classes based on the actions of the incretin hormones have recently been approved for therapy of T2DM; injectable long-acting stable analogues of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4348 | 19275672 | This review article focuses on the therapeutic potential of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in treating type 2 diabetes mellitus (T2DM). |
| 4349 | 19275672 | Therefore, the actions of GLP-1 and GIP, which include potentation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4350 | 19275672 | Two new drug classes based on the actions of the incretin hormones have recently been approved for therapy of T2DM; injectable long-acting stable analogues of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4351 | 19279000 | Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 modulate beta-cell chromatin structure. |
| 4352 | 19279000 | In the present study, we examined whether nuclear actions of the incretin hormones, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, involve modulation of beta-cell chromatin structure. |
| 4353 | 19279000 | Stimulation of INS-1(832/13) beta-cells or dispersed mouse islets with glucose-dependent insulinotropic polypeptide or glucagon-like peptide-1 resulted in the post-translational modification of core H3 histones, through acetylation and phosphorylation. |
| 4354 | 19279000 | Subsequent studies demonstrated that incretin-mediated histone H3 modifications involved activation of protein kinase A, p42/44 mitogen-activated protein kinase (MAPK), and p38 MAPK signaling modules, resulting in the activation of mitogen- and stress-activated kinase-1. |
| 4355 | 19279000 | Incretin-activated CREB-related Bcl-2 transcription was greatly reduced by a histone acetyltransferase inhibitor, demonstrating the functional importance of histone H3 modification. |
| 4356 | 19279000 | Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 modulate beta-cell chromatin structure. |
| 4357 | 19279000 | In the present study, we examined whether nuclear actions of the incretin hormones, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, involve modulation of beta-cell chromatin structure. |
| 4358 | 19279000 | Stimulation of INS-1(832/13) beta-cells or dispersed mouse islets with glucose-dependent insulinotropic polypeptide or glucagon-like peptide-1 resulted in the post-translational modification of core H3 histones, through acetylation and phosphorylation. |
| 4359 | 19279000 | Subsequent studies demonstrated that incretin-mediated histone H3 modifications involved activation of protein kinase A, p42/44 mitogen-activated protein kinase (MAPK), and p38 MAPK signaling modules, resulting in the activation of mitogen- and stress-activated kinase-1. |
| 4360 | 19279000 | Incretin-activated CREB-related Bcl-2 transcription was greatly reduced by a histone acetyltransferase inhibitor, demonstrating the functional importance of histone H3 modification. |
| 4361 | 19279000 | Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 modulate beta-cell chromatin structure. |
| 4362 | 19279000 | In the present study, we examined whether nuclear actions of the incretin hormones, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, involve modulation of beta-cell chromatin structure. |
| 4363 | 19279000 | Stimulation of INS-1(832/13) beta-cells or dispersed mouse islets with glucose-dependent insulinotropic polypeptide or glucagon-like peptide-1 resulted in the post-translational modification of core H3 histones, through acetylation and phosphorylation. |
| 4364 | 19279000 | Subsequent studies demonstrated that incretin-mediated histone H3 modifications involved activation of protein kinase A, p42/44 mitogen-activated protein kinase (MAPK), and p38 MAPK signaling modules, resulting in the activation of mitogen- and stress-activated kinase-1. |
| 4365 | 19279000 | Incretin-activated CREB-related Bcl-2 transcription was greatly reduced by a histone acetyltransferase inhibitor, demonstrating the functional importance of histone H3 modification. |
| 4366 | 19332493 | High-fat feeding increased fasting levels of plasma adiponectin, leptin and gastric inhibitory peptide (GIP). |
| 4367 | 19332493 | The increased insulin secretion may compensate for hepatic insulin resistance possibly mediated by elevated GIP secretion. |
| 4368 | 19332493 | Increased insulin secretion precedes the development of peripheral insulin resistance, mitochondrial dysfunction and obesity in response to overfeeding, suggesting a role for insulin per se as well GIP, in the development of peripheral insulin resistance and obesity. |
| 4369 | 19332493 | High-fat feeding increased fasting levels of plasma adiponectin, leptin and gastric inhibitory peptide (GIP). |
| 4370 | 19332493 | The increased insulin secretion may compensate for hepatic insulin resistance possibly mediated by elevated GIP secretion. |
| 4371 | 19332493 | Increased insulin secretion precedes the development of peripheral insulin resistance, mitochondrial dysfunction and obesity in response to overfeeding, suggesting a role for insulin per se as well GIP, in the development of peripheral insulin resistance and obesity. |
| 4372 | 19332493 | High-fat feeding increased fasting levels of plasma adiponectin, leptin and gastric inhibitory peptide (GIP). |
| 4373 | 19332493 | The increased insulin secretion may compensate for hepatic insulin resistance possibly mediated by elevated GIP secretion. |
| 4374 | 19332493 | Increased insulin secretion precedes the development of peripheral insulin resistance, mitochondrial dysfunction and obesity in response to overfeeding, suggesting a role for insulin per se as well GIP, in the development of peripheral insulin resistance and obesity. |
| 4375 | 19375579 | In normal subjects, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for 70% of the insulin response during a meal; but in diabetic subjects and other insulin-resistant conditions, the incretin effect is impaired. |
| 4376 | 19375579 | Plasma concentrations of GIP and GLP-1 were determined frequently during a 75-g glucose tolerance test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp. |
| 4377 | 19375579 | Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). |
| 4378 | 19375579 | The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS. |
| 4379 | 19375579 | In normal subjects, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for 70% of the insulin response during a meal; but in diabetic subjects and other insulin-resistant conditions, the incretin effect is impaired. |
| 4380 | 19375579 | Plasma concentrations of GIP and GLP-1 were determined frequently during a 75-g glucose tolerance test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp. |
| 4381 | 19375579 | Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). |
| 4382 | 19375579 | The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS. |
| 4383 | 19375579 | In normal subjects, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for 70% of the insulin response during a meal; but in diabetic subjects and other insulin-resistant conditions, the incretin effect is impaired. |
| 4384 | 19375579 | Plasma concentrations of GIP and GLP-1 were determined frequently during a 75-g glucose tolerance test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp. |
| 4385 | 19375579 | Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). |
| 4386 | 19375579 | The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS. |
| 4387 | 19375579 | In normal subjects, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for 70% of the insulin response during a meal; but in diabetic subjects and other insulin-resistant conditions, the incretin effect is impaired. |
| 4388 | 19375579 | Plasma concentrations of GIP and GLP-1 were determined frequently during a 75-g glucose tolerance test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp. |
| 4389 | 19375579 | Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). |
| 4390 | 19375579 | The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS. |
| 4391 | 19464426 | The key endogenous hormones of incretin system are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1); a key enzymatic regulator of these hormones is dipeptidyl peptidase-4, which rapidly inactivates/degrades the incretin hormones. |
| 4392 | 19533083 | Gastric inhibitory polypeptide (GIP) is a physiological gut peptide secreted from the intestinal K-cells with well documented insulin-releasing actions. |
| 4393 | 19533083 | However, the GIP receptor is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex and brain, suggesting that it may have other functions. |
| 4394 | 19533083 | The presence of functional GIP receptors on adipocytes and the key role played by GIP in lipid metabolism and fat deposition suggest a possible beneficial effect of compromised GIP action in obesity and insulin resistance. |
| 4395 | 19533083 | Thus, obese diabetic animals with compromised GIP action due to peptide-based GIP receptor antagonists, small molecular weight GIP receptor antagonists, vaccination against GIP, genetic knockout of GIP receptor or targeted K-cell destruction are protected against obesity and associated metabolic disturbances. |
| 4396 | 19533083 | In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. |
| 4397 | 19533083 | Gastric inhibitory polypeptide (GIP) is a physiological gut peptide secreted from the intestinal K-cells with well documented insulin-releasing actions. |
| 4398 | 19533083 | However, the GIP receptor is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex and brain, suggesting that it may have other functions. |
| 4399 | 19533083 | The presence of functional GIP receptors on adipocytes and the key role played by GIP in lipid metabolism and fat deposition suggest a possible beneficial effect of compromised GIP action in obesity and insulin resistance. |
| 4400 | 19533083 | Thus, obese diabetic animals with compromised GIP action due to peptide-based GIP receptor antagonists, small molecular weight GIP receptor antagonists, vaccination against GIP, genetic knockout of GIP receptor or targeted K-cell destruction are protected against obesity and associated metabolic disturbances. |
| 4401 | 19533083 | In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. |
| 4402 | 19533083 | Gastric inhibitory polypeptide (GIP) is a physiological gut peptide secreted from the intestinal K-cells with well documented insulin-releasing actions. |
| 4403 | 19533083 | However, the GIP receptor is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex and brain, suggesting that it may have other functions. |
| 4404 | 19533083 | The presence of functional GIP receptors on adipocytes and the key role played by GIP in lipid metabolism and fat deposition suggest a possible beneficial effect of compromised GIP action in obesity and insulin resistance. |
| 4405 | 19533083 | Thus, obese diabetic animals with compromised GIP action due to peptide-based GIP receptor antagonists, small molecular weight GIP receptor antagonists, vaccination against GIP, genetic knockout of GIP receptor or targeted K-cell destruction are protected against obesity and associated metabolic disturbances. |
| 4406 | 19533083 | In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. |
| 4407 | 19533083 | Gastric inhibitory polypeptide (GIP) is a physiological gut peptide secreted from the intestinal K-cells with well documented insulin-releasing actions. |
| 4408 | 19533083 | However, the GIP receptor is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex and brain, suggesting that it may have other functions. |
| 4409 | 19533083 | The presence of functional GIP receptors on adipocytes and the key role played by GIP in lipid metabolism and fat deposition suggest a possible beneficial effect of compromised GIP action in obesity and insulin resistance. |
| 4410 | 19533083 | Thus, obese diabetic animals with compromised GIP action due to peptide-based GIP receptor antagonists, small molecular weight GIP receptor antagonists, vaccination against GIP, genetic knockout of GIP receptor or targeted K-cell destruction are protected against obesity and associated metabolic disturbances. |
| 4411 | 19533083 | In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. |
| 4412 | 19533083 | Gastric inhibitory polypeptide (GIP) is a physiological gut peptide secreted from the intestinal K-cells with well documented insulin-releasing actions. |
| 4413 | 19533083 | However, the GIP receptor is widely distributed in peripheral organs, including the pancreas, gut, adipose tissue, heart, adrenal cortex and brain, suggesting that it may have other functions. |
| 4414 | 19533083 | The presence of functional GIP receptors on adipocytes and the key role played by GIP in lipid metabolism and fat deposition suggest a possible beneficial effect of compromised GIP action in obesity and insulin resistance. |
| 4415 | 19533083 | Thus, obese diabetic animals with compromised GIP action due to peptide-based GIP receptor antagonists, small molecular weight GIP receptor antagonists, vaccination against GIP, genetic knockout of GIP receptor or targeted K-cell destruction are protected against obesity and associated metabolic disturbances. |
| 4416 | 19533083 | In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. |
| 4417 | 19580949 | The key endogenous hormones of incretin system are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1); a key enzymatic regulator of these hormones is dipeptidyl peptidase-4, which rapidly inactivates/degrades the incretin hormones. |
| 4418 | 19590846 | The pathophysiology of i-IFG seems to include the following key defects: reduced hepatic insulin sensitivity, stationary beta cell dysfunction and/or chronic low beta cell mass, altered glucagon-like peptide-1 secretion and inappropriately elevated glucagon secretion. |
| 4419 | 19590846 | Conversely, the prediabetic state i-IGT is characterised by reduced peripheral insulin sensitivity, near-normal hepatic insulin sensitivity, progressive loss of beta cell function, reduced secretion of glucose-dependent insulinotropic polypeptide and inappropriately elevated glucagon secretion. |
| 4420 | 19595611 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are produced predominantly by enteroendocrine cells and have multiple blood glucose-lowering effects. |
| 4421 | 19595611 | Here, we review these recent advances and outline the multiple strategies being pursued to exploit the potential therapeutic benefits of GIP and GLP-1. |
| 4422 | 19595611 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are produced predominantly by enteroendocrine cells and have multiple blood glucose-lowering effects. |
| 4423 | 19595611 | Here, we review these recent advances and outline the multiple strategies being pursued to exploit the potential therapeutic benefits of GIP and GLP-1. |
| 4424 | 19672815 | Glucagon-like peptide-1 receptor (GLP-1R), glucose-dependent insulinotropic polypeptide receptor (GIPR), and G protein-coupled receptor 40 (GPR40) are members of G protein-coupled receptors (GPCR) family. |
| 4425 | 19672815 | The expressions of GLP-1R, GIPR, GPR40, and a nuclear transcription factor - peroxisome-proliferator activated receptor alpha (PPARalpha) - were analyzed by real-time RT-PCR and immunoblotting. |
| 4426 | 19672815 | We demonstrated that the expressions of GLP-1R, GIPR, and PPARalpha were downregulated when INS-1beta cells were treated with glucose, while their expressions were upregulated when treated with metformin or AICAR. |
| 4427 | 19672815 | These results indicate that glucose, metformin, and AICAR regulated the expressions of incretin receptors and PPARalpha, but not GPR40 in beta cells. |
| 4428 | 19689275 | Since implicated in the regulation of the biological activity of hormones and chemokines, such as glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, DPP4 inhibition offers a new potential therapeutic approach for type 2 diabetes mellitus, as monotherapy and adjunct therapy to other oral agents. |
| 4429 | 19689275 | The clinical use of presently available orally active inhibitors of DPP4, however, has been associated with side effects that have been in part attributed to the inhibition of related serine proteases, such as DPP8 and DPP9. |
| 4430 | 19721203 | Gastrointestinal hormones including gastric inhibitory polypeptide (GIP) and glucagon-like peptide (GLP) -1 are incretin, which are secreted immediately after meal ingestion and stimulate insulin secretion from pancreatic beta-cells. |
| 4431 | 19721203 | Characterization of extra-pancreatic GIP and GLP-1 receptors has revealed that these hormones regulate bone turnover. |
| 4432 | 19721203 | GIP intermittently stimulates osteoblasts and GLP-1 suppresses osteoclasts through a calcitonin-dependent pathway to increase the bone volume. |
| 4433 | 19721203 | Gastrointestinal hormones including gastric inhibitory polypeptide (GIP) and glucagon-like peptide (GLP) -1 are incretin, which are secreted immediately after meal ingestion and stimulate insulin secretion from pancreatic beta-cells. |
| 4434 | 19721203 | Characterization of extra-pancreatic GIP and GLP-1 receptors has revealed that these hormones regulate bone turnover. |
| 4435 | 19721203 | GIP intermittently stimulates osteoblasts and GLP-1 suppresses osteoclasts through a calcitonin-dependent pathway to increase the bone volume. |
| 4436 | 19721203 | Gastrointestinal hormones including gastric inhibitory polypeptide (GIP) and glucagon-like peptide (GLP) -1 are incretin, which are secreted immediately after meal ingestion and stimulate insulin secretion from pancreatic beta-cells. |
| 4437 | 19721203 | Characterization of extra-pancreatic GIP and GLP-1 receptors has revealed that these hormones regulate bone turnover. |
| 4438 | 19721203 | GIP intermittently stimulates osteoblasts and GLP-1 suppresses osteoclasts through a calcitonin-dependent pathway to increase the bone volume. |
| 4439 | 19748061 | In patients with type 2 diabetes, the incretin effect is markedly reduced, and this has been attributed to defects in the secretion and insulinotropic action of the two main incretin hormones, namely gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4440 | 19748061 | However, the secretion and action of GIP and GLP-1 is relatively unaltered in normal glucose-tolerant individuals at high risk for type 2 diabetes (e.g., first-degree relatives) and a diminished incretin effect is also detectable in other types of diabetes, thereby arguing against such reasoning. |
| 4441 | 19748061 | This article will describe the defects in the incretin system in patients with type 2 diabetes, summarise their relevance in the development of hyperglycaemia and discuss the potential individual roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. |
| 4442 | 19748061 | In patients with type 2 diabetes, the incretin effect is markedly reduced, and this has been attributed to defects in the secretion and insulinotropic action of the two main incretin hormones, namely gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4443 | 19748061 | However, the secretion and action of GIP and GLP-1 is relatively unaltered in normal glucose-tolerant individuals at high risk for type 2 diabetes (e.g., first-degree relatives) and a diminished incretin effect is also detectable in other types of diabetes, thereby arguing against such reasoning. |
| 4444 | 19748061 | This article will describe the defects in the incretin system in patients with type 2 diabetes, summarise their relevance in the development of hyperglycaemia and discuss the potential individual roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. |
| 4445 | 19748061 | In patients with type 2 diabetes, the incretin effect is markedly reduced, and this has been attributed to defects in the secretion and insulinotropic action of the two main incretin hormones, namely gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). |
| 4446 | 19748061 | However, the secretion and action of GIP and GLP-1 is relatively unaltered in normal glucose-tolerant individuals at high risk for type 2 diabetes (e.g., first-degree relatives) and a diminished incretin effect is also detectable in other types of diabetes, thereby arguing against such reasoning. |
| 4447 | 19748061 | This article will describe the defects in the incretin system in patients with type 2 diabetes, summarise their relevance in the development of hyperglycaemia and discuss the potential individual roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. |
| 4448 | 19748062 | Mechanisms underlying the rapid degradation and elimination of the incretin hormones GLP-1 and GIP. |
| 4449 | 19748062 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, gastric inhibitory peptide) are secreted from intestinal L and K cells and stimulate insulin secretion from pancreatic beta cells. |
| 4450 | 19748062 | However, they are immediately inactivated mainly via N-terminal degradation by dipeptidyl peptidase IV (DPP IV, CD26), a specialised enzyme located on the cell surface enzyme of endothelial, epithelial and some other cell types. |
| 4451 | 19748062 | Mechanisms underlying the rapid degradation and elimination of the incretin hormones GLP-1 and GIP. |
| 4452 | 19748062 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, gastric inhibitory peptide) are secreted from intestinal L and K cells and stimulate insulin secretion from pancreatic beta cells. |
| 4453 | 19748062 | However, they are immediately inactivated mainly via N-terminal degradation by dipeptidyl peptidase IV (DPP IV, CD26), a specialised enzyme located on the cell surface enzyme of endothelial, epithelial and some other cell types. |
| 4454 | 19748067 | Therapeutic potential for GIP receptor agonists and antagonists. |
| 4455 | 19748067 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4456 | 19748067 | Thus, GIP receptor agonists offer one of the newest classes of potential antidiabetic drug. |
| 4457 | 19748067 | Strong parallels exist with the beneficial metabolic effects of Roux-en-Y gastric bypass in obese, insulin-resistant humans that surgically ablates GIP-secreting K cells. |
| 4458 | 19748067 | Therapeutic potential for GIP receptor agonists and antagonists. |
| 4459 | 19748067 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4460 | 19748067 | Thus, GIP receptor agonists offer one of the newest classes of potential antidiabetic drug. |
| 4461 | 19748067 | Strong parallels exist with the beneficial metabolic effects of Roux-en-Y gastric bypass in obese, insulin-resistant humans that surgically ablates GIP-secreting K cells. |
| 4462 | 19748067 | Therapeutic potential for GIP receptor agonists and antagonists. |
| 4463 | 19748067 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4464 | 19748067 | Thus, GIP receptor agonists offer one of the newest classes of potential antidiabetic drug. |
| 4465 | 19748067 | Strong parallels exist with the beneficial metabolic effects of Roux-en-Y gastric bypass in obese, insulin-resistant humans that surgically ablates GIP-secreting K cells. |
| 4466 | 19748067 | Therapeutic potential for GIP receptor agonists and antagonists. |
| 4467 | 19748067 | Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. |
| 4468 | 19748067 | Thus, GIP receptor agonists offer one of the newest classes of potential antidiabetic drug. |
| 4469 | 19748067 | Strong parallels exist with the beneficial metabolic effects of Roux-en-Y gastric bypass in obese, insulin-resistant humans that surgically ablates GIP-secreting K cells. |
