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Gene Information
Gene symbol: SST
Gene name: somatostatin
HGNC ID: 11329
Synonyms: SMST
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 5326 | Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. |
| 2 | 44799 | The different mode of secretion of the gut hormones (paracrine secretion--somatostatin. endocrine and neurocrine secretion--gastrin, CCK; neurocrine secretion--VIP, substance P), obscures the physiological significance of these hormones. |
| 3 | 45064 | Hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 4 | 45064 | The aim of the present study was to evaluate possible hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 5 | 45064 | For this purpose, 7 insulin-requiring juvenile-onset diabetics were submitted to a short-term infusion of cyclic somatostatin (250 micrograms/h, over 2 h) or saline in randomized order. |
| 6 | 45064 | We conclude that somatostatin exerts a negative inotropic effect in insulin-dependent diabetes. |
| 7 | 45064 | Hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 8 | 45064 | The aim of the present study was to evaluate possible hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 9 | 45064 | For this purpose, 7 insulin-requiring juvenile-onset diabetics were submitted to a short-term infusion of cyclic somatostatin (250 micrograms/h, over 2 h) or saline in randomized order. |
| 10 | 45064 | We conclude that somatostatin exerts a negative inotropic effect in insulin-dependent diabetes. |
| 11 | 45064 | Hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 12 | 45064 | The aim of the present study was to evaluate possible hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 13 | 45064 | For this purpose, 7 insulin-requiring juvenile-onset diabetics were submitted to a short-term infusion of cyclic somatostatin (250 micrograms/h, over 2 h) or saline in randomized order. |
| 14 | 45064 | We conclude that somatostatin exerts a negative inotropic effect in insulin-dependent diabetes. |
| 15 | 45064 | Hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 16 | 45064 | The aim of the present study was to evaluate possible hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. |
| 17 | 45064 | For this purpose, 7 insulin-requiring juvenile-onset diabetics were submitted to a short-term infusion of cyclic somatostatin (250 micrograms/h, over 2 h) or saline in randomized order. |
| 18 | 45064 | We conclude that somatostatin exerts a negative inotropic effect in insulin-dependent diabetes. |
| 19 | 55530 | In three patients 2 to 3 h somatostatin infusions were twice superimposed upon a continuous 9-5 h insulin infusion (1 unit/h). |
| 20 | 62113 | A double immunofluorescence technique, with antisera to pancreatic glucagon, insulin, somatostatin, and human pancreatic polypeptide was used to show that 13 of the sera contained anitbodies reacting specifically with glucagon cells, while the other 4 reacted with somatostatin cells. |
| 21 | 63040 | Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. |
| 22 | 83463 | Several commercial insulin preparations were found to contain significant quantities of pancreatic glucagon, pancreatic polypeptide (P.P.), vasoactive intestinal peptide (V.I.P.), and somatostatin, though these substances were effectively absent from the new highly purified or monocomponent insulins. |
| 23 | 99048 | We studied the morphology of intraportally transplanted islets with the aid of the immunoperoxidase staining technique to identify insulin-, glucagon-, somatostatin-, and pancreatic polypeptide-containing cells at 24 hours, 48 hours, 1 week, 2 weeks, 4 weeks, 39 weeks, and 65 weeks after transplant. |
| 24 | 106734 | Insulin dependence of paradoxical overeating: effect of mannoheptulose, somatostatin, and cycloheximide. |
| 25 | 113327 | Efficacy of combined insulin and somatostatin infusion for the treatment of experimental diabetic ketoacidosis. |
| 26 | 130991 | Insulin-, glucagon-, and somatostatin-containing cells were evaluated by morphometry in sections of pancreas treated for immunofluorescence. |
| 27 | 131313 | Insulin-, glucagon-, and somatostatin-contianing cells, identified by immunofluorescent staining, were quantitated morphometrically in sections of pancreas obtained from diabetic and nondiabetic humans and rats. |
| 28 | 149656 | By the enzyme-labeled antibody method, cells containing somatostatin (SRIF) as well as insulin or glucagon were identified in pancreatic islets of the rat. |
| 29 | 158032 | Plasma somatostatin immunoreactivity (SIR) was elevated 40-fold in an insulin-treated diabetic with disseminated pancreatic carcinoma. |
| 30 | 169176 | Effects of somatostatin on plasma GH, insulin, and glucagon in sheep. |
| 31 | 169176 | To determine whether synthetic somatostatin originally isolated from sheep hypothalamus can inhibit hormone secretion in the same species, we measured plasma levels of GH, insulin, glucagon, and glucose of normal sheep under a variety of experimental conditions in the presence and absence of somatostatin infusion. |
| 32 | 169176 | Propionate (0.5 mmole per kilogram) and arginine (10 gm.) induced a rise in plasma insulin and GH, and glucagon was effectively blocked by cyclic somatostatin (0.5 mg.). |
| 33 | 169176 | Similarly, somatostatin inhibited glucose, and glucagon provoked GH and insulin secretory responses without affecting glucose or FFA levels. |
| 34 | 169176 | Effects of somatostatin on plasma GH, insulin, and glucagon in sheep. |
| 35 | 169176 | To determine whether synthetic somatostatin originally isolated from sheep hypothalamus can inhibit hormone secretion in the same species, we measured plasma levels of GH, insulin, glucagon, and glucose of normal sheep under a variety of experimental conditions in the presence and absence of somatostatin infusion. |
| 36 | 169176 | Propionate (0.5 mmole per kilogram) and arginine (10 gm.) induced a rise in plasma insulin and GH, and glucagon was effectively blocked by cyclic somatostatin (0.5 mg.). |
| 37 | 169176 | Similarly, somatostatin inhibited glucose, and glucagon provoked GH and insulin secretory responses without affecting glucose or FFA levels. |
| 38 | 169176 | Effects of somatostatin on plasma GH, insulin, and glucagon in sheep. |
| 39 | 169176 | To determine whether synthetic somatostatin originally isolated from sheep hypothalamus can inhibit hormone secretion in the same species, we measured plasma levels of GH, insulin, glucagon, and glucose of normal sheep under a variety of experimental conditions in the presence and absence of somatostatin infusion. |
| 40 | 169176 | Propionate (0.5 mmole per kilogram) and arginine (10 gm.) induced a rise in plasma insulin and GH, and glucagon was effectively blocked by cyclic somatostatin (0.5 mg.). |
| 41 | 169176 | Similarly, somatostatin inhibited glucose, and glucagon provoked GH and insulin secretory responses without affecting glucose or FFA levels. |
| 42 | 169176 | Effects of somatostatin on plasma GH, insulin, and glucagon in sheep. |
| 43 | 169176 | To determine whether synthetic somatostatin originally isolated from sheep hypothalamus can inhibit hormone secretion in the same species, we measured plasma levels of GH, insulin, glucagon, and glucose of normal sheep under a variety of experimental conditions in the presence and absence of somatostatin infusion. |
| 44 | 169176 | Propionate (0.5 mmole per kilogram) and arginine (10 gm.) induced a rise in plasma insulin and GH, and glucagon was effectively blocked by cyclic somatostatin (0.5 mg.). |
| 45 | 169176 | Similarly, somatostatin inhibited glucose, and glucagon provoked GH and insulin secretory responses without affecting glucose or FFA levels. |
| 46 | 171190 | With the perfused pancreas, somatostatin caused 32 per cent inhibition of glucose-mediated insulin release and inhibited arginine-induced glucagon release by 72 per cent. |
| 47 | 198195 | Short term (30 min) infusion of cyclic somatostatin (50 microgram/rat), insulin (1 U/rat) or the two together significantly suppressed urinary cyclic AMP excretion in streptozotocin-diabetic rats. |
| 48 | 198195 | While somatostatin tended to increase cyclic GMP excretion, insulin had an opposite effect in diabetic but not in normal rats. |
| 49 | 198195 | It is suggested that somatostatin suppresses cyclic AMP excretion by inhibiting directly adenylate cyclase in liver and perhaps in other organs. |
| 50 | 198195 | Short term (30 min) infusion of cyclic somatostatin (50 microgram/rat), insulin (1 U/rat) or the two together significantly suppressed urinary cyclic AMP excretion in streptozotocin-diabetic rats. |
| 51 | 198195 | While somatostatin tended to increase cyclic GMP excretion, insulin had an opposite effect in diabetic but not in normal rats. |
| 52 | 198195 | It is suggested that somatostatin suppresses cyclic AMP excretion by inhibiting directly adenylate cyclase in liver and perhaps in other organs. |
| 53 | 198195 | Short term (30 min) infusion of cyclic somatostatin (50 microgram/rat), insulin (1 U/rat) or the two together significantly suppressed urinary cyclic AMP excretion in streptozotocin-diabetic rats. |
| 54 | 198195 | While somatostatin tended to increase cyclic GMP excretion, insulin had an opposite effect in diabetic but not in normal rats. |
| 55 | 198195 | It is suggested that somatostatin suppresses cyclic AMP excretion by inhibiting directly adenylate cyclase in liver and perhaps in other organs. |
| 56 | 205166 | Insulin, glucagon, and somatostatin secretion in the regulation of metabolism. |
| 57 | 211005 | The presence of somatostatin within the pancreatic D cells raises the possibility that it may function as a local regulator of insulin and glucagon release. |
| 58 | 264686 | Infusion of exogenous insulin so as to restore plasma insulin to preinfusion values or cessation of the somatostatin infusion with restoration of endogenous insulin secretion resulted in a prompt reduction of plasma glucose to baseline values. |
| 59 | 264686 | We conclude that somatostatin caused only transient hypoglycemia in normal subjects and that hyperglycemia eventually developes as a consequence of insulin deficiency. |
| 60 | 264686 | Infusion of exogenous insulin so as to restore plasma insulin to preinfusion values or cessation of the somatostatin infusion with restoration of endogenous insulin secretion resulted in a prompt reduction of plasma glucose to baseline values. |
| 61 | 264686 | We conclude that somatostatin caused only transient hypoglycemia in normal subjects and that hyperglycemia eventually developes as a consequence of insulin deficiency. |
| 62 | 320077 | The A-, D-, and B-cells--the islet cells that contain, respectively, immunoreactive glucagon, somatostatin, and insulin--are distributed within a specialized heterocellular region of the islets of Langerhans as if to permit heterologous contacts between all three cell types. |
| 63 | 320077 | Glucagon stimulates both insulin and somatostatin release, while insulin and somatostatin both inhibit glucagon release, providing the basis for a feedback relationship through which A-cell secretion may be restrained. |
| 64 | 320077 | In addition, glucagon-mediated insulin secretion may be estrained by glucagon-stimulated somatostatin release. |
| 65 | 320077 | The A-, D-, and B-cells--the islet cells that contain, respectively, immunoreactive glucagon, somatostatin, and insulin--are distributed within a specialized heterocellular region of the islets of Langerhans as if to permit heterologous contacts between all three cell types. |
| 66 | 320077 | Glucagon stimulates both insulin and somatostatin release, while insulin and somatostatin both inhibit glucagon release, providing the basis for a feedback relationship through which A-cell secretion may be restrained. |
| 67 | 320077 | In addition, glucagon-mediated insulin secretion may be estrained by glucagon-stimulated somatostatin release. |
| 68 | 320077 | The A-, D-, and B-cells--the islet cells that contain, respectively, immunoreactive glucagon, somatostatin, and insulin--are distributed within a specialized heterocellular region of the islets of Langerhans as if to permit heterologous contacts between all three cell types. |
| 69 | 320077 | Glucagon stimulates both insulin and somatostatin release, while insulin and somatostatin both inhibit glucagon release, providing the basis for a feedback relationship through which A-cell secretion may be restrained. |
| 70 | 320077 | In addition, glucagon-mediated insulin secretion may be estrained by glucagon-stimulated somatostatin release. |
| 71 | 324423 | Studies using synthetic somatostatin have provided evidence that glucagon is a physiologically important hormone that exacerbates the consequences of insulin deficiency in human diabetes mellitus. |
| 72 | 324423 | The ability of somatostatin to diminish both fasting and post-prandial hyperglycemia and to forestall the development of ketoacidosis after withdrawal of insulin in insulin-dependent diabetics suggests a potential therapeutic use of this agent in diabetes. |
| 73 | 324423 | Studies using synthetic somatostatin have provided evidence that glucagon is a physiologically important hormone that exacerbates the consequences of insulin deficiency in human diabetes mellitus. |
| 74 | 324423 | The ability of somatostatin to diminish both fasting and post-prandial hyperglycemia and to forestall the development of ketoacidosis after withdrawal of insulin in insulin-dependent diabetics suggests a potential therapeutic use of this agent in diabetes. |
| 75 | 326606 | Insulin release from rat islets treated by somatostatin antiserum. |
| 76 | 326606 | In order to clarify the physiologic role of somatostatin in insulin release, rat pancreatic islets treated by somatostatin antiserum were incubated in media containing various concentrations of glucose. |
| 77 | 326606 | It is suggested that somatostatin plays an important role in the regulation of insulin release in the physiologic range of glucose concentration. |
| 78 | 326606 | Insulin release from rat islets treated by somatostatin antiserum. |
| 79 | 326606 | In order to clarify the physiologic role of somatostatin in insulin release, rat pancreatic islets treated by somatostatin antiserum were incubated in media containing various concentrations of glucose. |
| 80 | 326606 | It is suggested that somatostatin plays an important role in the regulation of insulin release in the physiologic range of glucose concentration. |
| 81 | 326606 | Insulin release from rat islets treated by somatostatin antiserum. |
| 82 | 326606 | In order to clarify the physiologic role of somatostatin in insulin release, rat pancreatic islets treated by somatostatin antiserum were incubated in media containing various concentrations of glucose. |
| 83 | 326606 | It is suggested that somatostatin plays an important role in the regulation of insulin release in the physiologic range of glucose concentration. |
| 84 | 338404 | Morphometric quantitation of the pancreatic insulin-, glucagon-, and somatostatin-positive cell populations in normal and alloxan-diabetic rats. |
| 85 | 338404 | The pancreatic insulin-, glucagon-, and somatostatin-positive cell populations were quantitated in normal and alloxan-diabetic rats. |
| 86 | 338404 | Morphometric quantitation of the pancreatic insulin-, glucagon-, and somatostatin-positive cell populations in normal and alloxan-diabetic rats. |
| 87 | 338404 | The pancreatic insulin-, glucagon-, and somatostatin-positive cell populations were quantitated in normal and alloxan-diabetic rats. |
| 88 | 340309 | In severely diabetic mice, islets presented a reduced proportion of insulin containing cells but increased glucagon-, somatostatin-, and pancreatic polypeptide (PP)-containing cells, as compared with islets of control (+/+) mice. |
| 89 | 340309 | An inverse change was observed in islets of mildly diabetic mice: islets were hypertrophic and composed mostly of insulin-containing cells, with decreased proportions of glucagon-, somatostatin-, and PP-containing cells. |
| 90 | 340309 | In severely diabetic mice, islets presented a reduced proportion of insulin containing cells but increased glucagon-, somatostatin-, and pancreatic polypeptide (PP)-containing cells, as compared with islets of control (+/+) mice. |
| 91 | 340309 | An inverse change was observed in islets of mildly diabetic mice: islets were hypertrophic and composed mostly of insulin-containing cells, with decreased proportions of glucagon-, somatostatin-, and PP-containing cells. |
| 92 | 355737 | We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. |
| 93 | 359389 | Using the morphometric technique of linear scanning, the insulin, glucagon, and somatostatin immunocytochemically positive, cell masses of the fetal pancreatic implants were quantitated. |
| 94 | 369928 | The insulin-,glucagon-, and somatostatin-positive islet cell masses of the fetal pancreatic implants were quantitated. |
| 95 | 374172 | Freshly isolated islets are relatively insensitive to somatostatin, requiring 100 ng/ml to suppress partially the glucose-induced insulin secretion. |
| 96 | 376377 | Effect of fasting on the release of insulin and somatostatin from perifused islets of Langerhans. |
| 97 | 376377 | Release of somatostatin and insulin from perifused islets of fasted and control rats was compared. |
| 98 | 376377 | After a fasting period of 48 h glucose-induced insulin release but not somatostatin release was diminished. |
| 99 | 376377 | Effect of fasting on the release of insulin and somatostatin from perifused islets of Langerhans. |
| 100 | 376377 | Release of somatostatin and insulin from perifused islets of fasted and control rats was compared. |
| 101 | 376377 | After a fasting period of 48 h glucose-induced insulin release but not somatostatin release was diminished. |
| 102 | 376377 | Effect of fasting on the release of insulin and somatostatin from perifused islets of Langerhans. |
| 103 | 376377 | Release of somatostatin and insulin from perifused islets of fasted and control rats was compared. |
| 104 | 376377 | After a fasting period of 48 h glucose-induced insulin release but not somatostatin release was diminished. |
| 105 | 377887 | Somatostatin exeits a diabetogenic action by inhibition of insulin release. |
| 106 | 377888 | Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. |
| 107 | 383555 | Effect of norepinephrine on insulin, glucagon, and somatostatin secretion in isolated perifused rat islets. |
| 108 | 383555 | The rate of insulin, glucagon, and somatostatin secretion was measured from isolated rat islets maintained in a perifusion system. |
| 109 | 383555 | During the initial maximal stimulation of glucagon, NE inhibition of somatostatin and insulin was prevented, possibly by the high level of glucagon released. |
| 110 | 383555 | Effect of norepinephrine on insulin, glucagon, and somatostatin secretion in isolated perifused rat islets. |
| 111 | 383555 | The rate of insulin, glucagon, and somatostatin secretion was measured from isolated rat islets maintained in a perifusion system. |
| 112 | 383555 | During the initial maximal stimulation of glucagon, NE inhibition of somatostatin and insulin was prevented, possibly by the high level of glucagon released. |
| 113 | 383555 | Effect of norepinephrine on insulin, glucagon, and somatostatin secretion in isolated perifused rat islets. |
| 114 | 383555 | The rate of insulin, glucagon, and somatostatin secretion was measured from isolated rat islets maintained in a perifusion system. |
| 115 | 383555 | During the initial maximal stimulation of glucagon, NE inhibition of somatostatin and insulin was prevented, possibly by the high level of glucagon released. |
| 116 | 395006 | In the diabetic pancreas addition of insulin to the perfusate (25,000 microU/ml) for periods from 10 to 75 minutes aimed at restoring normal extracellular insulin levels in the islets failed to restore either somatostatin or glucagon secretion to normal. |
| 117 | 395066 | In 8 insulin-dependent diabetics, the effect of D-Trp8-D-Cys14-somatostatin on blood glucose, growth hormone, and glucagon levels as well as on insulin requirements from an artificial endocrine pancreas was studied during a balanced meal. |
| 118 | 405569 | Somatostatin is available as a supplement to insulin therapy because it eliminates the growth hormone as possible source of diabetic vascular complications and it blocks the secretion of hormones with a contrainsular effect. |
| 119 | 421970 | To examine the mechanism of the arginine-induced rise in blood glucose concentration, splanchnic glucose output (SGO) and precursor uptake were studied during i.v. infusion of arginine (30 g/30 min) with and without somatostatin infusion (500 microgram/h, 90 min) in postabsorptive and in 60-h fasted healthy subjects. |
| 120 | 421970 | When both arginine and somatostatin were administered, glucagon rose threefold, whereas the insulin response was abolished. |
| 121 | 421970 | In the 60-h fasted group, arginine infusion was accompanied by a minimal increase in insulin but a fivefold elevation of the glucagon level. |
| 122 | 421970 | Combined arginine and somatostatin infusion did not boost insulin significantly but the glucagon level rose threefold above the basal value. |
| 123 | 421970 | To examine the mechanism of the arginine-induced rise in blood glucose concentration, splanchnic glucose output (SGO) and precursor uptake were studied during i.v. infusion of arginine (30 g/30 min) with and without somatostatin infusion (500 microgram/h, 90 min) in postabsorptive and in 60-h fasted healthy subjects. |
| 124 | 421970 | When both arginine and somatostatin were administered, glucagon rose threefold, whereas the insulin response was abolished. |
| 125 | 421970 | In the 60-h fasted group, arginine infusion was accompanied by a minimal increase in insulin but a fivefold elevation of the glucagon level. |
| 126 | 421970 | Combined arginine and somatostatin infusion did not boost insulin significantly but the glucagon level rose threefold above the basal value. |
| 127 | 421970 | To examine the mechanism of the arginine-induced rise in blood glucose concentration, splanchnic glucose output (SGO) and precursor uptake were studied during i.v. infusion of arginine (30 g/30 min) with and without somatostatin infusion (500 microgram/h, 90 min) in postabsorptive and in 60-h fasted healthy subjects. |
| 128 | 421970 | When both arginine and somatostatin were administered, glucagon rose threefold, whereas the insulin response was abolished. |
| 129 | 421970 | In the 60-h fasted group, arginine infusion was accompanied by a minimal increase in insulin but a fivefold elevation of the glucagon level. |
| 130 | 421970 | Combined arginine and somatostatin infusion did not boost insulin significantly but the glucagon level rose threefold above the basal value. |
| 131 | 426056 | To study the importance of glucagon and insulin in diabetes, somatostatin (ST) was infused, alone or with insulin or glucagon, in 11 conscious dogs. |
| 132 | 426056 | Plasma immunoreactive insulin (IRI) and glucagon (IRG) levels fell 65 +/- 4% and 33 +/- 3%, respectively, with somatostatin infusion. |
| 133 | 426056 | To study the importance of glucagon and insulin in diabetes, somatostatin (ST) was infused, alone or with insulin or glucagon, in 11 conscious dogs. |
| 134 | 426056 | Plasma immunoreactive insulin (IRI) and glucagon (IRG) levels fell 65 +/- 4% and 33 +/- 3%, respectively, with somatostatin infusion. |
| 135 | 437374 | These results indicate the possible inclusion of the adenylate cyclase--cyclic AMP system in the regulatory mechanism of rat pancreatic somatostatin secretion. |
| 136 | 437378 | We examined splanchnic metabolism of alanine in 15 normal males under three sets of conditions: infusion of saline (control studies); infusion of somatostatin (SRIF) (bihormonal deficiency of insulin and glucagon); and infusion of somatostatin plus insulin (selective glucagon deficiency). |
| 137 | 446917 | Possible role of endogenous somatostatin on insulin release. |
| 138 | 446917 | In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. |
| 139 | 446917 | The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. |
| 140 | 446917 | These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet. |
| 141 | 446917 | Possible role of endogenous somatostatin on insulin release. |
| 142 | 446917 | In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. |
| 143 | 446917 | The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. |
| 144 | 446917 | These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet. |
| 145 | 446917 | Possible role of endogenous somatostatin on insulin release. |
| 146 | 446917 | In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. |
| 147 | 446917 | The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. |
| 148 | 446917 | These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet. |
| 149 | 446917 | Possible role of endogenous somatostatin on insulin release. |
| 150 | 446917 | In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. |
| 151 | 446917 | The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. |
| 152 | 446917 | These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet. |
| 153 | 488547 | A simplified method using somatostatin to assess in vivo insulin resistance over a range of obesity. |
| 154 | 488547 | Twenty-one nondiabetic subjects, their weights ranging from 56 to 165 kg, received an infusion of glucose (420 mg/min), insulin (0.77 mU/kg/min), and somatostatin (500 microgram/h) for 150 min. |
| 155 | 488547 | A simplified method using somatostatin to assess in vivo insulin resistance over a range of obesity. |
| 156 | 488547 | Twenty-one nondiabetic subjects, their weights ranging from 56 to 165 kg, received an infusion of glucose (420 mg/min), insulin (0.77 mU/kg/min), and somatostatin (500 microgram/h) for 150 min. |
| 157 | 499100 | Increase by somatostatin of the arginine induced rise in blood glucose in untreated insulin requiring diabetics. |
| 158 | 499100 | These findings indicate a diabetogenic action of somatostatin also in insulin requiring diabetics as long as some residual capacity for insulin release is retained. |
| 159 | 499100 | Increase by somatostatin of the arginine induced rise in blood glucose in untreated insulin requiring diabetics. |
| 160 | 499100 | These findings indicate a diabetogenic action of somatostatin also in insulin requiring diabetics as long as some residual capacity for insulin release is retained. |
| 161 | 499633 | Insulin-induced hypoglycemia is not aggravated by somatostatin in insulin-dependent diabetes. |
| 162 | 570136 | In 12 insulin-dependent diabetics the 24 h plasma prolactin pattern was identical to that found in normals. |
| 163 | 570136 | Somatostatin infusion (4 mg/24 h in normals; 2--6 mg/24 h in diabetics) had no effect on the 24 h plasma prolactin pattern in either normals or in diabetics. |
| 164 | 621284 | To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. |
| 165 | 621284 | A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. |
| 166 | 621284 | In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. |
| 167 | 621284 | Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. |
| 168 | 621284 | It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established. |
| 169 | 621284 | To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. |
| 170 | 621284 | A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. |
| 171 | 621284 | In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. |
| 172 | 621284 | Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. |
| 173 | 621284 | It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established. |
| 174 | 621284 | To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. |
| 175 | 621284 | A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. |
| 176 | 621284 | In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. |
| 177 | 621284 | Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. |
| 178 | 621284 | It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established. |
| 179 | 621284 | To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. |
| 180 | 621284 | A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. |
| 181 | 621284 | In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. |
| 182 | 621284 | Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. |
| 183 | 621284 | It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established. |
| 184 | 621284 | To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. |
| 185 | 621284 | A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. |
| 186 | 621284 | In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. |
| 187 | 621284 | Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. |
| 188 | 621284 | It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established. |
| 189 | 640235 | In the normals, somatostatin suppressed plasma growth hormone, glucagon, and insulin but increased plasma glucose. |
| 190 | 640235 | The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion. |
| 191 | 640235 | In the normals, somatostatin suppressed plasma growth hormone, glucagon, and insulin but increased plasma glucose. |
| 192 | 640235 | The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion. |
| 193 | 661568 | Somatostatin inhibited glucose-stimulated insulin release and reduced plasma glucagon by 50%--65%. |
| 194 | 681570 | They received three injections per day for 3 days each week of 3 U of protamine zinc insulin, .25 mg of zinc glucagon, 50 microgram of protamine zinc somatostatin (SRIF), or protamine zinc vehicle. |
| 195 | 683012 | Diabetogenic effects of somatostatin in maturity-onset diabetes and normal man: primacy of insulin deficiency rather than glucagon excess in the pathogenesis of diabetes. |
| 196 | 683013 | Diabetogenic action of somatostatin in healthy subjects: effect of amino acids and somatostatin upon blood glucose, serum insulin, and glucagon. |
| 197 | 683015 | Glucose, insulin, and somatostatin infusion for the determination of insulin sensitivity in vivo. |
| 198 | 690190 | A selective deficiency of insulin or a combined deficiency of both pancreatic hormones was created by infusing somatostatin alone or in combination with an intraportal replacement infusion of glucagon. |
| 199 | 694712 | Conventional insulins contain impurities which are immunogenic; these include pancreatic polypeptide (PP), glucagon and somatostatin and intermediates of insulin synthesis co-extracted during purification. |
| 200 | 700256 | Immunoreactive glucagon responses to oral glucose, insulin infusion and deprivation, and somatostatin in pancreatectomized man. |
| 201 | 700256 | In a group of pancreatectomized subjects, immunoreactive glucagon (IRG) concentrations were normal after an overnight fast, increased after oral glucose, were not suppressed by somatostatin (SRIF) or insulin, and in two of four subjects they rose with an arginine infusion. |
| 202 | 700256 | Immunoreactive glucagon responses to oral glucose, insulin infusion and deprivation, and somatostatin in pancreatectomized man. |
| 203 | 700256 | In a group of pancreatectomized subjects, immunoreactive glucagon (IRG) concentrations were normal after an overnight fast, increased after oral glucose, were not suppressed by somatostatin (SRIF) or insulin, and in two of four subjects they rose with an arginine infusion. |
| 204 | 700257 | Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. |
| 205 | 700257 | Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. |
| 206 | 700257 | The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration. |
| 207 | 700257 | Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. |
| 208 | 700257 | Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. |
| 209 | 700257 | The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration. |
| 210 | 700257 | Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. |
| 211 | 700257 | Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. |
| 212 | 700257 | The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration. |
| 213 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 214 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 215 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 216 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 217 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 218 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 219 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 220 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 221 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 222 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 223 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 224 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 225 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 226 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 227 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 228 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 229 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 230 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 231 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 232 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 233 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 234 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 235 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 236 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 237 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 238 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 239 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 240 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 241 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 242 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 243 | 759249 | Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. |