| 4470 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4471 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4472 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4473 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4474 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4475 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4476 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4477 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4478 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4479 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4480 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4481 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4482 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4483 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4484 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4485 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4486 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4487 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4488 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4489 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4490 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4491 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4492 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4493 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4494 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4495 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4496 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4497 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4498 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4499 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4500 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4501 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4502 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4503 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4504 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4505 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4506 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4507 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4508 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4509 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4510 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4511 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4512 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4513 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4514 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4515 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4516 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4517 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4518 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4519 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4520 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4521 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4522 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4523 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4524 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4525 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4526 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4527 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4528 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4529 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4530 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4531 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4532 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4533 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 4534 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 4535 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 4536 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 4537 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 4538 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 4539 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 4540 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 4541 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 4542 | 19766644 | Differential importance of glucose-dependent insulinotropic polypeptide vs glucagon-like peptide 1 receptor signaling for beta cell survival in mice. |
| 4543 | 19791828 | Saxagliptin and its active metabolite M2 are dipeptidyl peptidase-4 inhibitors that improve glycaemic control by preventing the inactivation of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide. |
| 4544 | 19791828 | This increases GLP-1 levels, stimulates insulin secretion and reduces postprandial glucagon and glucose levels. |
| 4545 | 19808907 | Injection of glucose at 1 g/kg in the upper intestine significantly increased plasma GIP and GLP-1 levels, whereas injection of glucose in the colon did not increase GIP or GLP-1 levels. |
| 4546 | 19808907 | Coadministration of a sodium-glucose cotransporter-1 (SGLT1) inhibitor, phloridzin, with glucose in the upper intestine blocked glucose absorption and glucose-induced incretin secretion. alpha-methyl-d-glucopyranoside (MDG), an SGLT1 substrate that is a nonmetabolizable sugar, significantly increased plasma GIP and GLP-1 levels, whereas phloridzin blocked these increases, indicating that concomitant transport of sodium ions and glucose (substrate) via SGLT1 itself triggers incretin secretion without the need for subsequent glucose metabolism. |
| 4547 | 19808907 | Interestingly, oral administration of MDG significantly increased plasma GIP, GLP-1, and insulin levels and reduced blood glucose levels during an intraperitoneal glucose tolerance test. |
| 4548 | 19808907 | Injection of glucose at 1 g/kg in the upper intestine significantly increased plasma GIP and GLP-1 levels, whereas injection of glucose in the colon did not increase GIP or GLP-1 levels. |
| 4549 | 19808907 | Coadministration of a sodium-glucose cotransporter-1 (SGLT1) inhibitor, phloridzin, with glucose in the upper intestine blocked glucose absorption and glucose-induced incretin secretion. alpha-methyl-d-glucopyranoside (MDG), an SGLT1 substrate that is a nonmetabolizable sugar, significantly increased plasma GIP and GLP-1 levels, whereas phloridzin blocked these increases, indicating that concomitant transport of sodium ions and glucose (substrate) via SGLT1 itself triggers incretin secretion without the need for subsequent glucose metabolism. |
| 4550 | 19808907 | Interestingly, oral administration of MDG significantly increased plasma GIP, GLP-1, and insulin levels and reduced blood glucose levels during an intraperitoneal glucose tolerance test. |
| 4551 | 19808907 | Injection of glucose at 1 g/kg in the upper intestine significantly increased plasma GIP and GLP-1 levels, whereas injection of glucose in the colon did not increase GIP or GLP-1 levels. |
| 4552 | 19808907 | Coadministration of a sodium-glucose cotransporter-1 (SGLT1) inhibitor, phloridzin, with glucose in the upper intestine blocked glucose absorption and glucose-induced incretin secretion. alpha-methyl-d-glucopyranoside (MDG), an SGLT1 substrate that is a nonmetabolizable sugar, significantly increased plasma GIP and GLP-1 levels, whereas phloridzin blocked these increases, indicating that concomitant transport of sodium ions and glucose (substrate) via SGLT1 itself triggers incretin secretion without the need for subsequent glucose metabolism. |
| 4553 | 19808907 | Interestingly, oral administration of MDG significantly increased plasma GIP, GLP-1, and insulin levels and reduced blood glucose levels during an intraperitoneal glucose tolerance test. |
| 4554 | 19846181 | The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate postprandial insulin release from the beta-cells. |
| 4555 | 19846181 | Non-model-based and model-based estimates of beta-cell function and incremental areas under the curve of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP were calculated. |
| 4556 | 19846181 | Fat preferentially stimulates GIP secretion, whereas CH stimulates GLP-1 secretion. |
| 4557 | 19846181 | The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate postprandial insulin release from the beta-cells. |
| 4558 | 19846181 | Non-model-based and model-based estimates of beta-cell function and incremental areas under the curve of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP were calculated. |
| 4559 | 19846181 | Fat preferentially stimulates GIP secretion, whereas CH stimulates GLP-1 secretion. |
| 4560 | 19846181 | The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate postprandial insulin release from the beta-cells. |
| 4561 | 19846181 | Non-model-based and model-based estimates of beta-cell function and incremental areas under the curve of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP were calculated. |
| 4562 | 19846181 | Fat preferentially stimulates GIP secretion, whereas CH stimulates GLP-1 secretion. |
| 4563 | 19881250 | Intact GLP-1, GIP, and dipeptidyl peptidase (DPP)-IV were measured by ELISA. |
| 4564 | 19881250 | There were no significant differences in GLP-1 or GIP levels at each sampling time among NGT, IGT, and T2DM after the ingestions; hence the incremental areas under the curve (IAUC) for the three groups were quite similar. |
| 4565 | 19881250 | We concluded that intact GLP-1 levels are comparable between non-diabetics and T2DM, suggesting that impaired insulin secretion in Japanese T2DM is not attributable to defect in GLP-1 secretion. |
| 4566 | 19881250 | Intact GLP-1, GIP, and dipeptidyl peptidase (DPP)-IV were measured by ELISA. |
| 4567 | 19881250 | There were no significant differences in GLP-1 or GIP levels at each sampling time among NGT, IGT, and T2DM after the ingestions; hence the incremental areas under the curve (IAUC) for the three groups were quite similar. |
| 4568 | 19881250 | We concluded that intact GLP-1 levels are comparable between non-diabetics and T2DM, suggesting that impaired insulin secretion in Japanese T2DM is not attributable to defect in GLP-1 secretion. |
| 4569 | 19881341 | Glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide: new advances. |
| 4570 | 19947814 | The incretin effect, mediated by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), plays an important role in the regulation of insulin secretion in response to oral glucose. |
| 4571 | 19947814 | Increased awareness of the differences among incretin mimetics, GLP-1 analogs, and DPP-4 inhibitors, including their structures, half-lives, dosages, hemoglobin A(1c)-lowering capacities, effects on weight, and adverse events will help shape the future of these therapeutic agents. |
| 4572 | 19952298 | Nutrient intake stimulates the secretion of the gastrointestinal incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which exert glucose-dependent insulinotropic effects and assist pancreatic insulin and glucagon in maintaining glucose homeostasis. |
| 4573 | 19952298 | An impaired incretin system, characterized by decreased responsiveness to GIP and markedly reduced GLP-1 concentration, occurs in individuals with type 2 diabetes mellitus (T2DM). |
| 4574 | 19952298 | The administration of GLP-1 improves glycemic control, but GLP-1 is rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). |
| 4575 | 19952298 | Exenatide, a DPP-4-resistant exendin-4 GLP-1 receptor agonist, exhibits the glucoregulatory actions of GLP-1 and reduces body weight in patients with T2DM. |
| 4576 | 19952298 | DPP-4 inhibitors such as sitagliptin and saxagliptin increase endogenous GLP-1 concentration and demonstrate incretin-associated glucoregulatory actions in patients with T2DM. |
| 4577 | 19952298 | Nutrient intake stimulates the secretion of the gastrointestinal incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which exert glucose-dependent insulinotropic effects and assist pancreatic insulin and glucagon in maintaining glucose homeostasis. |
| 4578 | 19952298 | An impaired incretin system, characterized by decreased responsiveness to GIP and markedly reduced GLP-1 concentration, occurs in individuals with type 2 diabetes mellitus (T2DM). |
| 4579 | 19952298 | The administration of GLP-1 improves glycemic control, but GLP-1 is rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). |
| 4580 | 19952298 | Exenatide, a DPP-4-resistant exendin-4 GLP-1 receptor agonist, exhibits the glucoregulatory actions of GLP-1 and reduces body weight in patients with T2DM. |
| 4581 | 19952298 | DPP-4 inhibitors such as sitagliptin and saxagliptin increase endogenous GLP-1 concentration and demonstrate incretin-associated glucoregulatory actions in patients with T2DM. |
| 4582 | 20115929 | The incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are secreted in the gut upon meal ingestion and lower blood glucose by glucose-dependent stimulation of insulin secretion and production. |
| 4583 | 20115929 | Thus, injectable DPP-4-resistant GLP-1 receptor agonists (GLP-1RA) and oral DPP-4 inhibitors have been developed. |
| 4584 | 20122751 | A case of insulinoma following total gastrectomy--effects of an alpha-glucosidase inhibitor on suppressing GIP and GLP-1 elevations. |
| 4585 | 20122751 | GIP and GLP-1 levels after a mixed meal were extremely increased. |
| 4586 | 20122751 | Administration of miglitol, an alpha-glucosidase inhibitor, suppressed the GIP and GLP-1 elevations. |
| 4587 | 20122751 | A case of insulinoma following total gastrectomy--effects of an alpha-glucosidase inhibitor on suppressing GIP and GLP-1 elevations. |
| 4588 | 20122751 | GIP and GLP-1 levels after a mixed meal were extremely increased. |
| 4589 | 20122751 | Administration of miglitol, an alpha-glucosidase inhibitor, suppressed the GIP and GLP-1 elevations. |
| 4590 | 20122751 | A case of insulinoma following total gastrectomy--effects of an alpha-glucosidase inhibitor on suppressing GIP and GLP-1 elevations. |
| 4591 | 20122751 | GIP and GLP-1 levels after a mixed meal were extremely increased. |
| 4592 | 20122751 | Administration of miglitol, an alpha-glucosidase inhibitor, suppressed the GIP and GLP-1 elevations. |
| 4593 | 20152741 | Indeed, increased levels of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) may lead to improved beta-cell function and insulin secretion as well as reduced insulin resistance associated with weight loss. |
| 4594 | 20204054 | The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted postprandially from intestinal K- and L-cells, respectively. |
| 4595 | 20204054 | Whilst the enteroendocrine cells producing GIP and GLP-1 are therefore attractive targets for the treatment of diabetes and obesity, our understanding of their physiology is fairly limited. |
| 4596 | 20204054 | The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted postprandially from intestinal K- and L-cells, respectively. |
| 4597 | 20204054 | Whilst the enteroendocrine cells producing GIP and GLP-1 are therefore attractive targets for the treatment of diabetes and obesity, our understanding of their physiology is fairly limited. |
| 4598 | 20206729 | Glucagonlike peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, secreted from the L-cells of the lower gut and K-cells of the intestines, respectively, are responsible for these incretin effects, which are reduced in patients with type 2 diabetes mellitus. |
| 4599 | 20206729 | Sitagliptin inhibits the DPP-4 enzyme, thus increasing the half-life of endogenous GLP-1. |
| 4600 | 20206729 | This review examines data from recent GLP-1 receptor agonist and DPP-4 inhibitor studies in patients with type 2 diabetes, as well as data on other incretin-based therapies in clinical development. |
| 4601 | 20217513 | The long-term improvement was demonstrated with short-term intensive insulin therapy of newly diagnosed DM2, the use of antiapoptotic drugs such as glitazones, and the use of glucagon-like peptide-1 receptor agonists (GLP-1 mimetics), not inactivated by the enzyme dipeptidyl peptidase 4 and/or to inhibit that enzyme (GLP-1 enhancers). |
| 4602 | 20217513 | From the two major incretins, GLP-1 and GIP (glucose-dependent insulinotropic polypeptide), only the first one or its mimetics or enhancers can be used for treatment. |
| 4603 | 20332343 | Physiologic and pharmacologic modulation of glucose-dependent insulinotropic polypeptide (GIP) receptor expression in beta-cells by peroxisome proliferator-activated receptor (PPAR)-gamma signaling: possible mechanism for the GIP resistance in type 2 diabetes. |
| 4604 | 20337586 | The receptors for GIP and GLP-1 are expressed in neurons, and both GIP and GLP-1 are expressed and released as transmitters by neurons. |
| 4605 | 20337586 | GIP analogues such as DAla(2)GIP and GLP-1 analogues such as liraglutide enhance synaptic plasticity in the brain and also reverse the betaamyloid induced impairment of synaptic plasticity. |
| 4606 | 20337586 | The receptors for GIP and GLP-1 are expressed in neurons, and both GIP and GLP-1 are expressed and released as transmitters by neurons. |
| 4607 | 20337586 | GIP analogues such as DAla(2)GIP and GLP-1 analogues such as liraglutide enhance synaptic plasticity in the brain and also reverse the betaamyloid induced impairment of synaptic plasticity. |
| 4608 | 20389106 | Effects of fat supplementation on postprandial GIP, GLP-1, ghrelin and IGFBP-1 levels: a pilot study on adolescents with type 1 diabetes. |
| 4609 | 20425582 | The gastrointestinal hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), termed incretins, are essential regulators of normal glucose homeostasis. |
| 4610 | 20425582 | This review describes the defects in the incretin system seen in diabetic patients and discusses the potential roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. |
| 4611 | 20425582 | The gastrointestinal hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), termed incretins, are essential regulators of normal glucose homeostasis. |
| 4612 | 20425582 | This review describes the defects in the incretin system seen in diabetic patients and discusses the potential roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. |
| 4613 | 20483270 | These genes can also potentially be proteolytically processed in identical patterns as observed in the mammalian sequences that would yield a GIP hormone that is only one amino shorter than the mammalian sequences due to the removal of an extra basic residue by carboxypeptidase E. |
| 4614 | 20484128 | Sex steroids affect triglyceride handling, glucose-dependent insulinotropic polypeptide, and insulin sensitivity: a 1-week randomized clinical trial in healthy young men. |
| 4615 | 20501678 | Impact of exogenous hyperglucagonemia on postprandial concentrations of gastric inhibitory polypeptide and glucagon-like peptide-1 in humans. |
| 4616 | 20519806 | alpha-glucosidase inhibitors (alphaGIs) increase active glucagon-like peptide-1 (GLP-1) and reduce the total glucosedependent insulinotropic polypeptide (GIP) levels, but their ability to prevent diabetes remains uncertain. |
| 4617 | 20519806 | Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin, increase active GLP-1 and GIP levels and improve hyperglycemia in a glucose-dependent fashion. |
| 4618 | 20519806 | alpha-glucosidase inhibitors (alphaGIs) increase active glucagon-like peptide-1 (GLP-1) and reduce the total glucosedependent insulinotropic polypeptide (GIP) levels, but their ability to prevent diabetes remains uncertain. |
| 4619 | 20519806 | Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin, increase active GLP-1 and GIP levels and improve hyperglycemia in a glucose-dependent fashion. |
| 4620 | 20532013 | The Incretins and Pancreatic beta-Cells: Use of Glucagon-Like Peptide-1 and Glucose-Dependent Insulinotropic Polypeptide to Cure Type 2 Diabetes Mellitus. |
| 4621 | 20532013 | Incretin hormones, such as glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), have been shown to lower the postprandial and fasting glucose and the glycated hemoglobin levels, suppress the elevated glucagon level, and stimulate glucose-dependent insulin synthesis and secretion. |
| 4622 | 20532013 | In this report, we will review the biological actions and mechanisms associated with the actions of incretin hormones, GLP-1 and GIP, on beta-cell health and compare the differences between GLP-1 and GIP. |
| 4623 | 20532013 | The Incretins and Pancreatic beta-Cells: Use of Glucagon-Like Peptide-1 and Glucose-Dependent Insulinotropic Polypeptide to Cure Type 2 Diabetes Mellitus. |
| 4624 | 20532013 | Incretin hormones, such as glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), have been shown to lower the postprandial and fasting glucose and the glycated hemoglobin levels, suppress the elevated glucagon level, and stimulate glucose-dependent insulin synthesis and secretion. |
| 4625 | 20532013 | In this report, we will review the biological actions and mechanisms associated with the actions of incretin hormones, GLP-1 and GIP, on beta-cell health and compare the differences between GLP-1 and GIP. |
| 4626 | 20532013 | The Incretins and Pancreatic beta-Cells: Use of Glucagon-Like Peptide-1 and Glucose-Dependent Insulinotropic Polypeptide to Cure Type 2 Diabetes Mellitus. |
| 4627 | 20532013 | Incretin hormones, such as glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), have been shown to lower the postprandial and fasting glucose and the glycated hemoglobin levels, suppress the elevated glucagon level, and stimulate glucose-dependent insulin synthesis and secretion. |
| 4628 | 20532013 | In this report, we will review the biological actions and mechanisms associated with the actions of incretin hormones, GLP-1 and GIP, on beta-cell health and compare the differences between GLP-1 and GIP. |
| 4629 | 20575217 | Two drug classes-namely, the injectable glucagon-like peptide 1 (GLP-1) receptor agonists, which produce pharmacological GLP receptor activity, and the oral dipeptidyl peptidase-4 (DPP-4) inhibitors, which raise levels of endogenously produced GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) by preventing enzymatic degradation--have been available for several years. |
| 4630 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4631 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4632 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4633 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4634 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4635 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4636 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4637 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4638 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4639 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4640 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4641 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4642 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4643 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4644 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4645 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4646 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4647 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4648 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4649 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4650 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4651 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4652 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4653 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4654 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4655 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4656 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4657 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4658 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4659 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4660 | 20580750 | Glucagon-like peptide-2, but not glucose-dependent insulinotropic polypeptide, stimulates glucagon release in patients with type 1 diabetes. |
| 4661 | 20580750 | This study investigated the glucagon-releasing properties of the hormones glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP) in 8 patients with type 1 diabetes mellitus (T1DM) without paracrine intraislet influence of insulin (C-peptide negative following a 5 g intravenous arginine stimulation; on study days only treated with basal insulin substitution). |
| 4662 | 20580750 | In randomised order either GIP, GLP-2, or saline were infused intravenously during first 50 min in both periods at rates designed to mimic postprandial hormone responses. |
| 4663 | 20580750 | The resulting incremental area under curve values of glucagon were in period 1 -38+/-44 (GIP), 120+/-48 (GLP-2), and -16+/-61 (saline) pMx90 min (p=0.087), respectively; and in period 2 -157+/-76, 135+/-52, and -77+/-77pMx90 min (p=0.019), respectively. |
| 4664 | 20580750 | Post hoc analysis showed significant differences only between the GLP-2 days versus the GIP and saline days. |
| 4665 | 20580750 | In conclusion, GLP-2, but not GIP, was found to stimulate the release of glucagon in patients with T1DM, suggesting a role for GLP-2 in the postprandial hyperglucagonaemia characterising individuals with T1DM. |
| 4666 | 20631047 | Recently, glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) have received much attention regarding possible roles in aetiology and treatment of type 2 diabetes. |
| 4667 | 20631047 | Xenin also exerted an additive effect on GIP, GLP1 and neurotensin-mediated insulin secretion. |
| 4668 | 20631047 | Recently, glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) have received much attention regarding possible roles in aetiology and treatment of type 2 diabetes. |
| 4669 | 20631047 | Xenin also exerted an additive effect on GIP, GLP1 and neurotensin-mediated insulin secretion. |
| 4670 | 20634437 | Changes in food intake, body weight and composition, glucose tolerance, insulin sensitivity and tissue glucose uptake, and insulin signaling as well as plasma concentrations of glucagon-like peptide-1 and glucose-dependent insulinotropic peptide were measured. |
| 4671 | 20634437 | Euglycemic, hyperinsulinemic clamp and 1-[(14)C]-2-deoxyglucose tracer studies indicate that IT improves whole body glucose disposal, insulin-stimulated glucose uptake, and the ratio of phospho- to total Akt (P < 0.01 vs. control) in striated muscle. |
| 4672 | 20634437 | After oral glucose, the plasma concentration of glucagon-like peptide-1 was increased, whereas GIP was decreased following IT. |
| 4673 | 20655673 | The incretin effect results from release of the incretin hormones Glucagon like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIP) from intestinal cells in response to glucose ingestion. |
| 4674 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4675 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4676 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4677 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4678 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4679 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4680 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4681 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4682 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4683 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4684 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4685 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4686 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4687 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4688 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4689 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4690 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4691 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4692 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4693 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4694 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4695 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4696 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4697 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4698 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4699 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4700 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4701 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4702 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4703 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4704 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4705 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4706 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4707 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4708 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4709 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4710 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4711 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4712 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4713 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4714 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4715 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4716 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4717 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4718 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4719 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4720 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4721 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4722 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4723 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4724 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4725 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4726 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4727 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4728 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4729 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4730 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4731 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4732 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4733 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4734 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4735 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4736 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4737 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4738 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4739 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4740 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4741 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4742 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4743 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4744 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4745 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4746 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4747 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4748 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4749 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4750 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4751 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4752 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4753 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4754 | 20693566 | GIP increases human adipocyte LPL expression through CREB and TORC2-mediated trans-activation of the LPL gene. |
| 4755 | 20693566 | Additionally, emerging evidence suggests an important physiological role for GIP in the regulation of adipocyte metabolism. |
| 4756 | 20693566 | In previous studies on the lipogenic effects of GIP, it was shown to increase adipocyte lipoprotein lipase (LPL) activity in both differentiated 3T3-L1 cells and human adipocytes through a pathway involving activation of protein kinase B (PKB)/Akt. |
| 4757 | 20693566 | In the current study, we examined the effects of GIP on LPL gene expression. |
| 4758 | 20693566 | GIP in the presence of insulin increased LPL gene expression in human adipocytes and LPL promoter activity in GIP receptor-expressing HEK-293 cells, and both effects were greatly reduced by the transcription inhibitor actinomycin D. |
| 4759 | 20693566 | Subsequent studies established that GIP increased phosphorylation of Serine 133 in cAMP-response element binding protein (CREB) and the nuclear localization of cAMP-responsive CREB coactivator 2 (TORC2) through a pathway involving phosphatidylinositol 3-kinase (PI3-K), PKB, and AMP-activated protein kinase (AMPK). |
| 4760 | 20693566 | However, in the presence of insulin, GIP failed to activate the cAMP/PKA pathway. |
| 4761 | 20693566 | Knockdown of CREB and TORC2 using RNA interference reduced LPL expression, supporting a functional regulatory role. |
| 4762 | 20693566 | GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. |
| 4763 | 20693566 | The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation. |
| 4764 | 20708812 | Since the launch of sitagliptin in 2006, a compelling body of evidence has accumulated showing that dipeptidyl peptidase-4 (DPP-4) inhibitors, which augment endogenous GLP-1 and GIP levels, represent an important advance in the management of T2DM. |
| 4765 | 20714888 | In humans, the incretin effect is mediated by the secretion and insulinotropic action of two peptide hormones, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. |
| 4766 | 20736387 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are now known to play major roles in endogenous glucose control, including regulation of insulin, glucagon, and hepatic glucose metabolism. |
| 4767 | 20736387 | Investigation of the incretin system has led to development of drugs that mimic or enhance the endogenous hormones, including GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors. |
| 4768 | 20737753 | Currently, there are 2 types of incretin hormones which have been identified, i.e.Glucose dependent insulinotropic polypeptide (GIP) and Glucagon like peptide-1 (GLP-1). |
| 4769 | 20737753 | Several in vitro studies have demonstrated that these two incretin hormones may increase the proliferation of pancreatic beta cell.There is a decrease of GIP function and GLP-1 amount in type-2 diabetes mellitus; thus the attempt to increase both incretin hormones - in this case by using GLP-1 agonist and DPP-IV inhibitor - is one of treatment modalities to control the glucose blood level, either as a monotherapy or a combination therapy. |
| 4770 | 20737753 | Currently, there are 2 types of incretin hormones which have been identified, i.e.Glucose dependent insulinotropic polypeptide (GIP) and Glucagon like peptide-1 (GLP-1). |
| 4771 | 20737753 | Several in vitro studies have demonstrated that these two incretin hormones may increase the proliferation of pancreatic beta cell.There is a decrease of GIP function and GLP-1 amount in type-2 diabetes mellitus; thus the attempt to increase both incretin hormones - in this case by using GLP-1 agonist and DPP-IV inhibitor - is one of treatment modalities to control the glucose blood level, either as a monotherapy or a combination therapy. |
| 4772 | 20871975 | The incretin hormones gastric inhibitory polypeptide and especially glucagon-like peptide (GLP) have an important physiological function in augmenting postprandial insulin secretion. |
| 4773 | 20871975 | Such a deficiency is the rationale for replacing endogenous incretins with GLP-1 receptor agonists or re-normalising active GLP-1 concentrations with dipeptidyl peptidase-4 inhibitors. |
| 4774 | 20954337 | Incretin, GIP and GLP-1, are blood glucose lowering hormones secreted from K cells and L cells, and are rapidly degenerated by DPP-4 within a few minutes. |
| 4775 | 20957343 | Carriers of the TCF7L2 rs7903146 TT genotype have elevated levels of plasma glucose, serum proinsulin and plasma gastric inhibitory polypeptide (GIP) during a meal test. |
| 4776 | 21039588 | Glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), and gastrin are gastrointestinal hormones that are secreted in response to nutrient intake, regulating digestion, insulin secretion, satiety, and β-cell mass. |
| 4777 | 21039588 | GLP-1 and GIP are well-studied gastrointestinal hormones and influence β-cell proliferation, apoptosis, and islet neogenesis. |
| 4778 | 21039588 | CCK regulates β-cell apoptosis and mitogenesis, and gastrin stimulates islet neogenesis. |
| 4779 | 21039588 | GLP-1 and GIP bind to G protein-coupled receptors and regulate β-cell mass via multiple signaling pathways. |
| 4780 | 21039588 | The protein kinase A pathway is central to this process because it directly regulates proliferative and anti-apoptotic genes and transactivates several signaling cascades, including Akt and mitogen-activated protein kinases. |
| 4781 | 21039588 | Glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), and gastrin are gastrointestinal hormones that are secreted in response to nutrient intake, regulating digestion, insulin secretion, satiety, and β-cell mass. |
| 4782 | 21039588 | GLP-1 and GIP are well-studied gastrointestinal hormones and influence β-cell proliferation, apoptosis, and islet neogenesis. |
| 4783 | 21039588 | CCK regulates β-cell apoptosis and mitogenesis, and gastrin stimulates islet neogenesis. |
| 4784 | 21039588 | GLP-1 and GIP bind to G protein-coupled receptors and regulate β-cell mass via multiple signaling pathways. |
| 4785 | 21039588 | The protein kinase A pathway is central to this process because it directly regulates proliferative and anti-apoptotic genes and transactivates several signaling cascades, including Akt and mitogen-activated protein kinases. |
| 4786 | 21039588 | Glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), and gastrin are gastrointestinal hormones that are secreted in response to nutrient intake, regulating digestion, insulin secretion, satiety, and β-cell mass. |
| 4787 | 21039588 | GLP-1 and GIP are well-studied gastrointestinal hormones and influence β-cell proliferation, apoptosis, and islet neogenesis. |
| 4788 | 21039588 | CCK regulates β-cell apoptosis and mitogenesis, and gastrin stimulates islet neogenesis. |
| 4789 | 21039588 | GLP-1 and GIP bind to G protein-coupled receptors and regulate β-cell mass via multiple signaling pathways. |
| 4790 | 21039588 | The protein kinase A pathway is central to this process because it directly regulates proliferative and anti-apoptotic genes and transactivates several signaling cascades, including Akt and mitogen-activated protein kinases. |
| 4791 | 21050845 | Prolonged GIP receptor activation improves cognitive function, hippocampal synaptic plasticity and glucose homeostasis in high-fat fed mice. |
| 4792 | 21050845 | (d-Ala(2))GIP did not affect food intake or plasma insulin levels irrespective of diet. |
| 4793 | 21050845 | Prolonged GIP receptor activation improves cognitive function, hippocampal synaptic plasticity and glucose homeostasis in high-fat fed mice. |
| 4794 | 21050845 | (d-Ala(2))GIP did not affect food intake or plasma insulin levels irrespective of diet. |
| 4795 | 21086586 | It increases the circulating levels of incretin hormones (GLP-1, GIP), which contributes to amplify the insulin secretory response to meals and to reduce postprandial hyperglycaemia and, subsequently, fasting glycaemia. |
| 4796 | 21094895 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are essential components in the regulation of blood glucose levels in mammals. |
| 4797 | 21094895 | Like the hormones, the incretin action of the receptors is not a product of a shared common ancestral history, as the receptors for GLP-1 and GIP are not most closely related. |
| 4798 | 21094895 | Further study of the physiological functions of GLP-1 and GIP in additional vertebrates is required to better understand the origin of incretin action. |
| 4799 | 21094895 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are essential components in the regulation of blood glucose levels in mammals. |
| 4800 | 21094895 | Like the hormones, the incretin action of the receptors is not a product of a shared common ancestral history, as the receptors for GLP-1 and GIP are not most closely related. |
| 4801 | 21094895 | Further study of the physiological functions of GLP-1 and GIP in additional vertebrates is required to better understand the origin of incretin action. |
| 4802 | 21094895 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are essential components in the regulation of blood glucose levels in mammals. |
| 4803 | 21094895 | Like the hormones, the incretin action of the receptors is not a product of a shared common ancestral history, as the receptors for GLP-1 and GIP are not most closely related. |
| 4804 | 21094895 | Further study of the physiological functions of GLP-1 and GIP in additional vertebrates is required to better understand the origin of incretin action. |
| 4805 | 21094897 | The incretin effect has hitherto been attributed to the secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells in the intestinal epithelium. |
| 4806 | 21094897 | A number of recent studies have yielded fundamental insights into the influence of individual nutrients on incretin release and the mechanisms involved in the detection of carbohydrates, fats, and proteins by enteroendocrine cells, including the K(ATP) channel, sodium-glucose cotransporter 1 (SGLT1), sweet taste receptors, G-protein-coupled receptors (GPRs), and oligopeptide transporter 1 (PepT1). |
| 4807 | 21094898 | In addition to GIP, K-cells secrete xenin, a peptide with as of yet poorly understood physiological functions, and GIP is often colocalized with the other incretin hormone glucagon-like peptide-1 (GLP-1). |
| 4808 | 21094898 | Its secretion is elicited by intraluminal nutrients, especially carbohydrate and fat, through the action of SGLT1, GPR40, GPR120, and GPR119. |
| 4809 | 21094898 | Intracellular signaling mechanisms of GIP secretion are still elusive but include activation of adenylyl cyclase, protein kinase A (PKA), and protein kinase C (PKC). |
| 4810 | 21094898 | In addition to GIP, K-cells secrete xenin, a peptide with as of yet poorly understood physiological functions, and GIP is often colocalized with the other incretin hormone glucagon-like peptide-1 (GLP-1). |
| 4811 | 21094898 | Its secretion is elicited by intraluminal nutrients, especially carbohydrate and fat, through the action of SGLT1, GPR40, GPR120, and GPR119. |
| 4812 | 21094898 | Intracellular signaling mechanisms of GIP secretion are still elusive but include activation of adenylyl cyclase, protein kinase A (PKA), and protein kinase C (PKC). |
| 4813 | 21094896 | Two incretins, Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), have so far been identified. |
| 4814 | 21094896 | Localization of the cognate G protein-coupled receptors for GIP and GLP-1 revealed that they are present in numerous tissues in addition to the endocrine pancreas, including the gastrointestinal, cardiovascular, central nervous and autonomic nervous systems (ANSs), adipose tissue, and bone. |
| 4815 | 21094896 | Here, we provide an overview of current knowledge relating to the physiological roles of GIP and GLP-1, with specific emphasis on their modes of action on islet hormone secretion, β-cell proliferation and survival, central and autonomic neuronal function, gastrointestinal motility, and glucose and lipid metabolism. |
| 4816 | 21094896 | Two incretins, Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), have so far been identified. |
| 4817 | 21094896 | Localization of the cognate G protein-coupled receptors for GIP and GLP-1 revealed that they are present in numerous tissues in addition to the endocrine pancreas, including the gastrointestinal, cardiovascular, central nervous and autonomic nervous systems (ANSs), adipose tissue, and bone. |
| 4818 | 21094896 | Here, we provide an overview of current knowledge relating to the physiological roles of GIP and GLP-1, with specific emphasis on their modes of action on islet hormone secretion, β-cell proliferation and survival, central and autonomic neuronal function, gastrointestinal motility, and glucose and lipid metabolism. |
| 4819 | 21094896 | Two incretins, Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), have so far been identified. |
| 4820 | 21094896 | Localization of the cognate G protein-coupled receptors for GIP and GLP-1 revealed that they are present in numerous tissues in addition to the endocrine pancreas, including the gastrointestinal, cardiovascular, central nervous and autonomic nervous systems (ANSs), adipose tissue, and bone. |
| 4821 | 21094896 | Here, we provide an overview of current knowledge relating to the physiological roles of GIP and GLP-1, with specific emphasis on their modes of action on islet hormone secretion, β-cell proliferation and survival, central and autonomic neuronal function, gastrointestinal motility, and glucose and lipid metabolism. |
| 4822 | 21094901 | The two incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key factors in the regulation of islet function and glucose metabolism, and incretin-based therapy for type 2 diabetes has gained considerable interest during recent years. |
| 4823 | 21094901 | The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. |
| 4824 | 21094901 | The two incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key factors in the regulation of islet function and glucose metabolism, and incretin-based therapy for type 2 diabetes has gained considerable interest during recent years. |
| 4825 | 21094901 | The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. |
| 4826 | 21094902 | The importance of the two incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), in health and disease is becoming more apparent as the prevalence of type 2 diabetes and other metabolic disorders escalates. |
| 4827 | 21094902 | Rodent models have become indispensable in the study of the physiological function of GIP and GLP-1; however, investigators have run into several roadblocks when untangling the regulation of incretin secretion in these systems. |
| 4828 | 21094902 | Because of these limitations, continuous monitoring of GIP and GLP-1 secretion becomes difficult. |
| 4829 | 21094902 | The importance of the two incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), in health and disease is becoming more apparent as the prevalence of type 2 diabetes and other metabolic disorders escalates. |
| 4830 | 21094902 | Rodent models have become indispensable in the study of the physiological function of GIP and GLP-1; however, investigators have run into several roadblocks when untangling the regulation of incretin secretion in these systems. |
| 4831 | 21094902 | Because of these limitations, continuous monitoring of GIP and GLP-1 secretion becomes difficult. |
| 4832 | 21094902 | The importance of the two incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), in health and disease is becoming more apparent as the prevalence of type 2 diabetes and other metabolic disorders escalates. |
| 4833 | 21094902 | Rodent models have become indispensable in the study of the physiological function of GIP and GLP-1; however, investigators have run into several roadblocks when untangling the regulation of incretin secretion in these systems. |
| 4834 | 21094902 | Because of these limitations, continuous monitoring of GIP and GLP-1 secretion becomes difficult. |
| 4835 | 21094903 | The glucose-dependent insulinotropic polypeptide (GIP) receptor and the glucagon-like peptide-1 (GLP-1) receptor are homologous G-protein-coupled receptors (GPCRs). |
| 4836 | 21094906 | The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), work together to reduce postprandial hyperglycemia by glucose-dependent insulin secretion and inhibition of glucagon release, as well as inhibition of GI motility and gastric emptying. |
| 4837 | 21094909 | This chapter focuses on the incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), and their therapeutic potential in treating patients with type 2 diabetes. |
| 4838 | 21094909 | Therefore, the actions of GLP-1 and GIP, which include potentiation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4839 | 21094909 | Two new drug classes based on the actions of the incretin hormones have been approved for therapy of type 2 diabetes: injectable long-acting stable analogs of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4840 | 21094909 | This chapter focuses on the incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), and their therapeutic potential in treating patients with type 2 diabetes. |