| 244 | 759249 | Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. |
| 245 | 759249 | The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. |
| 246 | 759249 | The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. |
| 247 | 759249 | Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. |
| 248 | 759249 | Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. |
| 249 | 791728 | Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. |
| 250 | 798428 | In addition to this the hormones insulin and somatostatin formed by the islets of Langerhans of the pancreas seem to be of importance for the local reactivity of the A-cells of the endocrine pancreas. |
| 251 | 804137 | To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma beta-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes. |
| 252 | 814025 | The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. |
| 253 | 814025 | Only somatostatin and the hypothalamic extract affected insulin secretion. |
| 254 | 814025 | In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. |
| 255 | 814025 | The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. |
| 256 | 814025 | Only somatostatin and the hypothalamic extract affected insulin secretion. |
| 257 | 814025 | In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. |
| 258 | 814025 | The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. |
| 259 | 814025 | Only somatostatin and the hypothalamic extract affected insulin secretion. |
| 260 | 814025 | In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. |
| 261 | 818514 | Increased hormone production may result from tumors of the islet cells (insulin: insulinoma; glucagon: glucagonoma; gastrin: Zollinger-Ellison syndrome). |
| 262 | 818514 | While the clinical application of somatostatin in diabetes mellitus seems problematic at present, the use of a glucose-controlled system of insulin infusion ("artificial pancreas") makes possible a metabolic state approaching the healthy condition. |
| 263 | 820717 | When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. |
| 264 | 820717 | After insulin was withdrawn, plasma beta-hydroxybutyrate, glycerol, and FFA all rose to higher levels (P less than 0.01) than those observed during infusion of somatostatin alone when growth hormone secretion was suppressed; no difference in plasma glucose, alanine, and glucagon levels was evident. |
| 265 | 820717 | When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. |
| 266 | 820717 | After insulin was withdrawn, plasma beta-hydroxybutyrate, glycerol, and FFA all rose to higher levels (P less than 0.01) than those observed during infusion of somatostatin alone when growth hormone secretion was suppressed; no difference in plasma glucose, alanine, and glucagon levels was evident. |
| 267 | 826063 | The presence of insulin, glucagon, somatostatin, and delete pancreatic polypeptide positive cells in the islets of normal rat pancreas has been confirmed. |
| 268 | 836610 | [The influence of somatostatin on serum gastrin concentrations in patients after total duodenopancreatectomy (author's transl)]. |
| 269 | 836610 | Serum gastrin concentrations were measured in insulin-dependent diabetics and in patients who had undergone total duodenopancreatectomy and gastrectomy. |
| 270 | 836610 | Administration of somatostatin markedly inhibited gastrin release in the diabetic patients with an intact gastrointestinal tract. |
| 271 | 836610 | This inhibitory effect of somatostatin, however, is not detectable in the group of operated patients, who display basically low plasma gastrin levels. |
| 272 | 836610 | A marked increase in the plasma gastrin level after withdrawal of somatostatin was observed in patients with a normal gastrointestinal tract. |
| 273 | 836610 | [The influence of somatostatin on serum gastrin concentrations in patients after total duodenopancreatectomy (author's transl)]. |
| 274 | 836610 | Serum gastrin concentrations were measured in insulin-dependent diabetics and in patients who had undergone total duodenopancreatectomy and gastrectomy. |
| 275 | 836610 | Administration of somatostatin markedly inhibited gastrin release in the diabetic patients with an intact gastrointestinal tract. |
| 276 | 836610 | This inhibitory effect of somatostatin, however, is not detectable in the group of operated patients, who display basically low plasma gastrin levels. |
| 277 | 836610 | A marked increase in the plasma gastrin level after withdrawal of somatostatin was observed in patients with a normal gastrointestinal tract. |
| 278 | 836610 | [The influence of somatostatin on serum gastrin concentrations in patients after total duodenopancreatectomy (author's transl)]. |
| 279 | 836610 | Serum gastrin concentrations were measured in insulin-dependent diabetics and in patients who had undergone total duodenopancreatectomy and gastrectomy. |
| 280 | 836610 | Administration of somatostatin markedly inhibited gastrin release in the diabetic patients with an intact gastrointestinal tract. |
| 281 | 836610 | This inhibitory effect of somatostatin, however, is not detectable in the group of operated patients, who display basically low plasma gastrin levels. |
| 282 | 836610 | A marked increase in the plasma gastrin level after withdrawal of somatostatin was observed in patients with a normal gastrointestinal tract. |
| 283 | 836610 | [The influence of somatostatin on serum gastrin concentrations in patients after total duodenopancreatectomy (author's transl)]. |
| 284 | 836610 | Serum gastrin concentrations were measured in insulin-dependent diabetics and in patients who had undergone total duodenopancreatectomy and gastrectomy. |
| 285 | 836610 | Administration of somatostatin markedly inhibited gastrin release in the diabetic patients with an intact gastrointestinal tract. |
| 286 | 836610 | This inhibitory effect of somatostatin, however, is not detectable in the group of operated patients, who display basically low plasma gastrin levels. |
| 287 | 836610 | A marked increase in the plasma gastrin level after withdrawal of somatostatin was observed in patients with a normal gastrointestinal tract. |
| 288 | 870353 | Hormonal and metabolic effects of a synthetic linear somatostatin were tested in insulin-dependent subjects submitted to an intravenous arginine infusion. |
| 289 | 870353 | Substrate responses to arginine were also modified by somatostatin: alanine disappearance was impaired, this effect being dose-related; plasma FFA and 3-hydroxybutyrate concentrations showed a significant increase rather than decrease, consistent with somatostatin suppression of residual insulin secretion. |
| 290 | 870353 | Hormonal and metabolic effects of a synthetic linear somatostatin were tested in insulin-dependent subjects submitted to an intravenous arginine infusion. |
| 291 | 870353 | Substrate responses to arginine were also modified by somatostatin: alanine disappearance was impaired, this effect being dose-related; plasma FFA and 3-hydroxybutyrate concentrations showed a significant increase rather than decrease, consistent with somatostatin suppression of residual insulin secretion. |
| 292 | 870515 | To determine whether cyclic somatostatin (GH-RIH) interferes with glucose utilization and gluconeogenesis we studied levels of blood glucose (BG), immunoreactive insulin (IRI), immunoreactive glucagon (IRG) and of human growth hormone (GH) after iv glucose (330 mg/kg) and iv arginine (0.5 g/kg) in healthy subjects (n=8) and in maturity onset diabetics (n=8; fasting BG less than 200 mg/dl) both in the presence and in the absence of GH-RIH (500 microng/h iv). |
| 293 | 876274 | Furthermore, accentuation by somatostatin of hyperglycemia, hyperketonemia and hyperaminoacidemia in maturity-onset diabetes argues against its use in patients with residual insulin secretion. |
| 294 | 894407 | At five months, the insulin, glucagon, and growth hormone responses to glucose and to somatostatin were normalized. |
| 295 | 908462 | Infusion of somatostatin along with insulin prevented the effects of diazoxide on plasma glucose and glucose production. |
| 296 | 908478 | Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. |
| 297 | 908478 | To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. |
| 298 | 908478 | During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. |
| 299 | 908478 | These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. |
| 300 | 908478 | A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes. |
| 301 | 908478 | Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. |
| 302 | 908478 | To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. |
| 303 | 908478 | During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. |
| 304 | 908478 | These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. |
| 305 | 908478 | A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes. |
| 306 | 908478 | Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. |
| 307 | 908478 | To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. |
| 308 | 908478 | During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. |
| 309 | 908478 | These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. |
| 310 | 908478 | A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes. |
| 311 | 908478 | Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. |
| 312 | 908478 | To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. |
| 313 | 908478 | During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. |
| 314 | 908478 | These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. |
| 315 | 908478 | A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes. |
| 316 | 908478 | Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. |
| 317 | 908478 | To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. |
| 318 | 908478 | During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. |
| 319 | 908478 | These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. |
| 320 | 908478 | A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes. |
| 321 | 925138 | Glucose, insulin and somatostatin infusion for the determination of insulin sensitivity. |
| 322 | 925138 | Glucose, insulin and somatostatin infusion over 2 hours effectively suppressed endogenous secretion of insulin, glucagon and growth hormones. |
| 323 | 925138 | Glucose, insulin and somatostatin infusion for the determination of insulin sensitivity. |
| 324 | 925138 | Glucose, insulin and somatostatin infusion over 2 hours effectively suppressed endogenous secretion of insulin, glucagon and growth hormones. |
| 325 | 934480 | [Changes in blood sugar, and insulin levels induced by somatostatin in normal, diabetic and acromegalic subjects]. |
| 326 | 934480 | The effect of somatostatin on plasma sugar and insulin levels was determined in 8 normal, 7 diabetic and 5 acromegalic subjects. |
| 327 | 934480 | [Changes in blood sugar, and insulin levels induced by somatostatin in normal, diabetic and acromegalic subjects]. |
| 328 | 934480 | The effect of somatostatin on plasma sugar and insulin levels was determined in 8 normal, 7 diabetic and 5 acromegalic subjects. |
| 329 | 976635 | Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. |
| 330 | 976635 | The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. |
| 331 | 976635 | Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. |
| 332 | 976635 | The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. |
| 333 | 992224 | Reversal of somatostatin inhibition of insulin and glucagon secretion. |
| 334 | 992224 | These studies were designed to elucidate the mechanism of inhibitory action of somatostatin (SRIF) on glucagon (IRG) and insulin (IRI) secretion. |
| 335 | 992224 | Reversal of somatostatin inhibition of insulin and glucagon secretion. |
| 336 | 992224 | These studies were designed to elucidate the mechanism of inhibitory action of somatostatin (SRIF) on glucagon (IRG) and insulin (IRI) secretion. |
| 337 | 992227 | Insulin, glucagon, and somatostatin in normal physiology and diabetes mellitus. |
| 338 | 1033640 | [ Somatostatin in insulin-dependent diabetics and in pancreatectomized patients (author's transl)]. |
| 339 | 1033640 | The inhibitory effect of somatostatin on the secretion of glucagon permits the examination of the effect of glucagon on some metabolic parameters in the insulin-dependent diabetic patient. |
| 340 | 1033640 | The results obtained in 5 insulin-dependent diabetics and in 4 pancreatectomized patients revealed an inhibitory effect of somatostatin on blood glucose in the juvenile-type diabetics, but failed to show this influence of somatostatin in the pancreatectomized patients. |
| 341 | 1033640 | [ Somatostatin in insulin-dependent diabetics and in pancreatectomized patients (author's transl)]. |
| 342 | 1033640 | The inhibitory effect of somatostatin on the secretion of glucagon permits the examination of the effect of glucagon on some metabolic parameters in the insulin-dependent diabetic patient. |
| 343 | 1033640 | The results obtained in 5 insulin-dependent diabetics and in 4 pancreatectomized patients revealed an inhibitory effect of somatostatin on blood glucose in the juvenile-type diabetics, but failed to show this influence of somatostatin in the pancreatectomized patients. |
| 344 | 1033640 | [ Somatostatin in insulin-dependent diabetics and in pancreatectomized patients (author's transl)]. |
| 345 | 1033640 | The inhibitory effect of somatostatin on the secretion of glucagon permits the examination of the effect of glucagon on some metabolic parameters in the insulin-dependent diabetic patient. |
| 346 | 1033640 | The results obtained in 5 insulin-dependent diabetics and in 4 pancreatectomized patients revealed an inhibitory effect of somatostatin on blood glucose in the juvenile-type diabetics, but failed to show this influence of somatostatin in the pancreatectomized patients. |
| 347 | 1089999 | Glucagon suppression by somatostatin reduces or abolishes hyperglycemia in dogs made insulin-deficient by somatostatin, alloxan, or total pancreatectomy. |
| 348 | 1102369 | By means of a glucose-controlled insulin- and glucose-infusion system (GCIGIS) we examined the effect of somatostatin on insulin and glucose requirements following meals or oral glucose loads in juvenile diabetics. |
| 349 | 1102369 | In six of seven patients the insulin requirement with somatostatin was remarkably reduced to between 38 per cent and 79 per cent of that of otherwise identical control experiments. |
| 350 | 1102369 | By means of a glucose-controlled insulin- and glucose-infusion system (GCIGIS) we examined the effect of somatostatin on insulin and glucose requirements following meals or oral glucose loads in juvenile diabetics. |
| 351 | 1102369 | In six of seven patients the insulin requirement with somatostatin was remarkably reduced to between 38 per cent and 79 per cent of that of otherwise identical control experiments. |
| 352 | 1152674 | Somatostatin or insulin infusion in depancreatized and alloxan-diabetic dogs resulted in disappearance of the 3500 molecular-weight fraction. |
| 353 | 1152862 | In five subjects, a four-hour infusion of somatostatin (500 micrograms per hour) had no definite effect on platelet count, leukocyte count, hematocrit, platelet adhesiveness and aggregation, bleeding time, partial thromboplastin time, prothrombin time, and fibrinogen levels. |
| 354 | 1159060 | The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. |
| 355 | 1159060 | The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. |
| 356 | 1159060 | In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. |
| 357 | 1159060 | Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. |
| 358 | 1159060 | In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. |
| 359 | 1159060 | The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. |