| 4841 | 21094909 | Therefore, the actions of GLP-1 and GIP, which include potentiation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4842 | 21094909 | Two new drug classes based on the actions of the incretin hormones have been approved for therapy of type 2 diabetes: injectable long-acting stable analogs of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4843 | 21094909 | This chapter focuses on the incretin hormones, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP), and their therapeutic potential in treating patients with type 2 diabetes. |
| 4844 | 21094909 | Therefore, the actions of GLP-1 and GIP, which include potentiation of meal-induced insulin secretion and trophic effects on the beta-cell, have attracted a lot of interest. |
| 4845 | 21094909 | Two new drug classes based on the actions of the incretin hormones have been approved for therapy of type 2 diabetes: injectable long-acting stable analogs of GLP-1, incretin mimetics, and orally available inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), the so-called incretin enhancers. |
| 4846 | 21094910 | The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion from pancreatic β-cells and increased release of the gut peptides GLP-1 (glucagon-like peptide 1), GIP (glucose-dependent insulinotropic peptide) and PYY (polypeptide YY). |
| 4847 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4848 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4849 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4850 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4851 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4852 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4853 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4854 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4855 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4856 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4857 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4858 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4859 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4860 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4861 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4862 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4863 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4864 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4865 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4866 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4867 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4868 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4869 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4870 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4871 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4872 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4873 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4874 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4875 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4876 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4877 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4878 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4879 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4880 | 21095180 | After intraperitoneal administration of GIP (50 nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. |
| 4881 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4882 | 21095180 | These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway. |
| 4883 | 21116606 | Moreover, they show that metformin enhances the expression of the genes encoding the receptors for both GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) in mouse islets and also increases the effects of GIP and GLP-1 on insulin secretion from beta cells. |
| 4884 | 21146561 | The glycaemic response to oral glucose was improved (p<0.01) in all cold exposed rats, with significantly (p<0.05) elevated GIP responses in ad libitum fed rats and significantly (p<0.05) reduced insulin responses in pair fed rats. |
| 4885 | 21146561 | By the end of the study, cold acclimated rats had significantly (p<0.01) increased BAT mass and intestinal concentrations of GIP and GLP-1 compared to controls, independent of food intake. |
| 4886 | 21146561 | The glycaemic response to oral glucose was improved (p<0.01) in all cold exposed rats, with significantly (p<0.05) elevated GIP responses in ad libitum fed rats and significantly (p<0.05) reduced insulin responses in pair fed rats. |
| 4887 | 21146561 | By the end of the study, cold acclimated rats had significantly (p<0.01) increased BAT mass and intestinal concentrations of GIP and GLP-1 compared to controls, independent of food intake. |
| 4888 | 21194578 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagonlike peptide-1 (GLP-1), which are secreted by cells of the gastrointestinal tract in response to meal ingestion, exercise important glucoregulatory effects, including the glucose-dependent potentiation of insulin secretion by pancreatic β-cells. |
| 4889 | 21212092 | Glucose-dependent insulinotropic polypeptide (GIP) is a 42 amino acid hormone secreted from intestinal K-cells, which exhibits a number of actions including stimulation of insulin release. |
| 4890 | 21212092 | The results reveal that sustained GIP receptor activation exerts a spectrum of beneficial metabolic effects in high-fat fed mice. |
| 4891 | 21212092 | Glucose-dependent insulinotropic polypeptide (GIP) is a 42 amino acid hormone secreted from intestinal K-cells, which exhibits a number of actions including stimulation of insulin release. |
| 4892 | 21212092 | The results reveal that sustained GIP receptor activation exerts a spectrum of beneficial metabolic effects in high-fat fed mice. |
| 4893 | 21332446 | Administration of an acylated GLP-1 and GIP preparation provides added beneficial glucose-lowering and insulinotropic actions over single incretins in mice with Type 2 diabetes and obesity. |
| 4894 | 21332446 | The present study examined the glucose-lowering and insulinotropic properties of acylated GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) peptides in Type 2 diabetes and obesity. |
| 4895 | 21332446 | GLP-1, GIP, Liraglutide, N-AcGIP(Lys(37)Myr) (N-acetylGIP with myristic acid conjugated at Lys(37)), a simple combination of both peptides and a Lira-AcGIP preparation [overnight preparation of Liraglutide and N-AcGIP(Lys(37)Myr)] were incubated with DPP-IV (dipeptidyl peptidase-IV) to assess peptide stability, and BRIN-BD11 cells were used to evaluate cAMP production and insulin secretion. |
| 4896 | 21332446 | Liraglutide, N-AcGIP(Lys(37)Myr), a simple combination of both peptides and the Lira-AcGIP preparation demonstrated improved DPP-IV resistance (P<0.001), while stimulating cAMP production and insulin secretion (1.4-2-fold; P<0.001). |
| 4897 | 21332446 | These findings demonstrate that a combined preparation of the acylated GLP-1 and GIP peptides Liraglutide and N-AcGIP(Lys(37)Myr) markedly improved glucose-lowering and insulinotropic properties in diabetic obesity compared with either incretin mimetic given individually. |
| 4898 | 21332446 | Administration of an acylated GLP-1 and GIP preparation provides added beneficial glucose-lowering and insulinotropic actions over single incretins in mice with Type 2 diabetes and obesity. |
| 4899 | 21332446 | The present study examined the glucose-lowering and insulinotropic properties of acylated GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) peptides in Type 2 diabetes and obesity. |
| 4900 | 21332446 | GLP-1, GIP, Liraglutide, N-AcGIP(Lys(37)Myr) (N-acetylGIP with myristic acid conjugated at Lys(37)), a simple combination of both peptides and a Lira-AcGIP preparation [overnight preparation of Liraglutide and N-AcGIP(Lys(37)Myr)] were incubated with DPP-IV (dipeptidyl peptidase-IV) to assess peptide stability, and BRIN-BD11 cells were used to evaluate cAMP production and insulin secretion. |
| 4901 | 21332446 | Liraglutide, N-AcGIP(Lys(37)Myr), a simple combination of both peptides and the Lira-AcGIP preparation demonstrated improved DPP-IV resistance (P<0.001), while stimulating cAMP production and insulin secretion (1.4-2-fold; P<0.001). |
| 4902 | 21332446 | These findings demonstrate that a combined preparation of the acylated GLP-1 and GIP peptides Liraglutide and N-AcGIP(Lys(37)Myr) markedly improved glucose-lowering and insulinotropic properties in diabetic obesity compared with either incretin mimetic given individually. |
| 4903 | 21332446 | Administration of an acylated GLP-1 and GIP preparation provides added beneficial glucose-lowering and insulinotropic actions over single incretins in mice with Type 2 diabetes and obesity. |
| 4904 | 21332446 | The present study examined the glucose-lowering and insulinotropic properties of acylated GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) peptides in Type 2 diabetes and obesity. |
| 4905 | 21332446 | GLP-1, GIP, Liraglutide, N-AcGIP(Lys(37)Myr) (N-acetylGIP with myristic acid conjugated at Lys(37)), a simple combination of both peptides and a Lira-AcGIP preparation [overnight preparation of Liraglutide and N-AcGIP(Lys(37)Myr)] were incubated with DPP-IV (dipeptidyl peptidase-IV) to assess peptide stability, and BRIN-BD11 cells were used to evaluate cAMP production and insulin secretion. |
| 4906 | 21332446 | Liraglutide, N-AcGIP(Lys(37)Myr), a simple combination of both peptides and the Lira-AcGIP preparation demonstrated improved DPP-IV resistance (P<0.001), while stimulating cAMP production and insulin secretion (1.4-2-fold; P<0.001). |
| 4907 | 21332446 | These findings demonstrate that a combined preparation of the acylated GLP-1 and GIP peptides Liraglutide and N-AcGIP(Lys(37)Myr) markedly improved glucose-lowering and insulinotropic properties in diabetic obesity compared with either incretin mimetic given individually. |
| 4908 | 21332446 | Administration of an acylated GLP-1 and GIP preparation provides added beneficial glucose-lowering and insulinotropic actions over single incretins in mice with Type 2 diabetes and obesity. |
| 4909 | 21332446 | The present study examined the glucose-lowering and insulinotropic properties of acylated GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) peptides in Type 2 diabetes and obesity. |
| 4910 | 21332446 | GLP-1, GIP, Liraglutide, N-AcGIP(Lys(37)Myr) (N-acetylGIP with myristic acid conjugated at Lys(37)), a simple combination of both peptides and a Lira-AcGIP preparation [overnight preparation of Liraglutide and N-AcGIP(Lys(37)Myr)] were incubated with DPP-IV (dipeptidyl peptidase-IV) to assess peptide stability, and BRIN-BD11 cells were used to evaluate cAMP production and insulin secretion. |
| 4911 | 21332446 | Liraglutide, N-AcGIP(Lys(37)Myr), a simple combination of both peptides and the Lira-AcGIP preparation demonstrated improved DPP-IV resistance (P<0.001), while stimulating cAMP production and insulin secretion (1.4-2-fold; P<0.001). |
| 4912 | 21332446 | These findings demonstrate that a combined preparation of the acylated GLP-1 and GIP peptides Liraglutide and N-AcGIP(Lys(37)Myr) markedly improved glucose-lowering and insulinotropic properties in diabetic obesity compared with either incretin mimetic given individually. |
| 4913 | 21335995 | Especially milk and whey protein-based products contribute to elevations of postprandial insulin and basal insulin-like growth factor-I (IGF-I) plasma levels. |
| 4914 | 21335995 | Whey proteins are most potent inducers of glucose-dependent insulinotropic polypeptide secreted by enteroendocrine K cells which in concert with hydrolyzed whey protein-derived essential amino acids stimulate insulin secretion of pancreatic β-cells. |
| 4915 | 21335995 | Increased insulin/IGF-I signaling activates the phosphoinositide-3 kinase/Akt pathway, thereby reducing the nuclear content of the transcription factor FoxO1, the key nutrigenomic regulator of acne target genes. |
| 4916 | 21335995 | Nuclear FoxO1 deficiency has been linked to all major factors of acne pathogenesis, i.e. androgen receptor transactivation, comedogenesis, increased sebaceous lipogenesis, and follicular inflammation. |
| 4917 | 21372167 | RYGB resulted in an improved glucose, insulin, and glucagon-like peptide-1 (GLP-1) area under the curve (AUC) in the first 6 wk postoperatively (all P ≤ 0.018); there was no effect of delivery route (all P ≥ 0.632) or route × time interaction (all P ≥ 0.084). |
| 4918 | 21372167 | The ratio of insulin AUC to GLP-1 and GIP AUC decreased after surgery (P =.001 and 0.061, respectively) without an effect of delivery route over time (both P ≥ 0.646). |
| 4919 | 21415556 | The glucose-dependent insulinotropic polypeptide (GIP) receptor was expressed at high levels in compact cells, suggesting that GIP is responsible for the development of AIMAH. |
| 4920 | 21415556 | Genetic abnormalities in the MEN1, p27, and p18 genes were not found, however, the present case may provide a clue to the understanding of the etiology of MEN1 and AIMAH. |
| 4921 | 21437082 | DPP-4 inhibitors elevate plasma concentrations of the incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). |
| 4922 | 21441754 | Incretins (glucose-dependent insulinotropic polypeptide [GIP] and glucagon-like peptide-1 [GLP-1]) are hormones released post-meal from intestinal endocrine cells that stimulate insulin secretion and suppress postprandial glucagon secretion in a glucose-dependent manner. |
| 4923 | 21441754 | "Incretin therapies," comprising the injectable GLP-1 analogs and oral dipeptidyl peptidase-4 (DPP-4) inhibitors, are promising new therapies for use in older patients because of their consistent efficacy and low risk of hypoglycemia. |
| 4924 | 21488836 | Among these factors, the cAMP-responsive element-binding protein (CREB) has emerged as a key transcriptional element for the maintenance of an efficient glucose sensing, insulin exocytosis, insulin gene transcription and β-cell survival. |
| 4925 | 21488836 | CREB activates the transcription of target genes within the β-cells in response to a diverse array of stimuli including glucose, incretin hormones such as the glucagon-like peptide-1 (GLP-1) or the gastric inhibitory polypeptide (GIP), the pituitary adenylate cyclase-activating polypeptide (PACAP), or growth factors such as the insulin like growth factor-1 (IGF-1). |
| 4926 | 21488836 | These mechanisms involve different protein kinases, scaffold proteins and cofactors which allow CREB to specifically regulate the expression of crucial genes such as insulin, BCL-2, cyclin D1, cyclin A2 or IRS-2. |
| 4927 | 21540554 | In mice, genetic deletion of the glucagon receptor (Gcgr) results in increased levels of the insulinotropic hormone glucagon-like peptide 1 (GLP-1), which may contribute to the alterations in glucose homeostasis observed in Gcgr-/- mice. |
| 4928 | 21540554 | Here, we assessed the contribution of GLP-1 receptor (GLP-1R) signaling to the phenotype of Gcgr-/- mice by generating Gcgr-/-Glp1r-/- mice. |
| 4929 | 21540554 | Unexpectedly, deletion of Glp1r in Gcgr-/- mice did not alter the improved oral glucose tolerance and increased insulin secretion characteristic of that genotype. |
| 4930 | 21540554 | Although Gcgr-/-Glp1r-/- islets exhibited increased sensitivity to the incretin glucose-dependent insulinotropic polypeptide (GIP), mice lacking both Glp1r and the GIP receptor (Gipr) maintained preservation of the enteroinsular axis following reduction of Gcgr signaling. |
| 4931 | 21540554 | Moreover, Gcgr-/-Glp1r-/- islets expressed increased levels of the cholecystokinin A receptor (Cckar) and G protein-coupled receptor 119 (Gpr119) mRNA transcripts, and Gcgr-/-Glp1r-/- mice exhibited increased sensitivity to exogenous CCK and the GPR119 agonist AR231453. |
| 4932 | 21554523 | Protein elicits a stronger early (30 min) glucose-dependent insulinotropic polypeptide (GIP) response than fat ingestion in lean individuals, with no difference in glucagon-like peptide-1 (GLP-1). |
| 4933 | 21554523 | Equicaloric (8 kcal/kg) fat (olive oil) or protein (whey protein) was ingested by non-diabetic obese male volunteers [body mass index (BMI) >30 kg/m(2) ; n = 12] and plasma GIP and GLP-1 were determined. |
| 4934 | 21554523 | We found no difference in the early GIP or GLP-1 responses to fat versus protein. |
| 4935 | 21554523 | However, the total 300-min GIP response was greater after fat than after protein ingestion (20.3 ± 3.9 vs. 10.0 ± 2.8 nmol/l × min; p = 0.026), whereas the 300-min GLP-1 responses were the same. |
| 4936 | 21554523 | Protein elicits a stronger early (30 min) glucose-dependent insulinotropic polypeptide (GIP) response than fat ingestion in lean individuals, with no difference in glucagon-like peptide-1 (GLP-1). |
| 4937 | 21554523 | Equicaloric (8 kcal/kg) fat (olive oil) or protein (whey protein) was ingested by non-diabetic obese male volunteers [body mass index (BMI) >30 kg/m(2) ; n = 12] and plasma GIP and GLP-1 were determined. |
| 4938 | 21554523 | We found no difference in the early GIP or GLP-1 responses to fat versus protein. |
| 4939 | 21554523 | However, the total 300-min GIP response was greater after fat than after protein ingestion (20.3 ± 3.9 vs. 10.0 ± 2.8 nmol/l × min; p = 0.026), whereas the 300-min GLP-1 responses were the same. |
| 4940 | 21554523 | Protein elicits a stronger early (30 min) glucose-dependent insulinotropic polypeptide (GIP) response than fat ingestion in lean individuals, with no difference in glucagon-like peptide-1 (GLP-1). |
| 4941 | 21554523 | Equicaloric (8 kcal/kg) fat (olive oil) or protein (whey protein) was ingested by non-diabetic obese male volunteers [body mass index (BMI) >30 kg/m(2) ; n = 12] and plasma GIP and GLP-1 were determined. |
| 4942 | 21554523 | We found no difference in the early GIP or GLP-1 responses to fat versus protein. |
| 4943 | 21554523 | However, the total 300-min GIP response was greater after fat than after protein ingestion (20.3 ± 3.9 vs. 10.0 ± 2.8 nmol/l × min; p = 0.026), whereas the 300-min GLP-1 responses were the same. |
| 4944 | 21554523 | Protein elicits a stronger early (30 min) glucose-dependent insulinotropic polypeptide (GIP) response than fat ingestion in lean individuals, with no difference in glucagon-like peptide-1 (GLP-1). |
| 4945 | 21554523 | Equicaloric (8 kcal/kg) fat (olive oil) or protein (whey protein) was ingested by non-diabetic obese male volunteers [body mass index (BMI) >30 kg/m(2) ; n = 12] and plasma GIP and GLP-1 were determined. |
| 4946 | 21554523 | We found no difference in the early GIP or GLP-1 responses to fat versus protein. |
| 4947 | 21554523 | However, the total 300-min GIP response was greater after fat than after protein ingestion (20.3 ± 3.9 vs. 10.0 ± 2.8 nmol/l × min; p = 0.026), whereas the 300-min GLP-1 responses were the same. |
| 4948 | 21605578 | The small intestine is not only responsible for the digestion and transport of dietary triacylglycerol, through the formation of chylomicrons, but it also secretes the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells. |
| 4949 | 21605578 | The importance of GIP and GLP-1 in health and disease is becoming more apparent, especially as the prevalence of type 2 diabetes and other metabolic disorders increases. |
| 4950 | 21605578 | The small intestine is not only responsible for the digestion and transport of dietary triacylglycerol, through the formation of chylomicrons, but it also secretes the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells. |
| 4951 | 21605578 | The importance of GIP and GLP-1 in health and disease is becoming more apparent, especially as the prevalence of type 2 diabetes and other metabolic disorders increases. |
| 4952 | 21620903 | In ob/ob islets the insulinotropic peptides glucagon, GLP-1 and GIP suppressed NOS activities and amplified glucose-stimulated insulin release. |
| 4953 | 21620903 | Islets from ob/ob mice existing in a hyperglycemic in vivo milieu maintain elevated insulin secretion and protection from glucotoxicity through a general suppression of islet NOS activities achieved by leptin deficiency, high CO production and insulinotropic cyclic-AMP-generating hormones. |
| 4954 | 21747410 | Association between the GIPR gene and the insulin level after glucose loading in schizophrenia patients treated with olanzapine. |
| 4955 | 21747410 | Glucose-dependent insulinotropic polypeptide (GIP) is known to affect insulin secretion by pancreatic β cells. |
| 4956 | 21747410 | Recently, a meta-analysis study reported an association between a GIP receptor (GIPR) gene polymorphism (rs10423928) and insulin secretion measured by an oral glucose tolerance test (OGTT). |
| 4957 | 21747410 | We performed repeated-measures analysis of variance (ANOVA) and one-way ANOVA for the glucose and insulin levels during OGTTs in four groups divided by the GIPR gene polymorphism and cohort (schizophrenia or control). |
| 4958 | 21747410 | We found significant effects of the GIPR gene and cohort on the insulin levels at 30 min. |
| 4959 | 21747410 | Association between the GIPR gene and the insulin level after glucose loading in schizophrenia patients treated with olanzapine. |
| 4960 | 21747410 | Glucose-dependent insulinotropic polypeptide (GIP) is known to affect insulin secretion by pancreatic β cells. |
| 4961 | 21747410 | Recently, a meta-analysis study reported an association between a GIP receptor (GIPR) gene polymorphism (rs10423928) and insulin secretion measured by an oral glucose tolerance test (OGTT). |
| 4962 | 21747410 | We performed repeated-measures analysis of variance (ANOVA) and one-way ANOVA for the glucose and insulin levels during OGTTs in four groups divided by the GIPR gene polymorphism and cohort (schizophrenia or control). |
| 4963 | 21747410 | We found significant effects of the GIPR gene and cohort on the insulin levels at 30 min. |
| 4964 | 21761282 | Characterization of beta cell and incretin function in patients with MODY1 (HNF4A MODY) and MODY3 (HNF1A MODY) in a Swedish patient collection. |
| 4965 | 21761282 | The aim of this study was to evaluate the beta cell and incretin function in patients with HNF4A and HNF1A MODY during a test meal. |
| 4966 | 21761282 | Clinical characteristics and biochemical data (glucose, proinsulin, insulin, C-peptide, GLP-1 and GIP) during a test meal were compared between MODY patients from eight different families. |
| 4967 | 21761282 | The early phase of insulin secretion was attenuated in HNF4A, HNF1A MODY and T2D (AUC0-30 controls: 558.2 ± 101.2, HNF4A MODY: 93.8 ± 57.0, HNF1A MODY: 170.2 ± 64.5, T2D: 211.2 ± 65.3, P < 0.01). |
| 4968 | 21761282 | Markedly reduced levels of proinsulin were found in HNF4A MODY compared to T2D and that tended to be so also in HNF1A MODY (HNF4A MODY: 3.7 ± 1.2, HNF1A MODY: 8.3 ± 3.8 vs. |
| 4969 | 21761282 | Patients with HNF4A MODY had similar total GLP-1 and GIP responses as controls (GLP-1 AUC: (control: 823.9 ± 703.8, T2D: 556.4 ± 698.2, HNF4A MODY: 1,257.0 ± 999.3, HNF1A MODY: 697.1 ± 818.4) but with a different secretion pattern. |
| 4970 | 21761282 | Patients with HNF4A and HNF1A MODY showed an attenuated early phase of insulin secretion similar to T2Ds. |
| 4971 | 21761282 | Thus, GIP may be a more important factor for insulin secretion than GLP-1 in MODY patients. |
| 4972 | 21761282 | Characterization of beta cell and incretin function in patients with MODY1 (HNF4A MODY) and MODY3 (HNF1A MODY) in a Swedish patient collection. |
| 4973 | 21761282 | The aim of this study was to evaluate the beta cell and incretin function in patients with HNF4A and HNF1A MODY during a test meal. |
| 4974 | 21761282 | Clinical characteristics and biochemical data (glucose, proinsulin, insulin, C-peptide, GLP-1 and GIP) during a test meal were compared between MODY patients from eight different families. |
| 4975 | 21761282 | The early phase of insulin secretion was attenuated in HNF4A, HNF1A MODY and T2D (AUC0-30 controls: 558.2 ± 101.2, HNF4A MODY: 93.8 ± 57.0, HNF1A MODY: 170.2 ± 64.5, T2D: 211.2 ± 65.3, P < 0.01). |
| 4976 | 21761282 | Markedly reduced levels of proinsulin were found in HNF4A MODY compared to T2D and that tended to be so also in HNF1A MODY (HNF4A MODY: 3.7 ± 1.2, HNF1A MODY: 8.3 ± 3.8 vs. |
| 4977 | 21761282 | Patients with HNF4A MODY had similar total GLP-1 and GIP responses as controls (GLP-1 AUC: (control: 823.9 ± 703.8, T2D: 556.4 ± 698.2, HNF4A MODY: 1,257.0 ± 999.3, HNF1A MODY: 697.1 ± 818.4) but with a different secretion pattern. |
| 4978 | 21761282 | Patients with HNF4A and HNF1A MODY showed an attenuated early phase of insulin secretion similar to T2Ds. |
| 4979 | 21761282 | Thus, GIP may be a more important factor for insulin secretion than GLP-1 in MODY patients. |
| 4980 | 21813733 | Incretin hormones, including glucagon-like peptide-1, or GLP-1, and glucose-dependent insulinotropic polypeptide, are vital to the control of glucose homeostasis and pancreatic β-cell preservation. |
| 4981 | 21818121 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the major incretin hormones that exert insulinotropic and anti-apoptotic actions on pancreatic β-cells. |
| 4982 | 21818121 | Overexpression of Kv2.1 in INS-1 β-cells potentiated apoptosis in response to mitochondrial and ER stress and, conversely, co-stimulation with GIP/GLP-1 uncoupled this potentiation, suppressing apoptosis. |
| 4983 | 21818121 | In parallel, incretins promoted phosphorylation and acetylation of Kv2.1 via pathways involving protein kinase A (PKA)/mitogen- and stress-activated kinase-1 (MSK-1) and histone acetyltransferase (HAT)/histone deacetylase (HDAC). |
| 4984 | 21818121 | Further studies demonstrated that acetylation of Kv2.1 was mediated by incretin actions on nuclear/cytoplasmic shuttling of CREB binding protein (CBP) and its interaction with Kv2.1. |
| 4985 | 21818121 | Regulation of β-cell survival by GIP and GLP-1 therefore involves post-translational modifications (PTMs) of Kv channels by PKA/MSK-1 and HAT/HDAC. |
| 4986 | 21818121 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the major incretin hormones that exert insulinotropic and anti-apoptotic actions on pancreatic β-cells. |
| 4987 | 21818121 | Overexpression of Kv2.1 in INS-1 β-cells potentiated apoptosis in response to mitochondrial and ER stress and, conversely, co-stimulation with GIP/GLP-1 uncoupled this potentiation, suppressing apoptosis. |
| 4988 | 21818121 | In parallel, incretins promoted phosphorylation and acetylation of Kv2.1 via pathways involving protein kinase A (PKA)/mitogen- and stress-activated kinase-1 (MSK-1) and histone acetyltransferase (HAT)/histone deacetylase (HDAC). |
| 4989 | 21818121 | Further studies demonstrated that acetylation of Kv2.1 was mediated by incretin actions on nuclear/cytoplasmic shuttling of CREB binding protein (CBP) and its interaction with Kv2.1. |
| 4990 | 21818121 | Regulation of β-cell survival by GIP and GLP-1 therefore involves post-translational modifications (PTMs) of Kv channels by PKA/MSK-1 and HAT/HDAC. |
| 4991 | 21818121 | Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the major incretin hormones that exert insulinotropic and anti-apoptotic actions on pancreatic β-cells. |
| 4992 | 21818121 | Overexpression of Kv2.1 in INS-1 β-cells potentiated apoptosis in response to mitochondrial and ER stress and, conversely, co-stimulation with GIP/GLP-1 uncoupled this potentiation, suppressing apoptosis. |
| 4993 | 21818121 | In parallel, incretins promoted phosphorylation and acetylation of Kv2.1 via pathways involving protein kinase A (PKA)/mitogen- and stress-activated kinase-1 (MSK-1) and histone acetyltransferase (HAT)/histone deacetylase (HDAC). |
| 4994 | 21818121 | Further studies demonstrated that acetylation of Kv2.1 was mediated by incretin actions on nuclear/cytoplasmic shuttling of CREB binding protein (CBP) and its interaction with Kv2.1. |
| 4995 | 21818121 | Regulation of β-cell survival by GIP and GLP-1 therefore involves post-translational modifications (PTMs) of Kv channels by PKA/MSK-1 and HAT/HDAC. |
| 4996 | 21820006 | Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation. |
| 4997 | 21820006 | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. |
| 4998 | 21820006 | GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. |
| 4999 | 21820006 | In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. |
| 5000 | 21820006 | However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. |
| 5001 | 21820006 | We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes. |
| 5002 | 21820006 | Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation. |
| 5003 | 21820006 | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. |
| 5004 | 21820006 | GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. |
| 5005 | 21820006 | In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. |
| 5006 | 21820006 | However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. |
| 5007 | 21820006 | We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes. |
| 5008 | 21820006 | Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation. |
| 5009 | 21820006 | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. |
| 5010 | 21820006 | GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. |
| 5011 | 21820006 | In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. |
| 5012 | 21820006 | However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. |
| 5013 | 21820006 | We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes. |
| 5014 | 21820006 | Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation. |
| 5015 | 21820006 | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. |
| 5016 | 21820006 | GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. |
| 5017 | 21820006 | In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. |
| 5018 | 21820006 | However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. |
| 5019 | 21820006 | We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes. |
| 5020 | 21820006 | Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation. |
| 5021 | 21820006 | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. |
| 5022 | 21820006 | GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. |
| 5023 | 21820006 | In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. |
| 5024 | 21820006 | However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. |
| 5025 | 21820006 | We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes. |
| 5026 | 21869539 | MTT findings suggest that this combination therapy improves blood glucose control by delaying carbohydrate absorption and modifying the responses of incretins, GIP, and GLP-1. |
| 5027 | 21893952 | Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. |
| 5028 | 21893952 | In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. |
| 5029 | 21893952 | No GLP-1 or GIP receptors are detected in normal human thyroids. |
| 5030 | 21893952 | Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. |
| 5031 | 21893952 | TT cells lack GLP-1 receptors but express GIP receptors. |
| 5032 | 21893952 | Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. |
| 5033 | 21893952 | In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. |
| 5034 | 21893952 | No GLP-1 or GIP receptors are detected in normal human thyroids. |
| 5035 | 21893952 | Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. |
| 5036 | 21893952 | TT cells lack GLP-1 receptors but express GIP receptors. |
| 5037 | 21893952 | Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. |
| 5038 | 21893952 | In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. |
| 5039 | 21893952 | No GLP-1 or GIP receptors are detected in normal human thyroids. |
| 5040 | 21893952 | Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. |
| 5041 | 21893952 | TT cells lack GLP-1 receptors but express GIP receptors. |
| 5042 | 21893952 | Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. |
| 5043 | 21893952 | In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. |
| 5044 | 21893952 | No GLP-1 or GIP receptors are detected in normal human thyroids. |
| 5045 | 21893952 | Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. |
| 5046 | 21893952 | TT cells lack GLP-1 receptors but express GIP receptors. |
| 5047 | 21893952 | Incretin receptors for GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) were therefore measured in various rodent and human thyroid conditions. |
| 5048 | 21893952 | In vitro GLP-1 and GIP receptor autoradiography were performed in normal thyroids, C-cell hyperplasia and medullary thyroid carcinomas in rodents. |
| 5049 | 21893952 | No GLP-1 or GIP receptors are detected in normal human thyroids. |
| 5050 | 21893952 | Whereas only 27% of all human medullary thyroid carcinomas express GLP-1 receptors, up to 89% express GIP receptors in a high density. |
| 5051 | 21893952 | TT cells lack GLP-1 receptors but express GIP receptors. |
| 5052 | 21898126 | Miglitol and dipeptidyl peptidase-4 inhibitors, such as sitagliptin, enhance plasma active GLP-1 concentrations via different mechanisms; therefore, combined therapy with these agents was more effective than monotherapy. |
| 5053 | 21898126 | We measured the plasma glucose, serum insulin and glucagon, plasma active GLP-1, and total glucose-dependent insulinotropic polypeptide levels before breakfast, at 120 min after breakfast, before lunch, and 60 and 120 min after lunch in patients with diabetes who are receiving sitagliptin. |
| 5054 | 21907232 | Although unresponsiveness of type 2 diabetes (T2D) patients to GIP has now been reconsidered, GLP-1 mimetics and inhibitors of the GLP-1 degradation enzyme dipeptidyl peptidase (DPP)-4 have now been launched as drugs against T2D. |
| 5055 | 21907232 | The major roles of GLP-1 in T2D are reduction of appetite, gastric motility, glucagon secretion, enhancement of insulin secretion and β-cell survival. |
| 5056 | 21907232 | For insulin secretion and peripheral insulin function, GLP-1 and its mimetics sensitise β-cells to glucose; accelerate blood glucose withdrawal, in-cell glucose utilisation and glycogen synthesis in insulin-sensitive tissues; and assist in the function and survival of neurons mainly using glucose as an energy source. |
| 5057 | 21907232 | On the basis of our recent research results, we also describe a mechanism that regulates GLP-1 for glucokinase activity. |
| 5058 | 21912382 | After GBP, the plasma concentrations of the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide increase postprandially by three- to fivefold. |
| 5059 | 21912382 | The improved insulin release and glucose tolerance after GBP were shown by others to be blocked by the administration of a GLP-1 antagonist, demonstrating that the favorable metabolic changes after GBP are, in part, GLP-1 dependent. |
| 5060 | 21917634 | In contrast to NBW subjects, the plasma leptin levels of LBW subjects did not increase, and the plasma gastric inhibitory polypeptide (GIP) as well as pancreatic polypeptide (PP) levels increased less in LBW compared with NBW subjects during HFO. |
| 5061 | 21917634 | Reduced increments in response to HFO of fasting plasma leptin, PP, and GIP levels may contribute to insulin resistance, lower satiety, and impaired insulin secretion in LBW subjects. |
| 5062 | 21917634 | In contrast to NBW subjects, the plasma leptin levels of LBW subjects did not increase, and the plasma gastric inhibitory polypeptide (GIP) as well as pancreatic polypeptide (PP) levels increased less in LBW compared with NBW subjects during HFO. |
| 5063 | 21917634 | Reduced increments in response to HFO of fasting plasma leptin, PP, and GIP levels may contribute to insulin resistance, lower satiety, and impaired insulin secretion in LBW subjects. |
| 5064 | 21958333 | The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate glucose-induced insulin secretion; however, in patients with type 2 diabetes, the incretin system is impaired by loss of the insulinotropic effects of GIP as well as a possible reduction in secretion of GLP-1. |
| 5065 | 21958333 | The currently available incretin-based therapies, GLP-1 receptor agonists (incretin mimetics) and dipeptidyl peptidase-4 (DPP-4) inhibitors (CD26 antigen inhibitors) [incretin enhancers], are safe and effective in the treatment of type 2 diabetes. |
| 5066 | 21958333 | Therapies that directly target intestinal L cells to stimulate secretion of endogenous GLP-1 could possibly prove more effective than treatment with GLP-1 receptor agonists and DPP-4 inhibitors. |
| 5067 | 21958333 | Potential new approaches to modifying intestinal GLP-1 secretion in patients with type 2 diabetes include G-protein-coupled receptor (GPCR) agonists, α-glucosidase inhibitors, peroxisome proliferator-activated receptor (PPAR) agonists, metformin, bile acid mimetics and bile acid sequestrants. |
| 5068 | 21958333 | Both the GPCR agonist AR231453 and the novel bile acid mimetic INT-777 have been shown to stimulate GLP-1 release, leading to increased insulin secretion and improved glucose tolerance in mice. |
| 5069 | 21958333 | Similarly, a study in insulin-resistant rats demonstrated that the bile acid sequestrant colesevelam increased GLP-1 secretion and improved glucose levels and insulin resistance. |
| 5070 | 21958333 | Evidence suggests that GPCR agonists, α-glucosidase inhibitors, PPAR agonists, metformin, bile acid mimetics and bile acid sequestrants may represent a new approach to management of type 2 diabetes via modification of endogenous GLP-1 secretion. |
| 5071 | 21966329 | It has been shown that the naturally occurring gut hormones incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) can preserve the morphology and function of pancreatic beta cell. |
| 5072 | 21966329 | In addition, GIP and GLP-1 act on insulin receptors to facilitate insulin-receptor binding, resulting in optimal glucose metabolism. |
| 5073 | 21966329 | The paper also identified and reviewed a number of inhibitors, which can block dipeptidyl peptidase 4 (DPP-4), the enzyme responsible for the rapid degradation of GLP-1. |
| 5074 | 21966329 | It has been shown that the naturally occurring gut hormones incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) can preserve the morphology and function of pancreatic beta cell. |
| 5075 | 21966329 | In addition, GIP and GLP-1 act on insulin receptors to facilitate insulin-receptor binding, resulting in optimal glucose metabolism. |
| 5076 | 21966329 | The paper also identified and reviewed a number of inhibitors, which can block dipeptidyl peptidase 4 (DPP-4), the enzyme responsible for the rapid degradation of GLP-1. |
| 5077 | 21984584 | Glucose-dependent insulinotropic polypeptide: a bifunctional glucose-dependent regulator of glucagon and insulin secretion in humans. |
| 5078 | 22043004 | Glucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion. |
| 5079 | 22043004 | Because obesity and diabetes are glucocorticoid dependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by glucocorticoids using pharmacological activation of GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells. |
| 5080 | 22043004 | [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner. |
| 5081 | 22043004 | [d-Ala(2)]GIP increased cAMP levels, activated extracellular signalx{2013}related kinase (ERK)1/2, increased expression of steroidogenic genes, and increased neutral lipid storage in Y1GIPR cells. |
| 5082 | 22043004 | Gipr(-/-) adrenal glands demonstrated a twofold upregulation of the ACTH receptor mRNA and increased sensitivity to ACTH ex vivo. |
| 5083 | 22043004 | Glucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion. |
| 5084 | 22043004 | Because obesity and diabetes are glucocorticoid dependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by glucocorticoids using pharmacological activation of GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells. |
| 5085 | 22043004 | [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner. |
| 5086 | 22043004 | [d-Ala(2)]GIP increased cAMP levels, activated extracellular signalx{2013}related kinase (ERK)1/2, increased expression of steroidogenic genes, and increased neutral lipid storage in Y1GIPR cells. |
| 5087 | 22043004 | Gipr(-/-) adrenal glands demonstrated a twofold upregulation of the ACTH receptor mRNA and increased sensitivity to ACTH ex vivo. |
| 5088 | 22043004 | Glucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion. |
| 5089 | 22043004 | Because obesity and diabetes are glucocorticoid dependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by glucocorticoids using pharmacological activation of GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells. |
| 5090 | 22043004 | [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner. |
| 5091 | 22043004 | [d-Ala(2)]GIP increased cAMP levels, activated extracellular signalx{2013}related kinase (ERK)1/2, increased expression of steroidogenic genes, and increased neutral lipid storage in Y1GIPR cells. |
| 5092 | 22043004 | Gipr(-/-) adrenal glands demonstrated a twofold upregulation of the ACTH receptor mRNA and increased sensitivity to ACTH ex vivo. |
| 5093 | 22043004 | Glucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion. |
| 5094 | 22043004 | Because obesity and diabetes are glucocorticoid dependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by glucocorticoids using pharmacological activation of GIP receptor (GIPR) signaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells. |
| 5095 | 22043004 | [d-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner. |
| 5096 | 22043004 | [d-Ala(2)]GIP increased cAMP levels, activated extracellular signalx{2013}related kinase (ERK)1/2, increased expression of steroidogenic genes, and increased neutral lipid storage in Y1GIPR cells. |
| 5097 | 22043004 | Gipr(-/-) adrenal glands demonstrated a twofold upregulation of the ACTH receptor mRNA and increased sensitivity to ACTH ex vivo. |
| 5098 | 22160540 | Glucose in the gut lumen activates gut endocrine cells to release 5-HT, glucagon-like peptide 1/2 (GLP-1/2), and glucose-dependent insulinotropic polypeptide (GIP), which act to change gastrointestinal function and regulate postprandial plasma glucose. |
| 5099 | 22160540 | Immunoreactivity for GLP-1, but not GIP, was significantly reduced in RD and 3MD compared with PD rats (P < 0.01). |
| 5100 | 22160540 | Glucose in the gut lumen activates gut endocrine cells to release 5-HT, glucagon-like peptide 1/2 (GLP-1/2), and glucose-dependent insulinotropic polypeptide (GIP), which act to change gastrointestinal function and regulate postprandial plasma glucose. |
| 5101 | 22160540 | Immunoreactivity for GLP-1, but not GIP, was significantly reduced in RD and 3MD compared with PD rats (P < 0.01). |
| 5102 | 22179810 | We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. |
| 5103 | 22179810 | GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fashion. |
| 5104 | 22179810 | Preinhibition of 11β-HSD1 completely abolished GIP-induced effects on FFA release. |
| 5105 | 22179810 | GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11β-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. |
| 5106 | 22179810 | In general, the presented data support that GIP has direct and insulin-independent effects on adipose tissue. |
| 5107 | 22179810 | We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. |
| 5108 | 22179810 | GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fashion. |
| 5109 | 22179810 | Preinhibition of 11β-HSD1 completely abolished GIP-induced effects on FFA release. |
| 5110 | 22179810 | GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11β-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. |
| 5111 | 22179810 | In general, the presented data support that GIP has direct and insulin-independent effects on adipose tissue. |
| 5112 | 22179810 | We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. |
| 5113 | 22179810 | GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fashion. |
| 5114 | 22179810 | Preinhibition of 11β-HSD1 completely abolished GIP-induced effects on FFA release. |
| 5115 | 22179810 | GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11β-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. |
| 5116 | 22179810 | In general, the presented data support that GIP has direct and insulin-independent effects on adipose tissue. |
| 5117 | 22179810 | We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. |
| 5118 | 22179810 | GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fashion. |
| 5119 | 22179810 | Preinhibition of 11β-HSD1 completely abolished GIP-induced effects on FFA release. |
| 5120 | 22179810 | GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11β-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. |
| 5121 | 22179810 | In general, the presented data support that GIP has direct and insulin-independent effects on adipose tissue. |
| 5122 | 22179810 | We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. |
| 5123 | 22179810 | GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fashion. |
| 5124 | 22179810 | Preinhibition of 11β-HSD1 completely abolished GIP-induced effects on FFA release. |
| 5125 | 22179810 | GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11β-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. |
| 5126 | 22179810 | In general, the presented data support that GIP has direct and insulin-independent effects on adipose tissue. |
| 5127 | 22260799 | Evaluation of the long-term effects of gastric inhibitory polypeptide-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy balance and cognition in high-fat-fed mice. |
| 5128 | 22260799 | The effects of active immunisation with gastric inhibitory polypeptide (GIP) or (proline3)GIP-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy expenditure and cognition were examined in high-fat-fed mice. |
| 5129 | 22260799 | Active immunisation resulted in GIP antibody generation and significantly (P < 0·01 to P < 0·001) reduced circulating non-fasting plasma insulin concentrations compared to high-fat control mice from day 70 onwards. |
| 5130 | 22260799 | Further tests established that coupling of GIP peptides to ovalbumin abolished any intrinsic insulin-releasing or glucose-lowering activity. |
| 5131 | 22260799 | Evaluation of the long-term effects of gastric inhibitory polypeptide-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy balance and cognition in high-fat-fed mice. |
| 5132 | 22260799 | The effects of active immunisation with gastric inhibitory polypeptide (GIP) or (proline3)GIP-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy expenditure and cognition were examined in high-fat-fed mice. |
| 5133 | 22260799 | Active immunisation resulted in GIP antibody generation and significantly (P < 0·01 to P < 0·001) reduced circulating non-fasting plasma insulin concentrations compared to high-fat control mice from day 70 onwards. |
| 5134 | 22260799 | Further tests established that coupling of GIP peptides to ovalbumin abolished any intrinsic insulin-releasing or glucose-lowering activity. |
| 5135 | 22260799 | Evaluation of the long-term effects of gastric inhibitory polypeptide-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy balance and cognition in high-fat-fed mice. |
| 5136 | 22260799 | The effects of active immunisation with gastric inhibitory polypeptide (GIP) or (proline3)GIP-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy expenditure and cognition were examined in high-fat-fed mice. |
| 5137 | 22260799 | Active immunisation resulted in GIP antibody generation and significantly (P < 0·01 to P < 0·001) reduced circulating non-fasting plasma insulin concentrations compared to high-fat control mice from day 70 onwards. |
| 5138 | 22260799 | Further tests established that coupling of GIP peptides to ovalbumin abolished any intrinsic insulin-releasing or glucose-lowering activity. |
| 5139 | 22260799 | Evaluation of the long-term effects of gastric inhibitory polypeptide-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy balance and cognition in high-fat-fed mice. |