| 360 | 1159060 | The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. |
| 361 | 1159060 | In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. |
| 362 | 1159060 | Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. |
| 363 | 1159060 | In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. |
| 364 | 1159060 | The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. |
| 365 | 1159060 | The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. |
| 366 | 1159060 | In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. |
| 367 | 1159060 | Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. |
| 368 | 1159060 | In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. |
| 369 | 1159060 | The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. |
| 370 | 1159060 | The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. |
| 371 | 1159060 | In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. |
| 372 | 1159060 | Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. |
| 373 | 1159060 | In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. |
| 374 | 1159060 | The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. |
| 375 | 1159060 | The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. |
| 376 | 1159060 | In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. |
| 377 | 1159060 | Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. |
| 378 | 1159060 | In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. |
| 379 | 1186499 | The effect of glucagon suppression by somatostatin upon endogenous hyperglycemia was studied in three forms of experimental insulin deficiency in dogs: alloxan diabetes, total pancreatectomy, and diazoxide administration. |
| 380 | 1186499 | However, when glucagon was suppressed after insulin withdrawal, glucose remained below 240 mg/dl, significantly less than the controls (p less than 0.005); when somatostatin was stopped, glucagon rose and glucose increased 88 +/- 19 mg/dl within an hour. |
| 381 | 1186499 | Glucagon suppression by somatostatin during diazoxide-induced blockade of insulin secretion in four normal dogs reduced hyperglycemia significantly but did not prevent it. |
| 382 | 1186499 | The effect of glucagon suppression by somatostatin upon endogenous hyperglycemia was studied in three forms of experimental insulin deficiency in dogs: alloxan diabetes, total pancreatectomy, and diazoxide administration. |
| 383 | 1186499 | However, when glucagon was suppressed after insulin withdrawal, glucose remained below 240 mg/dl, significantly less than the controls (p less than 0.005); when somatostatin was stopped, glucagon rose and glucose increased 88 +/- 19 mg/dl within an hour. |
| 384 | 1186499 | Glucagon suppression by somatostatin during diazoxide-induced blockade of insulin secretion in four normal dogs reduced hyperglycemia significantly but did not prevent it. |
| 385 | 1186499 | The effect of glucagon suppression by somatostatin upon endogenous hyperglycemia was studied in three forms of experimental insulin deficiency in dogs: alloxan diabetes, total pancreatectomy, and diazoxide administration. |
| 386 | 1186499 | However, when glucagon was suppressed after insulin withdrawal, glucose remained below 240 mg/dl, significantly less than the controls (p less than 0.005); when somatostatin was stopped, glucagon rose and glucose increased 88 +/- 19 mg/dl within an hour. |
| 387 | 1186499 | Glucagon suppression by somatostatin during diazoxide-induced blockade of insulin secretion in four normal dogs reduced hyperglycemia significantly but did not prevent it. |
| 388 | 1227012 | [Inhibition of endotoxin-, hyperthermia- as well as arginine-induced growth hormone secretion due to somatostatin in healthy subjects and insulin-dependent diabetics]. |
| 389 | 1242153 | The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. |
| 390 | 1242153 | Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia. |
| 391 | 1242153 | Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus. |
| 392 | 1242153 | The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. |
| 393 | 1242153 | Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia. |
| 394 | 1242153 | Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus. |
| 395 | 1242153 | The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. |
| 396 | 1242153 | Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia. |
| 397 | 1242153 | Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus. |
| 398 | 1248672 | Interaction of somatostatin, glucagon, and insulin on hepatic glucose output in the normal dog. |
| 399 | 1248672 | The interaction of insulin and glucagon during infusion of somatostatin (SRIF), which suppresses secretion of these hormones, was investigated in normal, postabsorptive, concious dogs. |
| 400 | 1248672 | Interaction of somatostatin, glucagon, and insulin on hepatic glucose output in the normal dog. |
| 401 | 1248672 | The interaction of insulin and glucagon during infusion of somatostatin (SRIF), which suppresses secretion of these hormones, was investigated in normal, postabsorptive, concious dogs. |
| 402 | 1254110 | The nonsuppressible insulin-like (NSILA-s) and somatomedin-like activities of the serum were not elevated, and the tumor did not release insulin-like activity on incubation nor did it contain somatostatin. |
| 403 | 1278605 | In nine children with clinically overt insulin-dependent diabetes mellitus the authors injected cyclic somatostatin (3 mug. |
| 404 | 1306783 | [Blunted growth hormone response to hGRF 1-29 NH2 in patients with non-insulin-dependent diabetes mellitus]. |
| 405 | 1306783 | There exists some defect in central GH control in diabetics with enhanced somatostatin secretion and abnormal sensitivity of the GH secretion cells to a variety of regulatory factors including GRF, glucose, amino-acids, free fat acid. |
| 406 | 1310640 | Receptors for vasoactive intestinal peptide (VIP) and muscarinic cholinergic agents occurred on 60%, bombesin and gastrin on 30%, beta-adrenergic agents and gastrin-releasing peptide (GRP) on 20%, and somatostatin, opiates, neuromedin B, and substance P on 10%. |
| 407 | 1310640 | Inhibition of binding by agonists revealed relative potencies of 125I-[Tyr4]bombesin greater than GRP much greater than neuromedin B, and two recently described antagonists were similar in potency to GRP. |
| 408 | 1310640 | These results demonstrate the presence of several different receptors for gastrointestinal hormones or neurotransmitters, some described for the first time, on human colon cancer cell lines, including bombesin-related peptides, VIP, somatostatin, substance P, beta-adrenergic agents, calcitonin gene-related peptide, gastrin, muscarinic cholinergic agents, and opiates. |
| 409 | 1310640 | Receptors for vasoactive intestinal peptide (VIP) and muscarinic cholinergic agents occurred on 60%, bombesin and gastrin on 30%, beta-adrenergic agents and gastrin-releasing peptide (GRP) on 20%, and somatostatin, opiates, neuromedin B, and substance P on 10%. |
| 410 | 1310640 | Inhibition of binding by agonists revealed relative potencies of 125I-[Tyr4]bombesin greater than GRP much greater than neuromedin B, and two recently described antagonists were similar in potency to GRP. |
| 411 | 1310640 | These results demonstrate the presence of several different receptors for gastrointestinal hormones or neurotransmitters, some described for the first time, on human colon cancer cell lines, including bombesin-related peptides, VIP, somatostatin, substance P, beta-adrenergic agents, calcitonin gene-related peptide, gastrin, muscarinic cholinergic agents, and opiates. |
| 412 | 1334975 | Nitric oxide has recently been implicated as the effector molecule that mediates IL-1 beta-induced inhibition of glucose-stimulated insulin secretion and beta-cell specific destruction. |
| 413 | 1334975 | The pancreatic islet represents a heterogeneous cell population containing both endocrine cells (beta-[insulin], alpha-]glucagon], gamma[somatostatin], and PP-[polypeptide] secreting cells) and non-endocrine cells (fibroblast, macrophage, endothelial, and dendritic cells). |
| 414 | 1334975 | The purpose of this investigation was to determine if the beta-cell, which is selectively destroyed during insulin-dependent diabetes mellitus, is both a source of IL-1 beta-induced nitric oxide production and also a site of action of this free radical. |
| 415 | 1334975 | Pretreatment of beta-cells, purified by FACS with IL-1 beta results in a 40% inhibition of glucose-stimulated insulin secretion that is prevented by the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (NMMA). |
| 416 | 1334975 | This is further demonstrated by IL-1 beta-induced inhibition of glucose oxidation by purified beta-cells, mitochondrial aconitase activity of dispersed islet cells, and mitochondrial aconitase activity of Rin-m5F cells, all of which are prevented by NMMA. |
| 417 | 1342235 | Acute effect of the somatostatin analogue SMS-201995 on plasma glucose and triglycerides in insulin-dependent diabetic patients. |
| 418 | 1342235 | The effect of the long-acting somatostatin analogue SMS-201995 on diabetes control was assessed in 6 insulin-dependent diabetic patients (3 men and 3 women aged 19-38 years). 2. |
| 419 | 1342235 | We conclude that administration of the somatostatin analogue SMS-201995 may be beneficial for insulin-dependent diabetic patients. |
| 420 | 1342235 | Acute effect of the somatostatin analogue SMS-201995 on plasma glucose and triglycerides in insulin-dependent diabetic patients. |
| 421 | 1342235 | The effect of the long-acting somatostatin analogue SMS-201995 on diabetes control was assessed in 6 insulin-dependent diabetic patients (3 men and 3 women aged 19-38 years). 2. |
| 422 | 1342235 | We conclude that administration of the somatostatin analogue SMS-201995 may be beneficial for insulin-dependent diabetic patients. |
| 423 | 1342235 | Acute effect of the somatostatin analogue SMS-201995 on plasma glucose and triglycerides in insulin-dependent diabetic patients. |
| 424 | 1342235 | The effect of the long-acting somatostatin analogue SMS-201995 on diabetes control was assessed in 6 insulin-dependent diabetic patients (3 men and 3 women aged 19-38 years). 2. |
| 425 | 1342235 | We conclude that administration of the somatostatin analogue SMS-201995 may be beneficial for insulin-dependent diabetic patients. |
| 426 | 1348382 | In addition to glucose levels in the peripheral venous blood, levels of insulin, C-peptide, glucagon, somatostatin, and pancreatic polypeptide were determined. |
| 427 | 1348664 | Half-life of exogenous growth hormone following suppression of endogenous growth hormone secretion with somatostatin in type I (insulin-dependent) diabetes mellitus. |
| 428 | 1349365 | Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma insulin concentrations. |
| 429 | 1350065 | Chronic insulin replacement therapy in diabetic animals partly normalized somatostatin levels as well as plasma GH and glucose levels. |
| 430 | 1350066 | In an attempt to determine if increased somatostatin (SRIF) secretion is responsible for the decreased GH secretion, we studied the effect of modulating SRIF tone on the GH response to GHRH in normal and streptozotocin-induced diabetic rats. |
| 431 | 1350066 | Rats were pretreated with either normal sheep serum and saline (NSS+SAL), somatostatin antibodies (SRIF-Ab), or pyridostigmine (PD), an acetylcholinesterase inhibitor hypothesized to reduce hypothalamic SRIF secretion. |
| 432 | 1350066 | In an attempt to determine if increased somatostatin (SRIF) secretion is responsible for the decreased GH secretion, we studied the effect of modulating SRIF tone on the GH response to GHRH in normal and streptozotocin-induced diabetic rats. |
| 433 | 1350066 | Rats were pretreated with either normal sheep serum and saline (NSS+SAL), somatostatin antibodies (SRIF-Ab), or pyridostigmine (PD), an acetylcholinesterase inhibitor hypothesized to reduce hypothalamic SRIF secretion. |
| 434 | 1350067 | In the present study we investigated the effects of modulating endogenous somatostatin (SRIF) on the GH response to growth hormone-releasing hormone (GHRH) in spontaneously diabetic BB/Wor rats and nondiabetic littermates. |
| 435 | 1350067 | Plasma growth hormone (GH) concentrations following injection of GHRH (500 ng/kg, i.v.) were measured in the rats after pretreatment with either normal sheep serum+saline (NSS+SAL), somatostatin antibody (SRIF-Ab), or pyridostigmine bromide (PD), an acetylcholine esterase inhibitor hypothesized to decrease hypothalamic SRIF tone. |
| 436 | 1350067 | In the present study we investigated the effects of modulating endogenous somatostatin (SRIF) on the GH response to growth hormone-releasing hormone (GHRH) in spontaneously diabetic BB/Wor rats and nondiabetic littermates. |
| 437 | 1350067 | Plasma growth hormone (GH) concentrations following injection of GHRH (500 ng/kg, i.v.) were measured in the rats after pretreatment with either normal sheep serum+saline (NSS+SAL), somatostatin antibody (SRIF-Ab), or pyridostigmine bromide (PD), an acetylcholine esterase inhibitor hypothesized to decrease hypothalamic SRIF tone. |
| 438 | 1353688 | Numerical changes of insulin-, glucagon- and somatostatin-positive cells in the pancreas of WBN/Kob male rats with spontaneously occurring diabetes were examined. |
| 439 | 1354649 | To establish a qualitative and quantitative model of blood glucose response to stress hormone exposure, healthy subjects (HS) on and off somatostatin (250 micrograms/h) as well as insulin dependent diabetic patients were infused with either epinephrine (E), glucagon (G), cortisol (F), growth hormone (GH) or with a cocktail of these hormones raising plasma stress hormones to values seen in severe diabetic ketoacidosis. |
| 440 | 1354686 | The modified insulin suppression test was combined with an infusion of regular insulin, 30 mU/min x m2; glucose, 6 mg/kg x min; and somatostatin, 500 micrograms/h, for 120 minutes followed by only a somatostatin infusion for 60 minutes. |
| 441 | 1355581 | Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics. |
| 442 | 1355581 | A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. |
| 443 | 1355581 | We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. |
| 444 | 1355581 | To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. |
| 445 | 1355581 | In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). |
| 446 | 1355581 | CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. |
| 447 | 1355581 | Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. |
| 448 | 1355581 | This CRH action may be due to an enhanced somatostatin release. |
| 449 | 1355581 | Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion. |
| 450 | 1355581 | Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics. |
| 451 | 1355581 | A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. |
| 452 | 1355581 | We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. |
| 453 | 1355581 | To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. |
| 454 | 1355581 | In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). |
| 455 | 1355581 | CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. |
| 456 | 1355581 | Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. |
| 457 | 1355581 | This CRH action may be due to an enhanced somatostatin release. |
| 458 | 1355581 | Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion. |
| 459 | 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. |
| 460 | 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). |
| 461 | 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). |
| 462 | 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. |
| 463 | 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). |
| 464 | 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). |
| 465 | 1360719 | Human cytomegalovirus in the pancreas of patients with type 2 diabetes: is there a relation to clinical features, mRNA and protein expression of insulin, somatostatin, and MHC class II? |
| 466 | 1360719 | The present study addresses the question as to whether type 2 diabetes with an HCMV-positive pancreas differs from those with HCMV-negative pancreases with respect to age, sex, treatment, duration of disease, volume densities of B-cells and D-cells, mRNA levels of insulin and somatostatin, islet amyloid peptide deposits and major histocompatibility complex (MHC) class I and class II gene transcription, and protein expression. |
| 467 | 1360719 | Human cytomegalovirus in the pancreas of patients with type 2 diabetes: is there a relation to clinical features, mRNA and protein expression of insulin, somatostatin, and MHC class II? |