| 5140 | 22260799 | The effects of active immunisation with gastric inhibitory polypeptide (GIP) or (proline3)GIP-ovalbumin conjugates on insulin resistance, metabolic dysfunction, energy expenditure and cognition were examined in high-fat-fed mice. |
| 5141 | 22260799 | Active immunisation resulted in GIP antibody generation and significantly (P < 0·01 to P < 0·001) reduced circulating non-fasting plasma insulin concentrations compared to high-fat control mice from day 70 onwards. |
| 5142 | 22260799 | Further tests established that coupling of GIP peptides to ovalbumin abolished any intrinsic insulin-releasing or glucose-lowering activity. |
| 5143 | 22262068 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are gut peptides which are secreted by endocrine cells in the intestinal mucosa. |
| 5144 | 22262068 | Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. |
| 5145 | 22262068 | Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, but interpretation of the precise relationship between disease and incretins is difficult. |
| 5146 | 22262068 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are gut peptides which are secreted by endocrine cells in the intestinal mucosa. |
| 5147 | 22262068 | Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. |
| 5148 | 22262068 | Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, but interpretation of the precise relationship between disease and incretins is difficult. |
| 5149 | 22262068 | The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are gut peptides which are secreted by endocrine cells in the intestinal mucosa. |
| 5150 | 22262068 | Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. |
| 5151 | 22262068 | Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, but interpretation of the precise relationship between disease and incretins is difficult. |
| 5152 | 22287358 | The changes of many hormones after surgery are different between BPD and RGBP, especially some gastrointestinal hormones such as GLP-1 and GIP,however it cannot be fully explained by the widely known hindgut hypothesis and the foregut hypothesis. |
| 5153 | 22287358 | This review is intended to compare the anatomical structures and postoperative gastrointestinal hormones GLP-1 and GIP changes between the two procedures according to the latest researches in the world, and discussed different mechanisms which may take effect in improving diabetes. |
| 5154 | 22287358 | The changes of many hormones after surgery are different between BPD and RGBP, especially some gastrointestinal hormones such as GLP-1 and GIP,however it cannot be fully explained by the widely known hindgut hypothesis and the foregut hypothesis. |
| 5155 | 22287358 | This review is intended to compare the anatomical structures and postoperative gastrointestinal hormones GLP-1 and GIP changes between the two procedures according to the latest researches in the world, and discussed different mechanisms which may take effect in improving diabetes. |
| 5156 | 22323472 | Glucagon-like peptide-1 (GLP-1) is an incretin hormone that enhances glucose-stimulated insulin secretion and exerts direct and indirect actions on the cardiovascular system. |
| 5157 | 22323472 | GLP-1 and its related incretin hormone, glucose-dependent insulinotropic polypeptide, are rapidly inactivated by the enzyme dipeptidyl peptidase 4 (DPP-4), a key determinant of incretin bioactivity. |
| 5158 | 22323472 | Two classes of medications that enhance incretin action, GLP-1 receptor (GLP-1R) agonists and DPP-4 inhibitors, are used for the treatment of type 2 diabetes mellitus. |
| 5159 | 22323472 | We review herein the cardiovascular biology of GLP-1R agonists and DPP-4 inhibitors, including direct and indirect effects on cardiomyocytes, blood vessels, adipocytes, the control of blood pressure, and postprandial lipoprotein secretion. |
| 5160 | 22323472 | Both GLP-1R activation and DPP-4 inhibition exert multiple cardioprotective actions in preclinical models of cardiovascular dysfunction, and short-term studies in human subjects appear to demonstrate modest yet beneficial actions on cardiac function in subjects with ischemic heart disease. |
| 5161 | 22425330 | They exert their action through inhibition of the catabolism of locally secreted incretins such as glucagon-like peptide-4 (GLP-4) and glucose-dependent insulinotropic polypeptide (GIP) by inhibiting enzyme DPP-4. |
| 5162 | 22425330 | GLP-1 and GIP are secreted from the gastrointestinal tract in response to food intake. |
| 5163 | 22425330 | GLP-1 is secreted from L cells present in the mucosa of the small intestine and colon, whereas GIP is secreted from K cells of the jejunum. |
| 5164 | 22425330 | They exert their action through inhibition of the catabolism of locally secreted incretins such as glucagon-like peptide-4 (GLP-4) and glucose-dependent insulinotropic polypeptide (GIP) by inhibiting enzyme DPP-4. |
| 5165 | 22425330 | GLP-1 and GIP are secreted from the gastrointestinal tract in response to food intake. |
| 5166 | 22425330 | GLP-1 is secreted from L cells present in the mucosa of the small intestine and colon, whereas GIP is secreted from K cells of the jejunum. |
| 5167 | 22425330 | They exert their action through inhibition of the catabolism of locally secreted incretins such as glucagon-like peptide-4 (GLP-4) and glucose-dependent insulinotropic polypeptide (GIP) by inhibiting enzyme DPP-4. |
| 5168 | 22425330 | GLP-1 and GIP are secreted from the gastrointestinal tract in response to food intake. |
| 5169 | 22425330 | GLP-1 is secreted from L cells present in the mucosa of the small intestine and colon, whereas GIP is secreted from K cells of the jejunum. |
| 5170 | 22465882 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) improve markers of cognitive function in obesity-diabetes, however, both are rapidly degraded to their major metabolites, GLP-1(9-36)amide and GIP(3-42), respectively. |
| 5171 | 22465882 | Therefore, the present study investigated effects of GLP-1(9-36)amide and GIP(3-42) on locomotor activity, cognitive function and hippocampal synaptic plasticity in mice with diet-induced obesity and insulin resistance. |
| 5172 | 22465882 | High-fat fed Swiss TO mice treated with GLP-1(9-36)amide, GIP(3-42) or exendin(9-39)amide (twice-daily for 60 days) did not exhibit any changes in bodyweight, non-fasting plasma glucose and plasma insulin concentrations or glucose tolerance compared with high-fat saline controls. |
| 5173 | 22465882 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) improve markers of cognitive function in obesity-diabetes, however, both are rapidly degraded to their major metabolites, GLP-1(9-36)amide and GIP(3-42), respectively. |
| 5174 | 22465882 | Therefore, the present study investigated effects of GLP-1(9-36)amide and GIP(3-42) on locomotor activity, cognitive function and hippocampal synaptic plasticity in mice with diet-induced obesity and insulin resistance. |
| 5175 | 22465882 | High-fat fed Swiss TO mice treated with GLP-1(9-36)amide, GIP(3-42) or exendin(9-39)amide (twice-daily for 60 days) did not exhibit any changes in bodyweight, non-fasting plasma glucose and plasma insulin concentrations or glucose tolerance compared with high-fat saline controls. |
| 5176 | 22465882 | The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) improve markers of cognitive function in obesity-diabetes, however, both are rapidly degraded to their major metabolites, GLP-1(9-36)amide and GIP(3-42), respectively. |
| 5177 | 22465882 | Therefore, the present study investigated effects of GLP-1(9-36)amide and GIP(3-42) on locomotor activity, cognitive function and hippocampal synaptic plasticity in mice with diet-induced obesity and insulin resistance. |
| 5178 | 22465882 | High-fat fed Swiss TO mice treated with GLP-1(9-36)amide, GIP(3-42) or exendin(9-39)amide (twice-daily for 60 days) did not exhibit any changes in bodyweight, non-fasting plasma glucose and plasma insulin concentrations or glucose tolerance compared with high-fat saline controls. |
| 5179 | 22482239 | Linagliptin (Trajenta) is a selective inhibitor of dipeptidyl peptidase-4, an enzyme that degrades two incretin hormones, GLP-1 ("Glucagon-Like Peptide-1") and GIP ("Glucose-dependent Insulinotropic Polypeptide"). |
| 5180 | 22492530 | Transgenic pigs expressing a dominant-negative glucose-dependent insulinotropic polypeptide receptor (GIPR(dn)) reveal progressive deterioration of glucose control and reduction of β-cell mass, providing a unique opportunity to study metabolic changes during the prediabetic period. |
| 5181 | 22522617 | Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes. |
| 5182 | 22522617 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). |
| 5183 | 22522617 | Xenin-25 is a 25-amino acid neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice. |
| 5184 | 22522617 | Although magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored to normal in subjects with IGT and T2DM. |
| 5185 | 22522617 | Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes. |
| 5186 | 22522617 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). |
| 5187 | 22522617 | Xenin-25 is a 25-amino acid neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice. |
| 5188 | 22522617 | Although magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored to normal in subjects with IGT and T2DM. |
| 5189 | 22522617 | Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes. |
| 5190 | 22522617 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). |
| 5191 | 22522617 | Xenin-25 is a 25-amino acid neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice. |
| 5192 | 22522617 | Although magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored to normal in subjects with IGT and T2DM. |
| 5193 | 22522617 | Xenin-25 amplifies GIP-mediated insulin secretion in humans with normal and impaired glucose tolerance but not type 2 diabetes. |
| 5194 | 22522617 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). |
| 5195 | 22522617 | Xenin-25 is a 25-amino acid neurotensin-related peptide that amplifies GIP-mediated GSIS in hyperglycemic mice. |
| 5196 | 22522617 | Although magnitudes of insulin secretory responses to GIP were similar in all groups, ISRs were not restored to normal in subjects with IGT and T2DM. |
| 5197 | 22535748 | Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent-insulinotropic polypeptide (GIP), and glucagon concentrations were measured. |
| 5198 | 22535748 | GIP secretion was unchanged, while GLP-1 secretion increased more than 10-fold in both groups. |
| 5199 | 22535748 | Improvement in glycemic control in T2D after RYGB occurs within days after surgery and is associated with increased insulin sensitivity and improved β-cell function, the latter of which may be explained by dramatic increases in GLP-1 secretion. |
| 5200 | 22535748 | Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent-insulinotropic polypeptide (GIP), and glucagon concentrations were measured. |
| 5201 | 22535748 | GIP secretion was unchanged, while GLP-1 secretion increased more than 10-fold in both groups. |
| 5202 | 22535748 | Improvement in glycemic control in T2D after RYGB occurs within days after surgery and is associated with increased insulin sensitivity and improved β-cell function, the latter of which may be explained by dramatic increases in GLP-1 secretion. |
| 5203 | 22536426 | Glucose-dependent insulinotropic polypeptide prevents the progression of macrophage-driven atherosclerosis in diabetic apolipoprotein E-null mice. |
| 5204 | 22555471 | The ability of the incretin agents (glucagon-like peptide 1 [GLP-1] agonists and dipeptidyl peptidase IV [DPP-4] inhibitors) to improve glycaemia with a low associated risk of hypoglycaemia, together with beneficial/neutral effects on body weight, offers a significant advantage for both patients and treating clinicians. |
| 5205 | 22555471 | In 1986 they first documented a reduced incretin effect in patients with type 2 diabetes (Diabetologia 29:46-52), and then in 1993 they demonstrated that, in patients with poorly controlled type 2 diabetes, a single exogenous infusion of an incretin (GLP-1) increased insulin levels in a glucose-dependent manner and normalised fasting hyperglycaemia (Diabetologia 36:741-744). |
| 5206 | 22555471 | In the ensuing 26 years, progress in the field of incretin hormones has resulted in a greater understanding of the relative roles of GLP-1 and glucose-dependent insulinotropic polypeptide secretion and activity in the pathogenesis of type 2 diabetes and the important recognition that native GLP-1 is quickly degraded by the ubiquitous protease DPP-4. |
| 5207 | 22555471 | This has led to the development of GLP-1 agonists that are resistant to degradation by DPP-4 and of selective inhibitors of DPP-4 activity as therapeutic agents. |
| 5208 | 22555471 | GLP-1 agonists (exenatide and liraglutide) and DPP-4 inhibitors (sitagliptin, vildagliptin, saxagliptin and linagliptin) currently represent effective treatment options for patients with type 2 diabetes. |
| 5209 | 22555471 | Several additional agents are in the pipeline, including longer acting DPP-4-resistant GLP-1 agonists. |
| 5210 | 22561048 | Degradation, insulin secretion, glucose-lowering and GIP additive actions of a palmitate-derivatised analogue of xenin-25. |
| 5211 | 22561048 | Insulinotropic responses of xenin-25(Lys(13)PAL) in clonal beta-cells were similar to native xenin-25, moreover xenin-25(Lys(13)PAL) significantly (p<0.05 to p<0.001) potentiated the insulin releasing action of (D-Ala(2))GIP. |
| 5212 | 22561048 | Degradation, insulin secretion, glucose-lowering and GIP additive actions of a palmitate-derivatised analogue of xenin-25. |
| 5213 | 22561048 | Insulinotropic responses of xenin-25(Lys(13)PAL) in clonal beta-cells were similar to native xenin-25, moreover xenin-25(Lys(13)PAL) significantly (p<0.05 to p<0.001) potentiated the insulin releasing action of (D-Ala(2))GIP. |
| 5214 | 22581648 | GIP receptor was expressed in HUVECs. |
| 5215 | 22581648 | GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. |
| 5216 | 22581648 | GLP-1 also blocked the AGE-induced increase in mRNA levels of vascular cell adhesion molecule-1 (VCAM-1) and plasminogen activator inhibitor-1 in HUVECs. |
| 5217 | 22581648 | In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. |
| 5218 | 22581648 | Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. |
| 5219 | 22581648 | GIP receptor was expressed in HUVECs. |
| 5220 | 22581648 | GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. |
| 5221 | 22581648 | GLP-1 also blocked the AGE-induced increase in mRNA levels of vascular cell adhesion molecule-1 (VCAM-1) and plasminogen activator inhibitor-1 in HUVECs. |
| 5222 | 22581648 | In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. |
| 5223 | 22581648 | Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. |
| 5224 | 22581648 | GIP receptor was expressed in HUVECs. |
| 5225 | 22581648 | GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. |
| 5226 | 22581648 | GLP-1 also blocked the AGE-induced increase in mRNA levels of vascular cell adhesion molecule-1 (VCAM-1) and plasminogen activator inhibitor-1 in HUVECs. |
| 5227 | 22581648 | In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. |
| 5228 | 22581648 | Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. |
| 5229 | 22581648 | GIP receptor was expressed in HUVECs. |
| 5230 | 22581648 | GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. |
| 5231 | 22581648 | GLP-1 also blocked the AGE-induced increase in mRNA levels of vascular cell adhesion molecule-1 (VCAM-1) and plasminogen activator inhibitor-1 in HUVECs. |
| 5232 | 22581648 | In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. |
| 5233 | 22581648 | Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. |
| 5234 | 22659620 | The G protein-coupled receptors (GPCRs) for glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon are emerging as targets to treat both hyperglycemia and obesity. |
| 5235 | 22659620 | GIP is rapidly released from intestinal K-cells following food intake and stimulates glucose-dependent insulin secretion from β-cells and the storage of fat in adipocytes. |
| 5236 | 22659620 | Both GIP receptor agonists and antagonists have been demonstrated to display therapeutic potential to treat diabetes and obesity. |
| 5237 | 22659620 | Similar to GIP, GLP-1 is released from intestinal L-cells following food intake and potentiates glucose-dependent insulin secretion from β-cells. |
| 5238 | 22659620 | Here we review the biology of GIP, GLP-1 and glucagon and examine the various therapeutic strategies to activate and antagonize the receptors of these peptides. |
| 5239 | 22659620 | The G protein-coupled receptors (GPCRs) for glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon are emerging as targets to treat both hyperglycemia and obesity. |
| 5240 | 22659620 | GIP is rapidly released from intestinal K-cells following food intake and stimulates glucose-dependent insulin secretion from β-cells and the storage of fat in adipocytes. |
| 5241 | 22659620 | Both GIP receptor agonists and antagonists have been demonstrated to display therapeutic potential to treat diabetes and obesity. |
| 5242 | 22659620 | Similar to GIP, GLP-1 is released from intestinal L-cells following food intake and potentiates glucose-dependent insulin secretion from β-cells. |
| 5243 | 22659620 | Here we review the biology of GIP, GLP-1 and glucagon and examine the various therapeutic strategies to activate and antagonize the receptors of these peptides. |
| 5244 | 22659620 | The G protein-coupled receptors (GPCRs) for glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon are emerging as targets to treat both hyperglycemia and obesity. |
| 5245 | 22659620 | GIP is rapidly released from intestinal K-cells following food intake and stimulates glucose-dependent insulin secretion from β-cells and the storage of fat in adipocytes. |
| 5246 | 22659620 | Both GIP receptor agonists and antagonists have been demonstrated to display therapeutic potential to treat diabetes and obesity. |
| 5247 | 22659620 | Similar to GIP, GLP-1 is released from intestinal L-cells following food intake and potentiates glucose-dependent insulin secretion from β-cells. |
| 5248 | 22659620 | Here we review the biology of GIP, GLP-1 and glucagon and examine the various therapeutic strategies to activate and antagonize the receptors of these peptides. |
| 5249 | 22659620 | The G protein-coupled receptors (GPCRs) for glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon are emerging as targets to treat both hyperglycemia and obesity. |
| 5250 | 22659620 | GIP is rapidly released from intestinal K-cells following food intake and stimulates glucose-dependent insulin secretion from β-cells and the storage of fat in adipocytes. |
| 5251 | 22659620 | Both GIP receptor agonists and antagonists have been demonstrated to display therapeutic potential to treat diabetes and obesity. |
| 5252 | 22659620 | Similar to GIP, GLP-1 is released from intestinal L-cells following food intake and potentiates glucose-dependent insulin secretion from β-cells. |
| 5253 | 22659620 | Here we review the biology of GIP, GLP-1 and glucagon and examine the various therapeutic strategies to activate and antagonize the receptors of these peptides. |
| 5254 | 22659620 | The G protein-coupled receptors (GPCRs) for glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) and glucagon are emerging as targets to treat both hyperglycemia and obesity. |
| 5255 | 22659620 | GIP is rapidly released from intestinal K-cells following food intake and stimulates glucose-dependent insulin secretion from β-cells and the storage of fat in adipocytes. |
| 5256 | 22659620 | Both GIP receptor agonists and antagonists have been demonstrated to display therapeutic potential to treat diabetes and obesity. |
| 5257 | 22659620 | Similar to GIP, GLP-1 is released from intestinal L-cells following food intake and potentiates glucose-dependent insulin secretion from β-cells. |
| 5258 | 22659620 | Here we review the biology of GIP, GLP-1 and glucagon and examine the various therapeutic strategies to activate and antagonize the receptors of these peptides. |
| 5259 | 22733799 | The incretin effect, reflecting the enhancement of postprandial insulin secretion by factors including the intestinal hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, increases in proportion to meal size. |
| 5260 | 22733799 | These findings indicate that the incretin contribution to postprandial insulin release is independent of glycemia in healthy individuals, despite differences in GLP-1 secretion. |
| 5261 | 22802954 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. |
| 5262 | 22802954 | Since GIP has also been shown to exert β-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). |
| 5263 | 22802954 | In contrast, although GIP Tg mice demonstrated enhanced β-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. |
| 5264 | 22802954 | Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis. |
| 5265 | 22802954 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. |
| 5266 | 22802954 | Since GIP has also been shown to exert β-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). |
| 5267 | 22802954 | In contrast, although GIP Tg mice demonstrated enhanced β-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. |
| 5268 | 22802954 | Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis. |
| 5269 | 22802954 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. |
| 5270 | 22802954 | Since GIP has also been shown to exert β-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). |
| 5271 | 22802954 | In contrast, although GIP Tg mice demonstrated enhanced β-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. |
| 5272 | 22802954 | Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis. |
| 5273 | 22802954 | Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. |
| 5274 | 22802954 | Since GIP has also been shown to exert β-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). |
| 5275 | 22802954 | In contrast, although GIP Tg mice demonstrated enhanced β-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. |
| 5276 | 22802954 | Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis. |
| 5277 | 22879789 | As understanding of the incretin hormones (GLP-1, GIP) expand we may see additional important non-glycemic effects that may affect the chronic management of type 2 diabetes mellitus. |
| 5278 | 22906726 | The aim of this review is to discuss the pathways by which food ingestion triggers secretion of cholecystokinin (CCK), glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and the altered patterns of gut hormone release observed following gastric bypass surgery. |
| 5279 | 22934027 | In addition to insulin and glucagon produced by pancreatic islets, two incretin hormones, namely glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP, also known as glucose-dependent insulinotropic peptide), also play important roles in blood glucose homeostasis. |
| 5280 | 22934027 | Interestingly, TCF7L2 and β-catenin (β-cat), another effector of Wnt signaling pathway, may also mediate the function of the incretin hormones as well as the expression of their receptors in pancreatic β-cells. |
| 5281 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5282 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5283 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5284 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5285 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5286 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5287 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5288 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5289 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5290 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5291 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5292 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5293 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5294 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5295 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5296 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5297 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5298 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5299 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5300 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5301 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5302 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5303 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5304 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5305 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5306 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5307 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5308 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5309 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5310 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5311 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5312 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5313 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5314 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5315 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5316 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5317 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5318 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5319 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5320 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5321 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 5322 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 5323 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 5324 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 5325 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 5326 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 5327 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 5328 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 5329 | 23052340 | Dominant-negative glucose-dependent insulinotropic polypeptide receptor (GIPR(dn)) transgenic mice exhibit defective postnatal islet growth, develop PNDM and progressive diabetes-associated kidney lesions. |
| 5330 | 23056280 | GPR40 (FFAR1 or FFA1) is a G-protein-coupled receptor (GPCR), primarily expressed in insulin-producing pancreatic β-cells and incretin-producing enteroendocrine cells of the small intestine. |
| 5331 | 23056280 | GPR40 full agonists AM-1638 and AM-6226 stimulate GLP-1 and GIP secretion from intestinal enteroendocrine cells and increase GSIS from pancreatic islets, leading to enhanced glucose control in the high fat fed, streptozotocin treated and NONcNZO10/LtJ mouse models of type 2 diabetes. |
| 5332 | 23064014 | A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin. |
| 5333 | 23064014 | Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin. |
| 5334 | 23064014 | The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared. |
| 5335 | 23064014 | It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity. |
| 5336 | 23064014 | A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin. |
| 5337 | 23064014 | Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin. |
| 5338 | 23064014 | The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared. |
| 5339 | 23064014 | It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity. |
| 5340 | 23064014 | A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin. |
| 5341 | 23064014 | Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin. |
| 5342 | 23064014 | The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared. |
| 5343 | 23064014 | It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity. |
| 5344 | 23064014 | A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin. |
| 5345 | 23064014 | Quantitative PCR and liquid chromatography-mass spectrometry proteomic analyses of isolated, FACS-purified CCK-eGFP-positive cells demonstrated expression of not only CCK but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP), peptide YY (PYY), neurotensin, and secretin, but not somatostatin. |
| 5346 | 23064014 | The coexpression pattern was further confirmed through a cell ablation study based on expression of the human diphtheria toxin receptor under the control of the proglucagon promoter, in which activation of the receptor resulted in a marked reduction not only in GLP-1 cells, but also PYY, neurotensin, GIP, CCK, and secretin cells, whereas somatostatin cells were spared. |
| 5347 | 23064014 | It is concluded that a lineage of mature enteroendocrine cells have the ability to coexpress members of a group of functionally related peptides: CCK, secretin, GIP, GLP-1, PYY, and neurotensin, suggesting a potential therapeutic target for the treatment and prevention of diabetes and obesity. |
| 5348 | 23087044 | Islet-associated protein-2 (IA-2) and IA-2β (also known as phogrin) are unique neuroendocrine-specific protein tyrosine phosphatases (PTPs). |
| 5349 | 23087044 | The IA-2 family of PTPs was originally identified from insulinoma cells and discovered to be major autoantigens in type 1 diabetes. |
| 5350 | 23087044 | Despite its expression in the neural and canonical endocrine tissues, data on expression of the IA-2 family of PTPs in gastrointestinal endocrine cells (GECs) are limited. |
| 5351 | 23087044 | Therefore, we immunohistochemically investigated the expression of the IA-2 family of PTPs in the rat gastrointestinal tract. |
| 5352 | 23087044 | In the stomach, IA-2 and IA-2β were expressed in GECs that secrete serotonin, somatostatin, and cholecystokinin/gastrin-1. |
| 5353 | 23087044 | In addition to these hormones, secretin, gastric inhibitory polypeptide (also known as the glucose-dependent insulinotropic peptide), glucagon-like peptide-1, and glucagon, but not ghrelin were coexpressed with IA-2 or IA-2β in duodenal GECs. |
| 5354 | 23087044 | Pancreatic islet cells that secrete gut hormones expressed the IA-2 family of PTPs. |
| 5355 | 23087044 | These results reveal that the IA-2 family of PTPs is expressed in a cell type-specific manner in rat GECs. |
| 5356 | 23087044 | The extensive expression of the IA-2 family of PTPs in pancreo-gastrointestinal endocrine cells and in the enteric plexus suggests their systemic contribution to nutritional control through a neuroendocrine signaling network. |
| 5357 | 23099862 | Ectopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides. |
| 5358 | 23099862 | The Gcg(gfp/gfp) mice displayed improved glucose tolerance and enhanced insulin secretion, as assessed by both oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT). |
| 5359 | 23099862 | Responses of glucose-dependent insulinotropic polypeptide (GIP) to both oral and intraperitoneal glucose loads were unexpectedly enhanced in Gcg(gfp/gfp) mice, and immunohistochemistry localized GIP to pancreatic β-cells of Gcg(gfp/gfp) mice. |
| 5360 | 23099862 | Furthermore, secretion of GIP in response to glucose was detected in isolated islets of Gcg(gfp/gfp) mice. |
| 5361 | 23099862 | Blockade of GIP action in vitro and in vivo by cAMP antagonism and genetic deletion of the GIP receptor, respectively, almost completely abrogated enhanced insulin secretion in Gcg(gfp/gfp) mice. |
| 5362 | 23099862 | These results indicate that ectopic GIP expression in β-cells maintains insulin secretion in the absence of proglucagon-derived peptides (PGDPs), revealing a novel compensatory mechanism for sustaining incretin hormone action in islets. |
| 5363 | 23099862 | Ectopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides. |
| 5364 | 23099862 | The Gcg(gfp/gfp) mice displayed improved glucose tolerance and enhanced insulin secretion, as assessed by both oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT). |
| 5365 | 23099862 | Responses of glucose-dependent insulinotropic polypeptide (GIP) to both oral and intraperitoneal glucose loads were unexpectedly enhanced in Gcg(gfp/gfp) mice, and immunohistochemistry localized GIP to pancreatic β-cells of Gcg(gfp/gfp) mice. |
| 5366 | 23099862 | Furthermore, secretion of GIP in response to glucose was detected in isolated islets of Gcg(gfp/gfp) mice. |
| 5367 | 23099862 | Blockade of GIP action in vitro and in vivo by cAMP antagonism and genetic deletion of the GIP receptor, respectively, almost completely abrogated enhanced insulin secretion in Gcg(gfp/gfp) mice. |
| 5368 | 23099862 | These results indicate that ectopic GIP expression in β-cells maintains insulin secretion in the absence of proglucagon-derived peptides (PGDPs), revealing a novel compensatory mechanism for sustaining incretin hormone action in islets. |
| 5369 | 23099862 | Ectopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides. |
| 5370 | 23099862 | The Gcg(gfp/gfp) mice displayed improved glucose tolerance and enhanced insulin secretion, as assessed by both oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT). |
| 5371 | 23099862 | Responses of glucose-dependent insulinotropic polypeptide (GIP) to both oral and intraperitoneal glucose loads were unexpectedly enhanced in Gcg(gfp/gfp) mice, and immunohistochemistry localized GIP to pancreatic β-cells of Gcg(gfp/gfp) mice. |
| 5372 | 23099862 | Furthermore, secretion of GIP in response to glucose was detected in isolated islets of Gcg(gfp/gfp) mice. |
| 5373 | 23099862 | Blockade of GIP action in vitro and in vivo by cAMP antagonism and genetic deletion of the GIP receptor, respectively, almost completely abrogated enhanced insulin secretion in Gcg(gfp/gfp) mice. |
| 5374 | 23099862 | These results indicate that ectopic GIP expression in β-cells maintains insulin secretion in the absence of proglucagon-derived peptides (PGDPs), revealing a novel compensatory mechanism for sustaining incretin hormone action in islets. |
| 5375 | 23099862 | Ectopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides. |
| 5376 | 23099862 | The Gcg(gfp/gfp) mice displayed improved glucose tolerance and enhanced insulin secretion, as assessed by both oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT). |
| 5377 | 23099862 | Responses of glucose-dependent insulinotropic polypeptide (GIP) to both oral and intraperitoneal glucose loads were unexpectedly enhanced in Gcg(gfp/gfp) mice, and immunohistochemistry localized GIP to pancreatic β-cells of Gcg(gfp/gfp) mice. |
| 5378 | 23099862 | Furthermore, secretion of GIP in response to glucose was detected in isolated islets of Gcg(gfp/gfp) mice. |
| 5379 | 23099862 | Blockade of GIP action in vitro and in vivo by cAMP antagonism and genetic deletion of the GIP receptor, respectively, almost completely abrogated enhanced insulin secretion in Gcg(gfp/gfp) mice. |
| 5380 | 23099862 | These results indicate that ectopic GIP expression in β-cells maintains insulin secretion in the absence of proglucagon-derived peptides (PGDPs), revealing a novel compensatory mechanism for sustaining incretin hormone action in islets. |
| 5381 | 23099862 | Ectopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides. |
| 5382 | 23099862 | The Gcg(gfp/gfp) mice displayed improved glucose tolerance and enhanced insulin secretion, as assessed by both oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT). |
| 5383 | 23099862 | Responses of glucose-dependent insulinotropic polypeptide (GIP) to both oral and intraperitoneal glucose loads were unexpectedly enhanced in Gcg(gfp/gfp) mice, and immunohistochemistry localized GIP to pancreatic β-cells of Gcg(gfp/gfp) mice. |
| 5384 | 23099862 | Furthermore, secretion of GIP in response to glucose was detected in isolated islets of Gcg(gfp/gfp) mice. |
| 5385 | 23099862 | Blockade of GIP action in vitro and in vivo by cAMP antagonism and genetic deletion of the GIP receptor, respectively, almost completely abrogated enhanced insulin secretion in Gcg(gfp/gfp) mice. |
| 5386 | 23099862 | These results indicate that ectopic GIP expression in β-cells maintains insulin secretion in the absence of proglucagon-derived peptides (PGDPs), revealing a novel compensatory mechanism for sustaining incretin hormone action in islets. |
| 5387 | 23103794 | The incretin analogue D-Ala2GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease. |
| 5388 | 23103794 | Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, normalises insulin signalling and also acts as a neuroprotective growth factor. |
| 5389 | 23103794 | D-Ala(2)GIP was injected for 35 days at 25 nmol/kg i.p. once daily in APP/PS1 male mice and wild-type (WT) littermates aged 6, 12 and 19 months. |
| 5390 | 23103794 | D-Ala(2)GIP reduced the amyloid plaque load in 12- and 19-month-old mice, and the inflammation response as shown in the reduction of activated astrocytes in 12- and 19-month old APP/PS1 mice. |
| 5391 | 23103794 | Chronic oxidative stress in the brain was reduced in 12- and 19-month-old mice as shown in the reduction of 8-oxoguanine levels in the cortex of D-Ala(2)GIP-injected APP/PS1 mice. |
| 5392 | 23103794 | The incretin analogue D-Ala2GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease. |
| 5393 | 23103794 | Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, normalises insulin signalling and also acts as a neuroprotective growth factor. |
| 5394 | 23103794 | D-Ala(2)GIP was injected for 35 days at 25 nmol/kg i.p. once daily in APP/PS1 male mice and wild-type (WT) littermates aged 6, 12 and 19 months. |
| 5395 | 23103794 | D-Ala(2)GIP reduced the amyloid plaque load in 12- and 19-month-old mice, and the inflammation response as shown in the reduction of activated astrocytes in 12- and 19-month old APP/PS1 mice. |
| 5396 | 23103794 | Chronic oxidative stress in the brain was reduced in 12- and 19-month-old mice as shown in the reduction of 8-oxoguanine levels in the cortex of D-Ala(2)GIP-injected APP/PS1 mice. |
| 5397 | 23103794 | The incretin analogue D-Ala2GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease. |
| 5398 | 23103794 | Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, normalises insulin signalling and also acts as a neuroprotective growth factor. |
| 5399 | 23103794 | D-Ala(2)GIP was injected for 35 days at 25 nmol/kg i.p. once daily in APP/PS1 male mice and wild-type (WT) littermates aged 6, 12 and 19 months. |
| 5400 | 23103794 | D-Ala(2)GIP reduced the amyloid plaque load in 12- and 19-month-old mice, and the inflammation response as shown in the reduction of activated astrocytes in 12- and 19-month old APP/PS1 mice. |
| 5401 | 23103794 | Chronic oxidative stress in the brain was reduced in 12- and 19-month-old mice as shown in the reduction of 8-oxoguanine levels in the cortex of D-Ala(2)GIP-injected APP/PS1 mice. |
| 5402 | 23103794 | The incretin analogue D-Ala2GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease. |
| 5403 | 23103794 | Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, normalises insulin signalling and also acts as a neuroprotective growth factor. |
| 5404 | 23103794 | D-Ala(2)GIP was injected for 35 days at 25 nmol/kg i.p. once daily in APP/PS1 male mice and wild-type (WT) littermates aged 6, 12 and 19 months. |
| 5405 | 23103794 | D-Ala(2)GIP reduced the amyloid plaque load in 12- and 19-month-old mice, and the inflammation response as shown in the reduction of activated astrocytes in 12- and 19-month old APP/PS1 mice. |
| 5406 | 23103794 | Chronic oxidative stress in the brain was reduced in 12- and 19-month-old mice as shown in the reduction of 8-oxoguanine levels in the cortex of D-Ala(2)GIP-injected APP/PS1 mice. |
| 5407 | 23125920 | The incretin therapies focus on the increasing levels of the two incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 5408 | 23125920 | DPP-4 inhibitors such as sitagliptin and linagliptin prevent the inactivation of endogenous GLP-1 and GIP through competitive inhibition of the DPP-4 enzyme. |
| 5409 | 23125920 | The incretin therapies focus on the increasing levels of the two incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). |
| 5410 | 23125920 | DPP-4 inhibitors such as sitagliptin and linagliptin prevent the inactivation of endogenous GLP-1 and GIP through competitive inhibition of the DPP-4 enzyme. |
| 5411 | 23159576 | GLP-1 and GIP are insulinotropic peptides which are thought to benefit to β-cell physiology. |
| 5412 | 23208416 | Menin and GIP are inversely regulated by food intake and diet via PI3/AKT signaling in the proximal duodenum. |
| 5413 | 23319869 | DPP-4 inhibitors act by increasing endogenous GLP-1 and GIP concentrations. |
| 5414 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5415 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5416 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5417 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5418 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5419 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5420 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5421 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5422 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5423 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5424 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5425 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5426 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5427 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5428 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5429 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5430 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5431 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5432 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5433 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5434 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5435 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5436 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5437 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5438 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5439 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5440 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5441 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5442 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5443 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5444 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5445 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5446 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5447 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5448 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5449 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5450 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5451 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5452 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5453 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5454 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5455 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5456 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5457 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5458 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5459 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5460 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5461 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5462 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5463 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5464 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5465 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5466 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5467 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5468 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5469 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5470 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5471 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5472 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5473 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5474 | 23349498 | Link between GIP and osteopontin in adipose tissue and insulin resistance. |
| 5475 | 23349498 | Low-grade inflammation in obesity is associated with accumulation of the macrophage-derived cytokine osteopontin (OPN) in adipose tissue and induction of local as well as systemic insulin resistance. |
| 5476 | 23349498 | Since glucose-dependent insulinotropic polypeptide (GIP) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate OPN expression in adipose tissue and thereby induce insulin resistance. |
| 5477 | 23349498 | GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. |
| 5478 | 23349498 | The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13 ± 0.04 vs. 0.04 ± 0.01, P < 0.05) and correlated inversely with measures of insulin sensitivity (r = -0.24, P = 0.001). |
| 5479 | 23349498 | A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with a lower amount of the exon 9-containing isoform required for transmembrane activity. |
| 5480 | 23349498 | Carriers of the A allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. |
| 5481 | 23349498 | Together, these data suggest a role for GIP not only as an incretin hormone but also as a trigger of inflammation and insulin resistance in adipose tissue. |
| 5482 | 23349498 | Carriers of the GIPR rs10423928 A allele showed protective properties via reduced GIP effects. |
| 5483 | 23349498 | Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions. |
| 5484 | 23478327 | We describe mechanisms of action for combinations of glucagon-like peptide 1, glucagon, gastric inhibitory polypeptide, gastrin, islet amyloid polypeptide and leptin, which enhance weight loss whilst preserving glucoregulatory efficacy in experimental models of obesity and T2DM. |
| 5485 | 23487174 | LX4211 increases serum glucagon-like peptide 1 and peptide YY levels by reducing sodium/glucose cotransporter 1 (SGLT1)-mediated absorption of intestinal glucose. |
| 5486 | 23487174 | LX4211 [(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-2H-pyran-3,4,5-triol], a dual sodium/glucose cotransporter 1 (SGLT1) and SGLT2 inhibitor, is thought to decrease both renal glucose reabsorption by inhibiting SGLT2 and intestinal glucose absorption by inhibiting SGLT1. |
| 5487 | 23487174 | In clinical trials in patients with type 2 diabetes mellitus (T2DM), LX4211 treatment improved glycemic control while increasing circulating levels of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). |
| 5488 | 23487174 | To better understand how LX4211 increases GLP-1 and PYY levels, we challenged SGLT1 knockout (-/-) mice, SGLT2-/- mice, and LX4211-treated mice with oral glucose. |
| 5489 | 23487174 | LX4211-treated mice and SGLT1-/- mice had increased levels of plasma GLP-1, plasma PYY, and intestinal glucose during the 6 hours after a glucose-containing meal, as reflected by area under the curve (AUC) values, whereas SGLT2-/- mice showed no response. |
| 5490 | 23487174 | LX4211-treated mice and SGLT1-/- mice also had increased GLP-1 AUC values, decreased glucose-dependent insulinotropic polypeptide (GIP) AUC values, and decreased blood glucose excursions during the 6 hours after a challenge with oral glucose alone. |
| 5491 | 23487174 | However, GLP-1 and GIP levels were not increased in LX4211-treated mice and were decreased in SGLT1-/- mice, 5 minutes after oral glucose, consistent with studies linking decreased intestinal SGLT1 activity with reduced GLP-1 and GIP levels 5 minutes after oral glucose. |
| 5492 | 23487174 | These data suggest that LX4211 reduces intestinal glucose absorption by inhibiting SGLT1, resulting in net increases in GLP-1 and PYY release and decreases in GIP release and blood glucose excursions. |
| 5493 | 23487174 | The ability to inhibit both intestinal SGLT1 and renal SGLT2 provides LX4211 with a novel dual mechanism of action for improving glycemic control in patients with T2DM. |
| 5494 | 23487174 | LX4211 increases serum glucagon-like peptide 1 and peptide YY levels by reducing sodium/glucose cotransporter 1 (SGLT1)-mediated absorption of intestinal glucose. |