| 468 | 1360719 | The present study addresses the question as to whether type 2 diabetes with an HCMV-positive pancreas differs from those with HCMV-negative pancreases with respect to age, sex, treatment, duration of disease, volume densities of B-cells and D-cells, mRNA levels of insulin and somatostatin, islet amyloid peptide deposits and major histocompatibility complex (MHC) class I and class II gene transcription, and protein expression. |
| 469 | 1361917 | Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. |
| 470 | 1361917 | Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. |
| 471 | 1361917 | In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. |
| 472 | 1361917 | In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. |
| 473 | 1361917 | On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. |
| 474 | 1361917 | Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. |
| 475 | 1361917 | Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. |
| 476 | 1361917 | In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. |
| 477 | 1361917 | In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. |
| 478 | 1361917 | On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. |
| 479 | 1361917 | Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. |
| 480 | 1361917 | Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. |
| 481 | 1361917 | In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. |
| 482 | 1361917 | In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. |
| 483 | 1361917 | On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. |
| 484 | 1361917 | Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. |
| 485 | 1361917 | Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. |
| 486 | 1361917 | In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. |
| 487 | 1361917 | In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. |
| 488 | 1361917 | On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. |
| 489 | 1361917 | Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. |
| 490 | 1361917 | Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. |
| 491 | 1361917 | In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. |
| 492 | 1361917 | In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. |
| 493 | 1361917 | On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. |
| 494 | 1362039 | We compared in vitro glucose-induced insulin secretion in ANM-USC and control mice, inhibition of secretion by somatostatin, and variability of insulin secretion over the two-year period it took to complete these experiments. |
| 495 | 1363588 | The content of the insulin in B-cells, glucagon in A-cells and somatostatin in D-cells was determined by method of indirect immunofluorescence with the use of monoclonal antibodies and antiserum. |
| 496 | 1363588 | It is established that an decrease of the insulin content in B-cells is followed by an increase of glucagon in A-cells and that of somatostatin in D-cells. |
| 497 | 1363588 | The content of the insulin in B-cells, glucagon in A-cells and somatostatin in D-cells was determined by method of indirect immunofluorescence with the use of monoclonal antibodies and antiserum. |
| 498 | 1363588 | It is established that an decrease of the insulin content in B-cells is followed by an increase of glucagon in A-cells and that of somatostatin in D-cells. |
| 499 | 1381831 | We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model. |
| 500 | 1381831 | Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay. |
| 501 | 1381831 | We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model. |
| 502 | 1381831 | Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay. |
| 503 | 1397705 | To determine the relationship between decreases in glucose and metabolic regulation in the absence of counterregulatory hormones, we infused overnight-fasted, conscious, adrenalectomized dogs (lacking cortisol and EPI) with somatostatin (to eliminate glucagon and growth hormone) and intraportal insulin (30 pmol.kg-1.min-1), creating arterial insulin levels of approximately 2000 pM. |
| 504 | 1452087 | A 22 year old insulin dependent diabetic with high volume, secretory chronic diarrhoea refractory to standard andiarrhoeal drugs was treated with the somatostatin analogue octreotide, 50 micrograms twice daily by subcutaneous injection. |
| 505 | 1492581 | The effect of somatostatin analog octreotide (Sandostatin) on luteinizing hormone and ovarian steroids in insulin-dependent diabetic women without residual insulin secretion. |
| 506 | 1492581 | In order to determine whether the inhibitory effect of octreotide on luteinizing hormone (LH) secretion and ovarian steroids observed in women with polycystic ovaries (PCO) is a direct or indirect action of the analog, we have investigated the effect of 7 days of octreotide on LH, follicle stimulating hormone (FSH) and ovarian steroids in nine insulin-dependent diabetic women without residual insulin secreting, as in these patients a possibly confusing inhibitory effect of octreotide on endogenous insulin production is excluded. |
| 507 | 1495454 | The metabolic effects of a long-acting somatostatin analogue, octreotide, in type I diabetic patients on conventional insulin therapy have been evaluated. |
| 508 | 1499870 | This strategy can avoid injections of somatostatin, which can have other affects in addition to the suppression of insulin and glucagon. |
| 509 | 1499870 | Application of different tracer strategies and use of the depancreatized dog as a model of diabetes, we investigated the importance of the indirect effects of insulin in the pathogenesis of diabetes. 1) Because, in the treatment of IDDM, insulin is administered by the peripheral routes we compared the relative importance of hepatic and peripheral effects of insulin in regulating the rate of glucose production. |
| 510 | 1516889 | The effect of the somatostatin analogue octreotide on growth hormone secretion in insulin-dependent diabetics without residual insulin secretion. |
| 511 | 1516889 | Growth hormone (GH) hypersecretion is well documented in insulin-dependent diabetes mellitus (IDDM). |
| 512 | 1516889 | Somatostatin inhibits GH in acromegalics and healthy subjects although data on its inhibitory effects on high GH levels in IDDM patients are controversial. |
| 513 | 1516889 | The effect of treatment with the somatostatin analogue octreotide ("Sandostatin") on GH secretion, IGF1 levels and metabolic control was investigated in insulin-dependent diabetics. |
| 514 | 1516889 | Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). |
| 515 | 1516889 | The effect of the somatostatin analogue octreotide on growth hormone secretion in insulin-dependent diabetics without residual insulin secretion. |
| 516 | 1516889 | Growth hormone (GH) hypersecretion is well documented in insulin-dependent diabetes mellitus (IDDM). |
| 517 | 1516889 | Somatostatin inhibits GH in acromegalics and healthy subjects although data on its inhibitory effects on high GH levels in IDDM patients are controversial. |
| 518 | 1516889 | The effect of treatment with the somatostatin analogue octreotide ("Sandostatin") on GH secretion, IGF1 levels and metabolic control was investigated in insulin-dependent diabetics. |
| 519 | 1516889 | Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). |
| 520 | 1516889 | The effect of the somatostatin analogue octreotide on growth hormone secretion in insulin-dependent diabetics without residual insulin secretion. |
| 521 | 1516889 | Growth hormone (GH) hypersecretion is well documented in insulin-dependent diabetes mellitus (IDDM). |
| 522 | 1516889 | Somatostatin inhibits GH in acromegalics and healthy subjects although data on its inhibitory effects on high GH levels in IDDM patients are controversial. |
| 523 | 1516889 | The effect of treatment with the somatostatin analogue octreotide ("Sandostatin") on GH secretion, IGF1 levels and metabolic control was investigated in insulin-dependent diabetics. |
| 524 | 1516889 | Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). |
| 525 | 1563319 | The effects of 48 days of streptozotocin-induced diabetes mellitus in rats on plasma concentrations of gastrin, somatostatin, pancreatic glucagon, and enteroglucagon have been assessed. |
| 526 | 1592883 | Transthyretin (prealbumin) in the pancreas and sera of newly diagnosed type I (insulin-dependent) diabetic patients. |
| 527 | 1592883 | On the contrary, insulin-positive B-cells, which normally show uneven and weak TTR immunoreactivity, decreased in number, and only a few residual B-cells showed faint immunoreactivity. |
| 528 | 1592883 | Neither somatostatin cells nor pancreatic polypeptide cells were positive for TTR. |
| 529 | 1639022 | The data indicate that exogenous TRH enhances basal glucagon secretion; inversely, anti-TRH serum inhibits glucose plus arginine-induced glucagon secretion and produces a concomitant slight inhibition of somatostatin secretion. |
| 530 | 1639022 | The present study shows a physiological contribution for endogenous TRH as a local modulator of intraislet hormone regulation; from these observations, we postulate a direct effect of pancreatic TRH on glucagon-containing (alpha) cell secretion, which, in turn, may produce the fluctuation in somatostatin secretion. |
| 531 | 1639022 | The data indicate that exogenous TRH enhances basal glucagon secretion; inversely, anti-TRH serum inhibits glucose plus arginine-induced glucagon secretion and produces a concomitant slight inhibition of somatostatin secretion. |
| 532 | 1639022 | The present study shows a physiological contribution for endogenous TRH as a local modulator of intraislet hormone regulation; from these observations, we postulate a direct effect of pancreatic TRH on glucagon-containing (alpha) cell secretion, which, in turn, may produce the fluctuation in somatostatin secretion. |
| 533 | 1647994 | Immunocytochemical staining of passage 18 cells showed most contained insulin, with less than 5% containing glucagon, and none containing pancreatic polypeptide or somatostatin. |
| 534 | 1647994 | Northern-blot analysis confirmed high levels of insulin mRNA but only trace glucagon mRNA and undetectable somatostatin mRNA. |
| 535 | 1647994 | Interferon-gamma (IFN-gamma)-induced MHC class I RNA expression was correlated with markedly increased antigen expression at the cell surface. |
| 536 | 1647994 | Similarly, a MHC-linked "occult" class I-like antigen detected by Cr release assay only after exposure of standard NOD/Lt islet cells to IFN-gamma was strongly induced by IFN-gamma in NIT-1 cells. |
| 537 | 1647994 | Cell surface MHC class II antigen was not constitutively expressed on NIT-1 cells and could not be detected after IFN-gamma incubation, despite demonstration of IFN-gamma-induced Aa, Ab, and Li invariant-chain RNA transcripts. |
| 538 | 1647994 | Similarly IFN-gamma induction of intercellular adhesion molecule 1 (Icam-1) transcripts was not accompanied by demonstrable cell surface expression of ICAM-1 antigen. |
| 539 | 1649812 | Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. |
| 540 | 1649812 | Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. |
| 541 | 1649812 | Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. |
| 542 | 1649812 | Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. |
| 543 | 1657666 | We also found binding of 125I-GLP-I to insulin-, glucagon-, and somatostatin-immunoreactive cells by combined autoradiographic and immunohistochemical analysis of pancreatic specimens using antisera against insulin, glucagon, and somatostatin. |
| 544 | 1670977 | Nutrient-induced release of insulin, glucagon, and somatostatin in overnight-fasted rats aged 2, 10, 18, 24, and 30 mo was studied. |
| 545 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 546 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 547 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 548 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 549 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 550 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 551 | 1672658 | Somatostatin did not inhibit the early exaggerated insulin release, suggesting that these increased insulin levels represented leakage of insulin from damaged HIT cells rather than functional insulin secretion. |
| 552 | 1674642 | To assess the role of catecholamines in the prevention of hypoglycemia during moderate exercise (approximately 60% peak O2 consumption for 60 min), normal humans were studied with combined alpha- and beta-adrenergic blockade and with adrenergic blockade while changes in insulin and glucagon were prevented with the islet clamp technique (somatostatin infusion with insulin and glucagon infused at fixed rates). |
| 553 | 1675542 | Additionally, the distribution of gastric inhibitory polypeptide, somatostatin, glucagon, and insulin immunoreactive cells was also quantitated. |
| 554 | 1675542 | The glucagon, gastric inhibitory polypeptide, and somatostatin containing cells were intermingled with the beta-cells. |
| 555 | 1675542 | Additionally, the distribution of gastric inhibitory polypeptide, somatostatin, glucagon, and insulin immunoreactive cells was also quantitated. |
| 556 | 1675542 | The glucagon, gastric inhibitory polypeptide, and somatostatin containing cells were intermingled with the beta-cells. |
| 557 | 1677226 | Hyperplasia of somatostatin and pancreatic polypeptide immunoreactive cells in dogs with idiopathic atrophy of the exocrine pancreas. |
| 558 | 1677226 | Cells producing insulin (B), glucagon (A), somatostatin (D), and pancreatic polypeptide (PP) were identified using specific antisera and the ABC technique. |
| 559 | 1677226 | Hyperplasia of somatostatin and pancreatic polypeptide immunoreactive cells in dogs with idiopathic atrophy of the exocrine pancreas. |
| 560 | 1677226 | Cells producing insulin (B), glucagon (A), somatostatin (D), and pancreatic polypeptide (PP) were identified using specific antisera and the ABC technique. |
| 561 | 1678384 | Thus, in this glucose intolerance after hepatectomy, somatostatin seems to play an important role as a paracrine hormone by inhibiting the secretion of insulin by islet B-cells in the pancreas itself. |
| 562 | 1678493 | Hypothalamic secretion of somatostatin and growth hormone-releasing factor into the hypophysial-portal circulation is reduced in streptozotocin diabetic male rats. |
| 563 | 1678493 | Alterations in hypothalamic growth hormone-releasing factor (GRF) or hypothalamic somatostatin (SRIF) secretion, increased systemic SRIF secretion, and changes in somatotroph sensitivity to these hypothalamic factors have been advanced as potential underlying mechanisms for the observed attenuation of GH secretion after STZ treatment. |
| 564 | 1678493 | Hypothalamic secretion of somatostatin and growth hormone-releasing factor into the hypophysial-portal circulation is reduced in streptozotocin diabetic male rats. |
| 565 | 1678493 | Alterations in hypothalamic growth hormone-releasing factor (GRF) or hypothalamic somatostatin (SRIF) secretion, increased systemic SRIF secretion, and changes in somatotroph sensitivity to these hypothalamic factors have been advanced as potential underlying mechanisms for the observed attenuation of GH secretion after STZ treatment. |
| 566 | 1679127 | Somatostatin, gastrin-releasing peptide and gastrin in the stomach of rats with streptozotocin-induced diabetes and insulinoma. |
| 567 | 1679127 | Somatostatin, gastrin-releasing peptide (GRP) and gastrin were measured in the stomach of rats with streptozotocin-induced diabetes, insulinoma-bearing rats and their respective controls. |
| 568 | 1679127 | Stomach weights, and the concentrations and total amounts of GRP and gastrin in the stomach, were similar to nondiabetic control rats. |
| 569 | 1679127 | Concentrations of GRP and gastrin in the stomach were 72% and 19% lower, respectively, than in control rats. |
| 570 | 1679127 | Stomach concentrations of somatostatin, and total stomach contents of somatostatin and gastrin, were similar in insulinoma-bearing and control rats. |
| 571 | 1679127 | Somatostatin, gastrin-releasing peptide and gastrin in the stomach of rats with streptozotocin-induced diabetes and insulinoma. |
| 572 | 1679127 | Somatostatin, gastrin-releasing peptide (GRP) and gastrin were measured in the stomach of rats with streptozotocin-induced diabetes, insulinoma-bearing rats and their respective controls. |
| 573 | 1679127 | Stomach weights, and the concentrations and total amounts of GRP and gastrin in the stomach, were similar to nondiabetic control rats. |
| 574 | 1679127 | Concentrations of GRP and gastrin in the stomach were 72% and 19% lower, respectively, than in control rats. |
| 575 | 1679127 | Stomach concentrations of somatostatin, and total stomach contents of somatostatin and gastrin, were similar in insulinoma-bearing and control rats. |
| 576 | 1679127 | Somatostatin, gastrin-releasing peptide and gastrin in the stomach of rats with streptozotocin-induced diabetes and insulinoma. |
| 577 | 1679127 | Somatostatin, gastrin-releasing peptide (GRP) and gastrin were measured in the stomach of rats with streptozotocin-induced diabetes, insulinoma-bearing rats and their respective controls. |
| 578 | 1679127 | Stomach weights, and the concentrations and total amounts of GRP and gastrin in the stomach, were similar to nondiabetic control rats. |
| 579 | 1679127 | Concentrations of GRP and gastrin in the stomach were 72% and 19% lower, respectively, than in control rats. |
| 580 | 1679127 | Stomach concentrations of somatostatin, and total stomach contents of somatostatin and gastrin, were similar in insulinoma-bearing and control rats. |
| 581 | 1680332 | The presence of Neuron Specific Enolase, Protein Gene Product 9.5, cytokeratin, microvilli, cytoplasmic electrodense granules and the secretion of insulin, glucagon and somatostatin supports the neuroendocrine origin of this cell line. |
| 582 | 1680332 | Flow cytometric analysis showed that HLA expression in this cell line is readily induced by IFN-gamma and modulated by TNF-alpha. |
| 583 | 1680775 | [The effect of somatostatin on specific binding of insulin to receptors in patients with non-insulin dependent diabetes]. |
| 584 | 1680775 | Tests were performed of the effects of the Somatostatin (SMS) upon the concentration of Insulin, Glucagon and STH, as well as of the effects of SMS upon the specific binding of the insulin to the receptors. |
| 585 | 1680775 | [The effect of somatostatin on specific binding of insulin to receptors in patients with non-insulin dependent diabetes]. |
| 586 | 1680775 | Tests were performed of the effects of the Somatostatin (SMS) upon the concentration of Insulin, Glucagon and STH, as well as of the effects of SMS upon the specific binding of the insulin to the receptors. |
| 587 | 1680786 | There was also a decrease in the staining intensity of the insulin-positive cells, an absolute increase in the glucagon-positive cells, and no significant change in the number of somatostatin-positive cells. |
| 588 | 1682193 | The effect of continuous infusions of somatostatin (SRIF) on growth hormone (GH) secretion induced by GH-releasing hormone (GHRH) bolus was compared in a dose-response manner between diabetic subjects in poor glycemic control and nondiabetic subjects to address the hypothesis that altered pituitary responsiveness to SRIF contributes to the hypersecretion of GH in diabetes mellitus in humans. |
| 589 | 1682193 | In diabetic subjects after 2 wk of intensive insulin management, the change in the dose-response curve persisted despite significant decrements in glycosylated hemoglobin and increments in plasma insulinlike growth factor I. |
| 590 | 1682197 | Effect of somatostatin-28 on dynamics of insulin secretion in perfused rat pancreas. |
| 591 | 1682198 | In addition, the concentration of pancreatic hormones in the culture medium, used as a marker of cytolysis, also demonstrated that insulin was significantly increased after 6 h of culture, whereas glucagon and somatostatin were not. |
| 592 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 593 | 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. |
| 594 | 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. |
| 595 | 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. |
| 596 | 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. |
| 597 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 598 | 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. |
| 599 | 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. |
| 600 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 601 | 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. |
| 602 | 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. |
| 603 | 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. |
| 604 | 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. |
| 605 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 606 | 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. |
| 607 | 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. |
| 608 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 609 | 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. |
| 610 | 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. |
| 611 | 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. |
| 612 | 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. |
| 613 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 614 | 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. |
| 615 | 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. |
| 616 | 1683622 | Effects of cholecystokinin (CCK)-8, CCK-33, and gastric inhibitory polypeptide (GIP) on basal and meal-stimulated pancreatic hormone secretion in man. |
| 617 | 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. |
| 618 | 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. |
| 619 | 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. |
| 620 | 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. |
| 621 | 1683622 | Plasma somatostatin levels after the meal were increased by GIP but not affected by CCK-8 or CCK-33. |
| 622 | 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. |
| 623 | 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. |
| 624 | 1684554 | To examine the relationship between the magnitude of the negative arterial-portal glucose gradient and net hepatic glucose uptake, two groups of 42-h fasted, conscious dogs were infused with somatostatin, to suppress endogenous insulin and glucagon secretion, and the hormones were replaced intraportally to create hyperinsulinemia (3- to 4-fold basal) and basal glucagon levels. |
| 625 | 1685274 | Blood glucose concentration and tissue content of insulin, glucagon, and somatostatin were also measured. |
| 626 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 627 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 628 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 629 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 630 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 631 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 632 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 633 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 634 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 635 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 636 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 637 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 638 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 639 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 640 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 641 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 642 | 1687718 | Increased somatostatin response to glucagon in insulin-dependent diabetes mellitus. |
| 643 | 1687718 | The dynamic study of somatostatin secretion was performed in patients with insulin-dependent diabetes mellitus and age- and sex matched volunteers. |
| 644 | 1687718 | Increased somatostatin response to glucagon in insulin-dependent diabetes mellitus. |
| 645 | 1687718 | The dynamic study of somatostatin secretion was performed in patients with insulin-dependent diabetes mellitus and age- and sex matched volunteers. |
| 646 | 1694655 | Five tumors were associated with Zollinger-Ellison syndrome and had immunohistochemical gastrin, but in the others there was no correlation between ulcer disease and gastrin positivity. |
| 647 | 1694655 | Immunohistochemical identification of somatostatin and gastrin has little clinical relevance. |
| 648 | 1695589 | Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas. |
| 649 | 1695589 | Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. |
| 650 | 1695589 | Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). |
| 651 | 1695589 | Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. |
| 652 | 1695589 | Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. |
| 653 | 1695589 | In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. |
| 654 | 1695589 | Galanin also behaves as a potent inhibitor of somatostatin release. |
| 655 | 1695589 | Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas. |
| 656 | 1695589 | Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. |
| 657 | 1695589 | Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). |
| 658 | 1695589 | Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. |
| 659 | 1695589 | Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. |
| 660 | 1695589 | In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. |
| 661 | 1695589 | Galanin also behaves as a potent inhibitor of somatostatin release. |
| 662 | 1695589 | Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas. |
| 663 | 1695589 | Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. |
| 664 | 1695589 | Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). |
| 665 | 1695589 | Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. |
| 666 | 1695589 | Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. |
| 667 | 1695589 | In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. |
| 668 | 1695589 | Galanin also behaves as a potent inhibitor of somatostatin release. |
| 669 | 1695589 | Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas. |
| 670 | 1695589 | Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. |
| 671 | 1695589 | Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). |
| 672 | 1695589 | Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. |
| 673 | 1695589 | Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. |
| 674 | 1695589 | In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. |
| 675 | 1695589 | Galanin also behaves as a potent inhibitor of somatostatin release. |
| 676 | 1695589 | Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas. |
| 677 | 1695589 | Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. |
| 678 | 1695589 | Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). |
| 679 | 1695589 | Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. |
| 680 | 1695589 | Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. |
| 681 | 1695589 | In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. |
| 682 | 1695589 | Galanin also behaves as a potent inhibitor of somatostatin release. |
| 683 | 1719570 | These data suggest that STZ-induced diabetes selectively alters a neuronal system that involves substance P but not somatostatin in the spinal cord. |
| 684 | 1720364 | In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. |
| 685 | 1720364 | The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. |
| 686 | 1720364 | NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. |
| 687 | 1720364 | In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. |
| 688 | 1720364 | The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. |
| 689 | 1720364 | NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. |
| 690 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 691 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 692 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 693 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 694 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 695 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 696 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 697 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 698 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 699 | 1734887 | Presence of islet amyloid polypeptide in rat islet B and D cells determines parallelism and dissociation between rat pancreatic islet amyloid polypeptide and insulin content. |
| 700 | 1734887 | The islet amyloid polypeptide (IAPP) immunoreactivity of the adult rat pancreas is located in insulin-containing B cells as well as in somatostatin-containing D cells. |
| 701 | 1748055 | Insulin resistance, hyperinsulinemia, hypertriglyceridemia, and high blood pressure can be produced in fructose-fed Sprague-Dawley rats, but the development of these changes is inhibited by exercise training or somatostatin infusion. |
| 702 | 1748062 | Short-term studies have shown that octreotide, a long-acting somatostatin analog, blunts postprandial glycemic responses and reduces insulin requirement in insulin treated diabetic patients. |
| 703 | 1770039 | We evaluated the effect of a somatostatin analogue (SMS 201-995) on diabetic nephropathy using urinary albumin excretion as a marker in a streptozocin-induced diabetic unilateral nephrectomized rat model. |
| 704 | 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%. |
| 705 | 1782606 | Islet content of other endocrine peptides, glucagon, somatostatin, and pancreatic polypeptide, was normal at onset and at 2 weeks post onset. |
| 706 | 1796306 | In vivo experiment, it was found that preinjection of bombesin (50 micrograms/kg, sublingual v.) could effectively prevent an increase of plasma glucose and decrease of plasma insulin in diabetic rat induced by alloxan (200 mg/kg, s.c.) (2). |
| 707 | 1796306 | In vitro experiment, isolated pancreas perfusion showed that alloxan-induced (14 mmol/L) perfusion fluid inhibition of insulin secretion could be reversed by pretreatment of bombesin (10(-3) mmol/L). (3). |
| 708 | 1796306 | Investigation on isolated and incubated islets demonstrated that alloxan induced decrease of insulin and somatostatin secretion and increase of glucagon secretion could be prevented by bombesin. |
| 709 | 1802476 | Glomerular filtration rate, renal plasma flow, and albumin excretion rate were measured together with plasma concentrations of glucagon, growth hormone, insulin-like growth factor 1 (IGF-1), somatostatin, serum insulin and free amino acids in blood. |
| 710 | 1802476 | Growth hormone, somatostatin, insulin, and other amino acids remained unchanged. |
| 711 | 1802476 | Albumin excretion rate was correlated to IGF-1 (r = 0.86, p less than 0.001) on the high protein diet. |
| 712 | 1802476 | Glomerular filtration rate, renal plasma flow, and albumin excretion rate were measured together with plasma concentrations of glucagon, growth hormone, insulin-like growth factor 1 (IGF-1), somatostatin, serum insulin and free amino acids in blood. |
| 713 | 1802476 | Growth hormone, somatostatin, insulin, and other amino acids remained unchanged. |
| 714 | 1802476 | Albumin excretion rate was correlated to IGF-1 (r = 0.86, p less than 0.001) on the high protein diet. |
| 715 | 1850691 | However, postprandial responses of insulin, C-peptide, glucagon, gastric inhibitory peptide and somatostatin were not influenced by an increased fiber intake in any group. |
| 716 | 1901807 | Gi mediates decreases in intracellular cAMP caused by inhibitors of insulin secretion, e.g., epinephrine, somatostatin, prostaglandin E2, and galanin. |
| 717 | 1916058 | During the study endogenous insulin secretion was suppressed by somatostatin (450 micrograms/h) and replaced by insulin infusion (0.15 mU.kg-1.min-1). 3H-glucose was infused for isotopic determination of glucose turnover. |
| 718 | 1936585 | On both occasions, a pancreatic clamp (0.12 micrograms.kg-1.min-1 somatostatin, 0.05 mU.kg-1.min-1 insulin, and 3 ng.kg-1.min-1 growth hormone) was used to maintain plasma hormone concentrations at desired levels. |
| 719 | 1936599 | With the recent demonstration that the 64,000-M, antigen associated with insulin-dependent diabetes mellitus is GAD, there is increased interest in understanding the role of GABA in islet function. |
| 720 | 1936599 | Effects of GABA on insulin, glucagon, and somatostatin secretion have been proposed. |
| 721 | 1943736 | Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?) |
| 722 | 1943742 | To determine the effect of insulin and glucagon on the transformation of nonesterified fatty acids (NEFA) into ketone bodies (KB), we measured simultaneously in normal subjects NEFA and KB kinetics at different NEFA levels in the presence of basal (control test) or increasing insulin concentrations with glucagopenia (somatostatin + insulin infusion, insulin test) and without glucagopenia (somatostatin + insulin + glucagon infusion, glucagon test). |