| 5495 | 23487174 | LX4211 [(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-2H-pyran-3,4,5-triol], a dual sodium/glucose cotransporter 1 (SGLT1) and SGLT2 inhibitor, is thought to decrease both renal glucose reabsorption by inhibiting SGLT2 and intestinal glucose absorption by inhibiting SGLT1. |
| 5496 | 23487174 | In clinical trials in patients with type 2 diabetes mellitus (T2DM), LX4211 treatment improved glycemic control while increasing circulating levels of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). |
| 5497 | 23487174 | To better understand how LX4211 increases GLP-1 and PYY levels, we challenged SGLT1 knockout (-/-) mice, SGLT2-/- mice, and LX4211-treated mice with oral glucose. |
| 5498 | 23487174 | LX4211-treated mice and SGLT1-/- mice had increased levels of plasma GLP-1, plasma PYY, and intestinal glucose during the 6 hours after a glucose-containing meal, as reflected by area under the curve (AUC) values, whereas SGLT2-/- mice showed no response. |
| 5499 | 23487174 | LX4211-treated mice and SGLT1-/- mice also had increased GLP-1 AUC values, decreased glucose-dependent insulinotropic polypeptide (GIP) AUC values, and decreased blood glucose excursions during the 6 hours after a challenge with oral glucose alone. |
| 5500 | 23487174 | However, GLP-1 and GIP levels were not increased in LX4211-treated mice and were decreased in SGLT1-/- mice, 5 minutes after oral glucose, consistent with studies linking decreased intestinal SGLT1 activity with reduced GLP-1 and GIP levels 5 minutes after oral glucose. |
| 5501 | 23487174 | These data suggest that LX4211 reduces intestinal glucose absorption by inhibiting SGLT1, resulting in net increases in GLP-1 and PYY release and decreases in GIP release and blood glucose excursions. |
| 5502 | 23487174 | The ability to inhibit both intestinal SGLT1 and renal SGLT2 provides LX4211 with a novel dual mechanism of action for improving glycemic control in patients with T2DM. |
| 5503 | 23487174 | LX4211 increases serum glucagon-like peptide 1 and peptide YY levels by reducing sodium/glucose cotransporter 1 (SGLT1)-mediated absorption of intestinal glucose. |
| 5504 | 23487174 | LX4211 [(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-2H-pyran-3,4,5-triol], a dual sodium/glucose cotransporter 1 (SGLT1) and SGLT2 inhibitor, is thought to decrease both renal glucose reabsorption by inhibiting SGLT2 and intestinal glucose absorption by inhibiting SGLT1. |
| 5505 | 23487174 | In clinical trials in patients with type 2 diabetes mellitus (T2DM), LX4211 treatment improved glycemic control while increasing circulating levels of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). |
| 5506 | 23487174 | To better understand how LX4211 increases GLP-1 and PYY levels, we challenged SGLT1 knockout (-/-) mice, SGLT2-/- mice, and LX4211-treated mice with oral glucose. |
| 5507 | 23487174 | LX4211-treated mice and SGLT1-/- mice had increased levels of plasma GLP-1, plasma PYY, and intestinal glucose during the 6 hours after a glucose-containing meal, as reflected by area under the curve (AUC) values, whereas SGLT2-/- mice showed no response. |
| 5508 | 23487174 | LX4211-treated mice and SGLT1-/- mice also had increased GLP-1 AUC values, decreased glucose-dependent insulinotropic polypeptide (GIP) AUC values, and decreased blood glucose excursions during the 6 hours after a challenge with oral glucose alone. |
| 5509 | 23487174 | However, GLP-1 and GIP levels were not increased in LX4211-treated mice and were decreased in SGLT1-/- mice, 5 minutes after oral glucose, consistent with studies linking decreased intestinal SGLT1 activity with reduced GLP-1 and GIP levels 5 minutes after oral glucose. |
| 5510 | 23487174 | These data suggest that LX4211 reduces intestinal glucose absorption by inhibiting SGLT1, resulting in net increases in GLP-1 and PYY release and decreases in GIP release and blood glucose excursions. |
| 5511 | 23487174 | The ability to inhibit both intestinal SGLT1 and renal SGLT2 provides LX4211 with a novel dual mechanism of action for improving glycemic control in patients with T2DM. |
| 5512 | 23503814 | A DPP-IV-resistant triple-acting agonist of GIP, GLP-1 and glucagon receptors with potent glucose-lowering and insulinotropic actions in high-fat-fed mice. |
| 5513 | 23518155 | A novel GIP-oxyntomodulin hybrid peptide acting through GIP, glucagon and GLP-1 receptors exhibits weight reducing and anti-diabetic properties. |
| 5514 | 23518155 | GIP is the principle physiological regulator of postprandial insulin secretion. |
| 5515 | 23518155 | Therefore, the primary aim was to design a novel GIP-Oxm peptide incorporating the actions of GIP, GLP-1 and glucagon in a single molecule. |
| 5516 | 23518155 | The first 11 N-terminal residues of Oxm were substituted with the sequence of stable dA(2)GIP molecule to generate a novel GIP-Oxm peptide (dA(2)GIP-Oxm). dA(2)GIP-Oxm was resistant to DPP-IV and significantly stimulated in vitro insulin release. dA(2)GIP-Oxm stimulated cAMP production in GIP-R, glucagon-R and GLP-1-R transfected cells by up to 95%, 83% and 77% of that elicited by respective native ligands. |
| 5517 | 23518155 | These improvements in metabolic control were independent of changes in food intake and insulin sensitivity. dA(2)GIP-Oxm exerts positive beneficial actions on glucose homeostasis, beta-cell insulin secretion and body weight, mediated through GIP, glucagon and GLP-1 receptors. |
| 5518 | 23518155 | A novel GIP-oxyntomodulin hybrid peptide acting through GIP, glucagon and GLP-1 receptors exhibits weight reducing and anti-diabetic properties. |
| 5519 | 23518155 | GIP is the principle physiological regulator of postprandial insulin secretion. |
| 5520 | 23518155 | Therefore, the primary aim was to design a novel GIP-Oxm peptide incorporating the actions of GIP, GLP-1 and glucagon in a single molecule. |
| 5521 | 23518155 | The first 11 N-terminal residues of Oxm were substituted with the sequence of stable dA(2)GIP molecule to generate a novel GIP-Oxm peptide (dA(2)GIP-Oxm). dA(2)GIP-Oxm was resistant to DPP-IV and significantly stimulated in vitro insulin release. dA(2)GIP-Oxm stimulated cAMP production in GIP-R, glucagon-R and GLP-1-R transfected cells by up to 95%, 83% and 77% of that elicited by respective native ligands. |
| 5522 | 23518155 | These improvements in metabolic control were independent of changes in food intake and insulin sensitivity. dA(2)GIP-Oxm exerts positive beneficial actions on glucose homeostasis, beta-cell insulin secretion and body weight, mediated through GIP, glucagon and GLP-1 receptors. |
| 5523 | 23518155 | A novel GIP-oxyntomodulin hybrid peptide acting through GIP, glucagon and GLP-1 receptors exhibits weight reducing and anti-diabetic properties. |
| 5524 | 23518155 | GIP is the principle physiological regulator of postprandial insulin secretion. |
| 5525 | 23518155 | Therefore, the primary aim was to design a novel GIP-Oxm peptide incorporating the actions of GIP, GLP-1 and glucagon in a single molecule. |
| 5526 | 23518155 | The first 11 N-terminal residues of Oxm were substituted with the sequence of stable dA(2)GIP molecule to generate a novel GIP-Oxm peptide (dA(2)GIP-Oxm). dA(2)GIP-Oxm was resistant to DPP-IV and significantly stimulated in vitro insulin release. dA(2)GIP-Oxm stimulated cAMP production in GIP-R, glucagon-R and GLP-1-R transfected cells by up to 95%, 83% and 77% of that elicited by respective native ligands. |
| 5527 | 23518155 | These improvements in metabolic control were independent of changes in food intake and insulin sensitivity. dA(2)GIP-Oxm exerts positive beneficial actions on glucose homeostasis, beta-cell insulin secretion and body weight, mediated through GIP, glucagon and GLP-1 receptors. |
| 5528 | 23518155 | A novel GIP-oxyntomodulin hybrid peptide acting through GIP, glucagon and GLP-1 receptors exhibits weight reducing and anti-diabetic properties. |
| 5529 | 23518155 | GIP is the principle physiological regulator of postprandial insulin secretion. |
| 5530 | 23518155 | Therefore, the primary aim was to design a novel GIP-Oxm peptide incorporating the actions of GIP, GLP-1 and glucagon in a single molecule. |
| 5531 | 23518155 | The first 11 N-terminal residues of Oxm were substituted with the sequence of stable dA(2)GIP molecule to generate a novel GIP-Oxm peptide (dA(2)GIP-Oxm). dA(2)GIP-Oxm was resistant to DPP-IV and significantly stimulated in vitro insulin release. dA(2)GIP-Oxm stimulated cAMP production in GIP-R, glucagon-R and GLP-1-R transfected cells by up to 95%, 83% and 77% of that elicited by respective native ligands. |
| 5532 | 23518155 | These improvements in metabolic control were independent of changes in food intake and insulin sensitivity. dA(2)GIP-Oxm exerts positive beneficial actions on glucose homeostasis, beta-cell insulin secretion and body weight, mediated through GIP, glucagon and GLP-1 receptors. |
| 5533 | 23518155 | A novel GIP-oxyntomodulin hybrid peptide acting through GIP, glucagon and GLP-1 receptors exhibits weight reducing and anti-diabetic properties. |
| 5534 | 23518155 | GIP is the principle physiological regulator of postprandial insulin secretion. |
| 5535 | 23518155 | Therefore, the primary aim was to design a novel GIP-Oxm peptide incorporating the actions of GIP, GLP-1 and glucagon in a single molecule. |
| 5536 | 23518155 | The first 11 N-terminal residues of Oxm were substituted with the sequence of stable dA(2)GIP molecule to generate a novel GIP-Oxm peptide (dA(2)GIP-Oxm). dA(2)GIP-Oxm was resistant to DPP-IV and significantly stimulated in vitro insulin release. dA(2)GIP-Oxm stimulated cAMP production in GIP-R, glucagon-R and GLP-1-R transfected cells by up to 95%, 83% and 77% of that elicited by respective native ligands. |
| 5537 | 23518155 | These improvements in metabolic control were independent of changes in food intake and insulin sensitivity. dA(2)GIP-Oxm exerts positive beneficial actions on glucose homeostasis, beta-cell insulin secretion and body weight, mediated through GIP, glucagon and GLP-1 receptors. |
| 5538 | 23522180 | Incretins (gastric inhibitory polypeptide and glucagon-like peptide 1 [GLP-1]) are hormones released from the gastrointestinal tract during food intake that potentiate insulin secretion. |
| 5539 | 23522180 | Native GLP-1 is quickly degraded by the enzyme dipeptidylpeptidase-4 (DPP-4), which has led to the development of GLP-1 agonists with resistance to degradation and to inhibitors of DPP-4 activity as therapeutic agents in humans with type 2 diabetes. |
| 5540 | 23522180 | In healthy cats, GLP-1 agonists and DPP-4 inhibitors have produced a substantial increase in insulin secretion. |
| 5541 | 23523778 | GLP-1 and another gut peptide, glucose-dependent insulinotropic polypeptide (GIP) are collectively referred to as 'incretin' hormones, and play an important role in glucose homeostasis. |
| 5542 | 23564338 | Mechanistic studies in healthy volunteers suggest that pasireotide-associated hyperglycemia is due to reduced secretion of glucagon-like peptide (GLP)-1, glucose-dependent insulinotropic polypeptide, and insulin; however, it is associated with intact postprandial glucagon secretion. |
| 5543 | 23564338 | Diabetes mellitus should be managed by initiation of medical therapy with metformin and staged treatment intensification with a dipeptidyl peptidase-4 inhibitor, with a switch to a GLP-1 receptor agonist and initiation of insulin, as required, to achieve and maintain glycemic control. |
| 5544 | 23601582 | Neuroprotective effects of D-Ala(2)GIP on Alzheimer's disease biomarkers in an APP/PS1 mouse model. |
| 5545 | 23643349 | The incretin effect is largely due to the release and action on beta-cells of the gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 5546 | 23643349 | Although the reports in the literature are mixed, most studies of GIP and GLP-1 secretory responses to oral glucose or a mixed meal have shown fairly normal results in type 2 diabetes. |
| 5547 | 23643349 | In contrast, the insulinotropic effects of both GIP and GLP-1 are impaired in type 2 diabetes with greater suppression of insulin secretion augmentation with GIP than with GLP-1. |
| 5548 | 23643349 | The incretin effect is largely due to the release and action on beta-cells of the gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 5549 | 23643349 | Although the reports in the literature are mixed, most studies of GIP and GLP-1 secretory responses to oral glucose or a mixed meal have shown fairly normal results in type 2 diabetes. |
| 5550 | 23643349 | In contrast, the insulinotropic effects of both GIP and GLP-1 are impaired in type 2 diabetes with greater suppression of insulin secretion augmentation with GIP than with GLP-1. |
| 5551 | 23643349 | The incretin effect is largely due to the release and action on beta-cells of the gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). |
| 5552 | 23643349 | Although the reports in the literature are mixed, most studies of GIP and GLP-1 secretory responses to oral glucose or a mixed meal have shown fairly normal results in type 2 diabetes. |
| 5553 | 23643349 | In contrast, the insulinotropic effects of both GIP and GLP-1 are impaired in type 2 diabetes with greater suppression of insulin secretion augmentation with GIP than with GLP-1. |
| 5554 | 23645229 | Dipeptidyl peptidase-4 (DPP-4 or CD26) inhibitors, a new class of oral anti-hyperglycemic agents that prolong the bioavailability of the endogenously secreted incretin hormone glucagon-like peptide-1 (GLP-1) and the glucose-dependent insulinotropic polypeptide (GIP), are effective in the treatment of diabetes. |
| 5555 | 23683065 | Dipeptidyl peptidase (DPP)-4 inhibitors are a new class of antidiabetic agents that reduce blood glucose by preventing the degradation of the endogenous incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. |
| 5556 | 23684623 | Incretin peptides, principally GLP-1 and GIP, regulate islet hormone secretion, glucose concentrations, lipid metabolism, gut motility, appetite and body weight, and immune function, providing a scientific basis for utilizing incretin-based therapies in the treatment of type 2 diabetes. |
| 5557 | 23684623 | Activation of GLP-1 and GIP receptors also leads to nonglycemic effects in multiple tissues, through direct actions on tissues expressing incretin receptors and indirect mechanisms mediated through neuronal and endocrine pathways. |
| 5558 | 23684623 | Incretin peptides, principally GLP-1 and GIP, regulate islet hormone secretion, glucose concentrations, lipid metabolism, gut motility, appetite and body weight, and immune function, providing a scientific basis for utilizing incretin-based therapies in the treatment of type 2 diabetes. |
| 5559 | 23684623 | Activation of GLP-1 and GIP receptors also leads to nonglycemic effects in multiple tissues, through direct actions on tissues expressing incretin receptors and indirect mechanisms mediated through neuronal and endocrine pathways. |
| 5560 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5561 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5562 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5563 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5564 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5565 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5566 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5567 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5568 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5569 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5570 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5571 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5572 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5573 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5574 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5575 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5576 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5577 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5578 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5579 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5580 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5581 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5582 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5583 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5584 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5585 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5586 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5587 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5588 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5589 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5590 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5591 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5592 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5593 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5594 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5595 | 23689510 | Glucose-dependent insulinotropic polypeptide (GIP) is an endogenous hormonal factor (incretin) that, upon binding to its receptor (GIPr; a class B G-protein-coupled receptor), stimulates insulin secretion by beta cells in the pancreas. |
| 5596 | 23689510 | There has been a lack of potent inhibitors of the GIPr with prolonged in vivo exposure to support studies on GIP biology. |
| 5597 | 23689510 | Gipg013 is a specific competitive antagonist with equally high potencies to mouse, rat, dog, and human GIP receptors with a Ki of 7 nm for the human GIPr. |
| 5598 | 23689510 | Gipg013 antagonizes the GIP receptor and inhibits GIP-induced insulin secretion in vitro and in vivo. |
| 5599 | 23689510 | A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal α-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. |
| 5600 | 23689510 | The antibody epitope overlaps with the GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor. |
| 5601 | 23689510 | This well characterized antagonizing antibody to the GIPr will be useful as a tool to further understand the biological roles of GIP. |
| 5602 | 23697612 | Type 2 diabetes patients have dysfunction in incretin hormones (as glucagon-like peptide-1 or GLP-1, and glucose-dependent insulinotropic polypeptide or GIP). |
| 5603 | 23697612 | By inhibiting the dipeptidyl peptidase-4 (DPP-4) enzyme, it is possible to slow the inactivation of GLP-1 and GIP, promoting blood glucose level reduction in a glucose-dependent manner. |
| 5604 | 23697612 | Type 2 diabetes patients have dysfunction in incretin hormones (as glucagon-like peptide-1 or GLP-1, and glucose-dependent insulinotropic polypeptide or GIP). |
| 5605 | 23697612 | By inhibiting the dipeptidyl peptidase-4 (DPP-4) enzyme, it is possible to slow the inactivation of GLP-1 and GIP, promoting blood glucose level reduction in a glucose-dependent manner. |
| 5606 | 23707531 | The incretin hormones such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released from the small intestine into the vasculature during a meal, and these incretins have a potential to release insulin from pancreatic beta cells of islets of Langerhans, affording a glucose-lowering action. |
| 5607 | 23707531 | Inhibitors of DPP-4, therefore, enhance the bioavailability of GLP-1 and GIP, and thus have been approved for better glycemic management in patients afflicted with type 2 diabetes mellitus (T2DM). |
| 5608 | 23707531 | The incretin hormones such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released from the small intestine into the vasculature during a meal, and these incretins have a potential to release insulin from pancreatic beta cells of islets of Langerhans, affording a glucose-lowering action. |
| 5609 | 23707531 | Inhibitors of DPP-4, therefore, enhance the bioavailability of GLP-1 and GIP, and thus have been approved for better glycemic management in patients afflicted with type 2 diabetes mellitus (T2DM). |
| 5610 | 23788637 | We have used in vitro and in vivo systems to show that FoxO1, an integrator of metabolic stimuli, inhibits PPARγ expression in β-cells, thus transcription of its target genes (Pdx1, glucose-dependent insulinotropic polypeptide (GIP) receptor, and pyruvate carboxylase) that are important regulators of β-cell function, survival, and compensation. |
| 5611 | 23818527 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones that control the secretion of insulin, glucagon, and somatostatin to facilitate glucose disposal. |
| 5612 | 23818527 | GLP-1 and GIP promote β-cell proliferation and survival in rodents. |
| 5613 | 23818527 | GLP-1 and GIP exert their actions predominantly through unique G protein-coupled receptors expressed on β-cells and other pancreatic cell types. |
| 5614 | 23818527 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones that control the secretion of insulin, glucagon, and somatostatin to facilitate glucose disposal. |
| 5615 | 23818527 | GLP-1 and GIP promote β-cell proliferation and survival in rodents. |
| 5616 | 23818527 | GLP-1 and GIP exert their actions predominantly through unique G protein-coupled receptors expressed on β-cells and other pancreatic cell types. |
| 5617 | 23818527 | Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretin hormones that control the secretion of insulin, glucagon, and somatostatin to facilitate glucose disposal. |
| 5618 | 23818527 | GLP-1 and GIP promote β-cell proliferation and survival in rodents. |
| 5619 | 23818527 | GLP-1 and GIP exert their actions predominantly through unique G protein-coupled receptors expressed on β-cells and other pancreatic cell types. |
| 5620 | 23834050 | In addition to these alterations, we must also consider the changes observed in incretins profiles like GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide 1) directly related to glucose homeostasis maintenance. |
| 5621 | 23835687 | The effect of exogenous glucose-dependent insulinotropic polypeptide in combination with glucagon-like peptide-1 on glycemia in the critically ill. |
| 5622 | 23859800 | In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect (that is, higher insulin release in response to an oral glucose challenge compared to an equal intravenous glucose load). |
| 5623 | 23859800 | Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, and the loss of incretin effect is likely to contribute importantly to the postprandial hyperglycaemia in type 2 diabetes. |
| 5624 | 23859800 | In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect (that is, higher insulin release in response to an oral glucose challenge compared to an equal intravenous glucose load). |
| 5625 | 23859800 | Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, and the loss of incretin effect is likely to contribute importantly to the postprandial hyperglycaemia in type 2 diabetes. |
| 5626 | 23939544 | Glucose excursions, insulin secretion rates (ISRs), and levels of glucagon, endogenous GLP-1, and gastric inhibitory polypeptide were measured after the meal or glucose loads. |
| 5627 | 24018562 | Pancreatic β cell dysfunction is pathognomonic of type 2 diabetes mellitus (T2DM) and is driven by environmental and genetic factors. β cell responses to glucose and to incretins such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are altered in the disease state. |
| 5628 | 24018562 | We found that GLP-1 and GIP recruit a highly coordinated subnetwork of β cells that are targeted by lipotoxicity to suppress insulin secretion. |
| 5629 | 24018562 | Pancreatic β cell dysfunction is pathognomonic of type 2 diabetes mellitus (T2DM) and is driven by environmental and genetic factors. β cell responses to glucose and to incretins such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are altered in the disease state. |
| 5630 | 24018562 | We found that GLP-1 and GIP recruit a highly coordinated subnetwork of β cells that are targeted by lipotoxicity to suppress insulin secretion. |