| 723 | 1954071 | We conclude that, despite accelerated lipolysis and provision of substrate for ketogenesis during insulin withdrawal, this somatostatin analogue significantly reduces ketogenesis resulting from insulin deprivation, probably secondary to decreasing glucagon secretion. |
| 724 | 1967164 | Altered pituitary growth hormone (GH) regulation in streptozotocin-diabetic rats: a combined defect of hypothalamic somatostatin and GH-releasing factor. |
| 725 | 1967164 | An interplay between hypothalamic GH-releasing factor (GRF) and inhibitory factor [somatostatin (SRIF)] secretion is thought to account for episodic pituitary GH release. |
| 726 | 1967164 | GH synthesis has been shown to be independent of SRIF regulation; however, insulin-like growth factor-I and GRF inhibit and stimulate GH synthesis, respectively. |
| 727 | 1967164 | In diabetic rats insulin-like growth factor-I levels were decreased, appropriate to low GH status, in serum (290 +/- 66 vs. 1662 +/- 92 ng/ml; P less than 0.001) and hypothalamus (6.8 +/- 1.0 vs. 13.0 +/- 0.4 pg/mg wet wt; P less than 0.001) and, thus, did not seem to account for the low AP GH content. |
| 728 | 1967164 | Altered pituitary growth hormone (GH) regulation in streptozotocin-diabetic rats: a combined defect of hypothalamic somatostatin and GH-releasing factor. |
| 729 | 1967164 | An interplay between hypothalamic GH-releasing factor (GRF) and inhibitory factor [somatostatin (SRIF)] secretion is thought to account for episodic pituitary GH release. |
| 730 | 1967164 | GH synthesis has been shown to be independent of SRIF regulation; however, insulin-like growth factor-I and GRF inhibit and stimulate GH synthesis, respectively. |
| 731 | 1967164 | In diabetic rats insulin-like growth factor-I levels were decreased, appropriate to low GH status, in serum (290 +/- 66 vs. 1662 +/- 92 ng/ml; P less than 0.001) and hypothalamus (6.8 +/- 1.0 vs. 13.0 +/- 0.4 pg/mg wet wt; P less than 0.001) and, thus, did not seem to account for the low AP GH content. |
| 732 | 1967178 | In control (saline-infused) experiments, endogenous glucose appearance (Ra) increased by 80-90% above baseline to match the increase in glucose disappearance in both normal and IDDM subjects, even though the latter exercised at fixed levels of plasma free insulin, averaging 203 +/- 19 pmol/L. |
| 733 | 1967178 | In other experiments, somatostatin was infused, and glucagon (1.0 ng/kg.min) and insulin (at two different rates) were maintained at constant levels. |
| 734 | 1967178 | However, insulin infusion at doses that normalized the portal insulin concentration (approximately 208 pmol/L) together with glucagon replacement inhibited the rise in glucose production in both normal and IDDM subjects. |
| 735 | 1967178 | When peripheral plasma free insulin (and presumably portal levels as well) were increased by about 20% in this experimental setting in IDDM (278 +/- 43 pmol/L), the suppression of Ra was even more profound, and Ra failed to increase at all with exercise. |
| 736 | 1967577 | Paradoxical reduction in pancreatic glucagon with normalization of somatostatin and decrease in insulin in normoglycemic alloxan-diabetic dogs: a putative mechanism of glucagon irresponsiveness to hypoglycemia. |
| 737 | 1967577 | Therefore, as in insulin-dependent diabetes mellitus (IDDM), increased glucose utilization is not matched by an increase in hepatic production. |
| 738 | 1967577 | Normoglycemia 1) normalizes somatostatin content, 2) further diminishes insulin and proinsulin synthesis presumably due to lack of hyperglycemic stimulus, and 3) paradoxically decreases pancreatic glucagon content 5-fold below its normal level. |
| 739 | 1967577 | Paradoxical reduction in pancreatic glucagon with normalization of somatostatin and decrease in insulin in normoglycemic alloxan-diabetic dogs: a putative mechanism of glucagon irresponsiveness to hypoglycemia. |
| 740 | 1967577 | Therefore, as in insulin-dependent diabetes mellitus (IDDM), increased glucose utilization is not matched by an increase in hepatic production. |
| 741 | 1967577 | Normoglycemia 1) normalizes somatostatin content, 2) further diminishes insulin and proinsulin synthesis presumably due to lack of hyperglycemic stimulus, and 3) paradoxically decreases pancreatic glucagon content 5-fold below its normal level. |
| 742 | 1969430 | Somatostatin was infused (250 micrograms/h) during the third h of glucose clamp to inhibit glucose-stimulated insulin secretion. |
| 743 | 1969430 | Plasma free fatty acid concentrations, which were similar in the two groups at fasting, decreased during hyperglycemia and glucose-induced hyperinsulinemia (0-120 min; 180-240 min), and rose during hyperglycemia and somatostatin-inhibited insulin secretion (120-180 min). |
| 744 | 1969430 | Somatostatin was infused (250 micrograms/h) during the third h of glucose clamp to inhibit glucose-stimulated insulin secretion. |
| 745 | 1969430 | Plasma free fatty acid concentrations, which were similar in the two groups at fasting, decreased during hyperglycemia and glucose-induced hyperinsulinemia (0-120 min; 180-240 min), and rose during hyperglycemia and somatostatin-inhibited insulin secretion (120-180 min). |
| 746 | 1969977 | The diagnosis remained unclear until immunohistochemical studies of the resected specimen revealed somatostatin and synaptophysin, suggesting a somatostatinoma. |
| 747 | 1970540 | Islet amyloid polypeptide response to glucose, insulin, and somatostatin analogue administration. |
| 748 | 1970540 | We determined islet amyloid polypeptide (IAPP) response in plasma to oral and intravenous glucose administration and intravenous insulin injection in nondiabetic subjects. |
| 749 | 1970706 | The in vivo labeling of somatostatin-14, somatostatin-28, arginine vasopressin, and oxytocin was studied in rat hypothalamus after third ventricular administration of [35S]cysteine to streptozotocin-diabetic and normal rats. |
| 750 | 1971441 | We have investigated the influence of non-insulin-dependent diabetes on the regulation of somatostatin secretion from the pancreatic D cell. |
| 751 | 1971774 | The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. |
| 752 | 1971774 | Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. |
| 753 | 1971774 | These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM. |
| 754 | 1971774 | The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. |
| 755 | 1971774 | Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. |
| 756 | 1971774 | These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM. |
| 757 | 1974025 | When sodium acetoacetate was infused with somatostatin (0.10 micrograms/kg/min) to suppress glucagon and insulin secretion, the decrease in both plasma glucose (13.3 +/- 0.9 to 10.2 +/- 0.7 mmol/L) and hepatic glucose output (17.2 +/- 1.6 to 9.4 +/- 0.6 mumols/kg/min) was greater than either acetoacetate or somatostatin infusion alone. |
| 758 | 1974102 | The glucose-induced insulin and somatostatin secretion from the isolated perfused pancreas was almost identical in all four groups. |
| 759 | 1974102 | The arginine-induced insulin and glucagon secretion was decreased in HF and HC rats, compared to both HP and BD rats, but somatostatin secretion was not. |
| 760 | 1974102 | The glucose-induced insulin and somatostatin secretion from the isolated perfused pancreas was almost identical in all four groups. |
| 761 | 1974102 | The arginine-induced insulin and glucagon secretion was decreased in HF and HC rats, compared to both HP and BD rats, but somatostatin secretion was not. |
| 762 | 1974524 | [The effect of growth hormone-releasing factor (GRF) on secretion of insulin, glucagon and somatostatin from perfused rat pancreas]. |
| 763 | 1974524 | To examine the effects of growth hormone-releasing factor (GRF) on islet hormone release, rat pancreas was perfused. rhGRF at the concentration of 10(-7) M or more enhanced insulin secretion stimulated by 16.7 mM glucose, hpGRF slightly enhanced insulin secretion as well. |
| 764 | 1974524 | We concluded that rhGRF stimulated insulin, glucagon and somatostatin secretion and the insulin secretion was inhibited by beta-blocker. hpGRF stimulated insulin and glucagon secretion as well. |
| 765 | 1974524 | [The effect of growth hormone-releasing factor (GRF) on secretion of insulin, glucagon and somatostatin from perfused rat pancreas]. |
| 766 | 1974524 | To examine the effects of growth hormone-releasing factor (GRF) on islet hormone release, rat pancreas was perfused. rhGRF at the concentration of 10(-7) M or more enhanced insulin secretion stimulated by 16.7 mM glucose, hpGRF slightly enhanced insulin secretion as well. |
| 767 | 1974524 | We concluded that rhGRF stimulated insulin, glucagon and somatostatin secretion and the insulin secretion was inhibited by beta-blocker. hpGRF stimulated insulin and glucagon secretion as well. |
| 768 | 1976213 | Originally characterized as a hypothalamic regulator of growth hormone secretion, somatostatin also regulates the secretion of several other pituitary, pancreatic, and gastrointestinal (GI) hormones including thyrotropin-stimulating hormone, insulin, glucagon, and gastrin. |
| 769 | 1976221 | Somatostatin secreted by pancreatic D cells is a potent inhibitor of insulin, glucagon and growth hormone secretion, as well as other cells. |
| 770 | 1976558 | Recent evidence suggests that somatostatin-28 (SRIF-28), cleaved from prosomatostatin by cells of the upper intestine, acts as a nutrient-stimulated inhibitor of insulin secretion in healthy men. |
| 771 | 1977322 | In the present study, six subjects with insulin-dependent diabetes and six nondiabetic volunteers were studied during infusion of somatostatin, growth hormone, and insulin at rates designed to maintain basal rates of lipolysis, which was traced using a constant infusion of [1-14C]palmitate. |
| 772 | 1979947 | Fasting plasma insulin and somatostatin were elevated in transplanted rats. |
| 773 | 1980258 | Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus. |
| 774 | 1980258 | The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). |
| 775 | 1980258 | A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. |
| 776 | 1980258 | Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. |
| 777 | 1980258 | It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion. |
| 778 | 1980258 | Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus. |
| 779 | 1980258 | The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). |
| 780 | 1980258 | A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. |
| 781 | 1980258 | Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. |
| 782 | 1980258 | It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion. |
| 783 | 1980258 | Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus. |
| 784 | 1980258 | The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). |
| 785 | 1980258 | A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. |
| 786 | 1980258 | Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. |
| 787 | 1980258 | It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion. |
| 788 | 1980258 | Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus. |
| 789 | 1980258 | The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). |
| 790 | 1980258 | A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. |
| 791 | 1980258 | Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. |
| 792 | 1980258 | It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion. |
| 793 | 1980258 | Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus. |
| 794 | 1980258 | The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). |
| 795 | 1980258 | A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. |
| 796 | 1980258 | Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. |
| 797 | 1980258 | It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion. |
| 798 | 1980453 | Other promising treatments (human proinsulin, nasal insulin, somatostatin) have not shown any advantage over conventional insulin therapy. |
| 799 | 1980735 | Radioimmunoassays for glucagon, somatostatin (SRIF) and insulin were also made on these extracts. |
| 800 | 1982400 | [Modification of gastrin and somatostatin cells in the gastric antrum in experimental diabetes]. |
| 801 | 1992187 | Somatostatin analogue, octreotide, reduces increased glomerular filtration rate and kidney size in insulin-dependent diabetes. |
| 802 | 1992187 | To determine whether treatment with a somatostatin analogue can reduce kidney hyperfiltration and hypertrophy in insulin-dependent diabetes mellitus, we studied 11 patients with insulin-dependent diabetes mellitus and glomerular hyperfiltration. |
| 803 | 1992187 | Somatostatin analogue, octreotide, reduces increased glomerular filtration rate and kidney size in insulin-dependent diabetes. |
| 804 | 1992187 | To determine whether treatment with a somatostatin analogue can reduce kidney hyperfiltration and hypertrophy in insulin-dependent diabetes mellitus, we studied 11 patients with insulin-dependent diabetes mellitus and glomerular hyperfiltration. |
| 805 | 2015054 | Depletion of islet amyloid polypeptide in the spontaneously diabetic (BB) Wistar rat. |
| 806 | 2015054 | Islet amyloid polypeptide (IAPP) in the pancreas of the spontaneously diabetic (BB) Wistar rat was examined by radioimmunoassay, and IAPP mRNA levels were determined by Northern blotting. |
| 807 | 2015054 | Insulin mRNA was dramatically reduced to only 4% of the control group and, in contrast, somatostatin was relatively unaffected, with the diabetic group retaining 86% of signal compared with the controls. |
| 808 | 2026051 | Combined with the use of tracer dilution technique, hepatic vein catheterization technique, infusion of somatostatin, forearm or leg techniques and indirect calorimetry, insight into several other major parameters of glucose kinetics has been achieved; i.e. insulin-mediated glucose uptake (IMGU), glucose-induced glucose uptake (GIGU), hepatic glucose production (HGP) splanchnic glucose uptake and oxidative and nonoxidative glucose disposal. |
| 809 | 2035626 | To assess the roles of decrements in insulin and increments in glucagon in the prevention of hypoglycemia during moderate exercise (approximately 60% peak O2 consumption for 60 min), normal young men were studied during somatostatin infusions with insulin and glucagon infused to 1) hold insulin and glucagon levels constant, 2) decrease insulin, 3) increase glucagon, and 4) decrease insulin and increase glucagon during exercise. |
| 810 | 2040385 | In study 2, LH or saline was infused as in study 1, but the compensatory insulin release was prevented by intravenous infusion of somatostatin and replacement of basal insulin and glucagon concentrations. |
| 811 | 2078850 | Islet amyloid polypeptide (IAPP) in the gastrointestinal tract and pancreas of man and rat. |
| 812 | 2078850 | An immunohistochemical study for islet amyloid polypeptide (IAPP) was made on the gastrointestinal (GI) tract and pancreas of man and rat, using antisera raised against a synthetic peptide of C-terminal human IAPP (24-37) and a synthetic peptide of rat IAPP (18-37). |
| 813 | 2078850 | An examination was made for evidence of colocalization of IAPP-immunoreactive material with material immunoreactive for gastrin, somatostatin, vasoactive intestinal polypeptide, pancreatic polypeptide, insulin, and glucagon, but none was found. |
| 814 | 2078850 | IAPP-immunoreactive cells were also found in the pancreas of non-diabetic and non-insulin-dependent diabetic patients, but they were completely absent from a patient with insulin-dependent diabetes mellitus despite the presence of IAPP in the plasma. |
| 815 | 2105656 | Subjects participated in four experimental protocols: 1) euglycemic insulin clamp (+80 microU/ml), 2) epinephrine infusion (50 ng.kg-1.min-1) plus somatostatin with basal replacement of insulin and glucagon, 3) combined epinephrine (50 ng.kg-1.min-1) plus insulin (+80 microU/ml) infusion, and 4) epinephrine and somatostatin as in study 2 plus basal amino acid replacement. |
| 816 | 2108069 | No somatostatin or pancreatic polypeptide was detected by immunohistochemical staining in alpha TC1 clones 6 or 9 or beta TC1 cells. |
| 817 | 2108069 | Rat recombinant gamma-interferon (IFN-gamma; 5-250 U/ml) or mouse recombinant interleukin 1 (IL-1; 1-25 U/ml) individually inhibited DNA synthesis in beta TC1 cells after 3 days of treatment. |
| 818 | 2111240 | Immunohistochemically, proislets contained scattered populations of insulin-, glucagon- and somatostatin-producing cells; following isotransplantation proislets developed into mature islet tissue with normal endocrine cell composition. |
| 819 | 2167806 | Insulin, glucagon and somatostatin were administered from 60 to 210 min in each study and euglycaemia was maintained. 3. |
| 820 | 2177367 | In addition, the insulin-stimulated glucose uptake was estimated in all subjects by measuring the final 30 min steady-state plasma glucose (SSPG) of a continuous infusion of somatostatin, insulin and glucose for 4 hours (modified insulin suppression test). |
| 821 | 2192226 | Arginine-induced serum insulin, glucagon, and somatostatin responses in the grafted pancreas were similar to those in normal pancreas. |
| 822 | 2197845 | Effect of one year continuous subcutaneous infusion of a somatostatin analogue, octreotide, on early retinopathy, metabolic control and thyroid function in Type I (insulin-dependent) diabetes mellitus. |
| 823 | 2197845 | In a randomized study we evaluated the possible effects of one year treatment with a somatostatin (SRIH) analogue, octreotide, on early retinopathy and on metabolism in Type I (insulin-dependent) diabetes mellitus. |
| 824 | 2197845 | We conclude that treatment with octreotide for one year has modest effects on GH, IGF-I, and glucose metabolism, but has no significant effect on early retinopathy in Type I (insulin-dependent) diabetes. |
| 825 | 2197845 | Effect of one year continuous subcutaneous infusion of a somatostatin analogue, octreotide, on early retinopathy, metabolic control and thyroid function in Type I (insulin-dependent) diabetes mellitus. |
| 826 | 2197845 | In a randomized study we evaluated the possible effects of one year treatment with a somatostatin (SRIH) analogue, octreotide, on early retinopathy and on metabolism in Type I (insulin-dependent) diabetes mellitus. |
| 827 | 2197845 | We conclude that treatment with octreotide for one year has modest effects on GH, IGF-I, and glucose metabolism, but has no significant effect on early retinopathy in Type I (insulin-dependent) diabetes. |
| 828 | 2210065 | Five conscious dogs fasted 18 h were given somatostatin and replacement insulin (245 +/- 34 microU.kg-1.min-1) and glucagon (0.65 ng.kg-1.min-1) infusions intraportally. |
| 829 | 2227272 | All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon. |
| 830 | 2227272 | Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient. |
| 831 | 2227272 | Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms. |
| 832 | 2227272 | All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon. |
| 833 | 2227272 | Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient. |
| 834 | 2227272 | Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms. |
| 835 | 2229305 | In the present study we investigated the effects of the acetylcholinesterase inhibitor pyridostigmine (PD), which is hypothesized to decrease hypothalamic somatostatin tone, alone and in association with GH-releasing hormone (GHRH) on GH secretion in 18 type 1 diabetic patients and 12 normal subjects using a randomized double blind placebo-controlled protocol. |
| 836 | 2233277 | In contrast, db/db mice of both C57BL/6J and C57BL/KsJ strains exhibited alterations in a total of four peptides in three brain areas: lower concentration of somatostatin-LI in median eminence, higher Met-enkephalin-LI in dorsal vagal complex of the medulla oblongata, higher substance P-LI and lower vasoactive intestinal polypeptide (VIP)-LI in amygdala. |
| 837 | 2262048 | The neuropeptides examined were vasoactive intestinal peptide, neuropeptide Y, substance P. calcitonin gene-related peptide, galanin and somatostatin. |
| 838 | 2262048 | Substance P and calcitonin gene-related peptide which are colocalized in a proportion of the somatostatin neurons were unaffected. |
| 839 | 2387655 | Effect of long-acting somatostatin analog (SMS 201-995) on high glomerular filtration rate in insulin dependent diabetic patients. |
| 840 | 2408435 | Effects of somatostatin on the behaviour of thromboxane B2 and beta-thromboglobulin in type I diabetes. |
| 841 | 2408435 | Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. |
| 842 | 2408435 | Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of beta-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 micrograms iv bolus followed by infusion of 300 micrograms over 3 h. |
| 843 | 2408435 | In both groups, after somatostatin infusion thromboxane B2 and beta-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. |
| 844 | 2408435 | Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of beta-thromboglobulin lower than in control subjects. |
| 845 | 2408435 | Effects of somatostatin on the behaviour of thromboxane B2 and beta-thromboglobulin in type I diabetes. |
| 846 | 2408435 | Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. |
| 847 | 2408435 | Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of beta-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 micrograms iv bolus followed by infusion of 300 micrograms over 3 h. |
| 848 | 2408435 | In both groups, after somatostatin infusion thromboxane B2 and beta-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. |
| 849 | 2408435 | Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of beta-thromboglobulin lower than in control subjects. |
| 850 | 2408435 | Effects of somatostatin on the behaviour of thromboxane B2 and beta-thromboglobulin in type I diabetes. |
| 851 | 2408435 | Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. |
| 852 | 2408435 | Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of beta-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 micrograms iv bolus followed by infusion of 300 micrograms over 3 h. |
| 853 | 2408435 | In both groups, after somatostatin infusion thromboxane B2 and beta-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. |
| 854 | 2408435 | Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of beta-thromboglobulin lower than in control subjects. |
| 855 | 2408435 | Effects of somatostatin on the behaviour of thromboxane B2 and beta-thromboglobulin in type I diabetes. |
| 856 | 2408435 | Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. |
| 857 | 2408435 | Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of beta-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 micrograms iv bolus followed by infusion of 300 micrograms over 3 h. |
| 858 | 2408435 | In both groups, after somatostatin infusion thromboxane B2 and beta-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. |
| 859 | 2408435 | Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of beta-thromboglobulin lower than in control subjects. |
| 860 | 2408435 | Effects of somatostatin on the behaviour of thromboxane B2 and beta-thromboglobulin in type I diabetes. |
| 861 | 2408435 | Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. |
| 862 | 2408435 | Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of beta-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 micrograms iv bolus followed by infusion of 300 micrograms over 3 h. |
| 863 | 2408435 | In both groups, after somatostatin infusion thromboxane B2 and beta-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. |
| 864 | 2408435 | Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of beta-thromboglobulin lower than in control subjects. |
| 865 | 2409805 | Ganglioneuronal amyloid had staining characteristics identical to those previously reported for islet amyloid, including 1) congophilia, 2) resistance to oxidation by KMnO4, 3) immunoreactivity (PAP technique) with antiserum to a B-chain-rich insulin fraction, and 4) no reactivity with antisera to insulin, glucagon, or somatostatin. |
| 866 | 2409805 | Nonneuronal cells with insulin, glucagon, and somatostatin immunoreactivity were seen in many pancreatic ganglia and nerves; and in a few instances, B cells were found near ganglioneuronal amyloid deposits. |
| 867 | 2409805 | The premise that these ganglioneuronal amyloid deposits (like islet amyloid) are insulin-related is supported by their immunoreactivity with antiserum to B-chain-rich insulin and the demonstration of B cells in pancreatic ganglia and nerves. |
| 868 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 869 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 870 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 871 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 872 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 873 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 874 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 875 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 876 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 877 | 2416604 | The immunohistochemical observation of somatostatin-like and avian pancreatic polypeptide-like immunoreactivity in certain cellular elements of diabetic lipodystrophic skin. |
| 878 | 2416604 | Somatostatin-like and avian pancreatic polypeptide-like immunoreactivities were found to occur within certain cellular elements of the dermis of a patient having diabetic lipodystrophic skin lesions. |
| 879 | 2416604 | The immunohistochemical observation of somatostatin-like and avian pancreatic polypeptide-like immunoreactivity in certain cellular elements of diabetic lipodystrophic skin. |
| 880 | 2416604 | Somatostatin-like and avian pancreatic polypeptide-like immunoreactivities were found to occur within certain cellular elements of the dermis of a patient having diabetic lipodystrophic skin lesions. |
| 881 | 2417865 | The effect of streptozotocin treatment (65 mg/kg i.v.) on plasma protein extravasation, nociception, and the content of substance P immunoreactivity (SP-IR) and somatostatin immunoreactivity (SOM-IR) was investigated in the rat. |
| 882 | 2433176 | Substance P and somatostatin content and transport in vagus and sciatic nerves of the streptozocin-induced diabetic rat. |
| 883 | 2433176 | Substance P (SP) and somatostatin (SS) are two widely distributed neuropeptides that within the vagus and sciatic nerves are localized predominantly in sensory fibers. |
| 884 | 2433176 | Substance P and somatostatin content and transport in vagus and sciatic nerves of the streptozocin-induced diabetic rat. |
| 885 | 2433176 | Substance P (SP) and somatostatin (SS) are two widely distributed neuropeptides that within the vagus and sciatic nerves are localized predominantly in sensory fibers. |
| 886 | 2436870 | The levels of insulin, C-peptide, gastric inhibitory polypeptide (GIP), glucagon, somatostatin, triglyceride and glycerol were followed after the breakfast meals. |
| 887 | 2444380 | At the developmental age of 15 days argyrophil insulin-immunoreactive cells were also present, and in the 18-day-old embryos a few somatostatin cells could occasionally be discovered, too. |
| 888 | 2446417 | The insulin cells of the diabetic mice were severely degranulated and many of the glucagon, somatostatin and pancreatic polypeptide cells were displaced from the mantle to the core of the islet tissue where the non-insulin cells appeared to lose their continuity. |
| 889 | 2446417 | The volume and numerical percents of the insulin cells were significantly increased whereas those of the glucagon and somatostatin cells were decreased in the KKAy mice. |
| 890 | 2446417 | Pancreatic insulin and somatostatin contents were markedly diminished in the islets of KKAy compared with those of C57BL/6 mice. |
| 891 | 2446417 | The insulin cells of the diabetic mice were severely degranulated and many of the glucagon, somatostatin and pancreatic polypeptide cells were displaced from the mantle to the core of the islet tissue where the non-insulin cells appeared to lose their continuity. |
| 892 | 2446417 | The volume and numerical percents of the insulin cells were significantly increased whereas those of the glucagon and somatostatin cells were decreased in the KKAy mice. |
| 893 | 2446417 | Pancreatic insulin and somatostatin contents were markedly diminished in the islets of KKAy compared with those of C57BL/6 mice. |
| 894 | 2446417 | The insulin cells of the diabetic mice were severely degranulated and many of the glucagon, somatostatin and pancreatic polypeptide cells were displaced from the mantle to the core of the islet tissue where the non-insulin cells appeared to lose their continuity. |
| 895 | 2446417 | The volume and numerical percents of the insulin cells were significantly increased whereas those of the glucagon and somatostatin cells were decreased in the KKAy mice. |
| 896 | 2446417 | Pancreatic insulin and somatostatin contents were markedly diminished in the islets of KKAy compared with those of C57BL/6 mice. |
| 897 | 2454647 | The plasma immunoreactive insulin profiles were determined during a 6 h post injection period in subjects receiving concomitantly somatostatin to suppress endogenous insulin secretion. 2. |
| 898 | 2457528 | The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation. |
| 899 | 2457528 | The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined. |
| 900 | 2457528 | If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response. |
| 901 | 2457528 | Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease. |
| 902 | 2457528 | The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation. |
| 903 | 2457528 | The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined. |
| 904 | 2457528 | If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response. |
| 905 | 2457528 | Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease. |
| 906 | 2457530 | By indirect immunofluorescence, an anti-insulin antibody reacted positively with cell cytoplasm, whereas anti-somatostatin and anti-glucagon antibodies did not. |
| 907 | 2461657 | Anterograde infusion of insulin antibody increased glucagon and somatostatin secretion (p less than 0.0005), whereas retrograde insulin antibody infusion was without effect. |
| 908 | 2461657 | Anterograde infusion of somatostatin antibody had no effect upon insulin or glucagon secretion. |
| 909 | 2461657 | In contrast, retrograde infusion of somatostatin antibody increased both insulin and glucagon secretion (p less than 0.0005). |
| 910 | 2461657 | In comparison, anterograde infusion of antiglucagon antibody decreased somatostatin secretion without influencing insulin, whereas retrograde antiglucagon antibody infusion decreased insulin without changing somatostatin secretion. |
| 911 | 2461657 | Anterograde infusion of insulin antibody increased glucagon and somatostatin secretion (p less than 0.0005), whereas retrograde insulin antibody infusion was without effect. |
| 912 | 2461657 | Anterograde infusion of somatostatin antibody had no effect upon insulin or glucagon secretion. |
| 913 | 2461657 | In contrast, retrograde infusion of somatostatin antibody increased both insulin and glucagon secretion (p less than 0.0005). |
| 914 | 2461657 | In comparison, anterograde infusion of antiglucagon antibody decreased somatostatin secretion without influencing insulin, whereas retrograde antiglucagon antibody infusion decreased insulin without changing somatostatin secretion. |
| 915 | 2461657 | Anterograde infusion of insulin antibody increased glucagon and somatostatin secretion (p less than 0.0005), whereas retrograde insulin antibody infusion was without effect. |
| 916 | 2461657 | Anterograde infusion of somatostatin antibody had no effect upon insulin or glucagon secretion. |
| 917 | 2461657 | In contrast, retrograde infusion of somatostatin antibody increased both insulin and glucagon secretion (p less than 0.0005). |
| 918 | 2461657 | In comparison, anterograde infusion of antiglucagon antibody decreased somatostatin secretion without influencing insulin, whereas retrograde antiglucagon antibody infusion decreased insulin without changing somatostatin secretion. |
| 919 | 2461657 | Anterograde infusion of insulin antibody increased glucagon and somatostatin secretion (p less than 0.0005), whereas retrograde insulin antibody infusion was without effect. |
| 920 | 2461657 | Anterograde infusion of somatostatin antibody had no effect upon insulin or glucagon secretion. |
| 921 | 2461657 | In contrast, retrograde infusion of somatostatin antibody increased both insulin and glucagon secretion (p less than 0.0005). |
| 922 | 2461657 | In comparison, anterograde infusion of antiglucagon antibody decreased somatostatin secretion without influencing insulin, whereas retrograde antiglucagon antibody infusion decreased insulin without changing somatostatin secretion. |
| 923 | 2465668 | Insulin-like growth factor I in the pancreas of normal and diabetic adult rats. |
| 924 | 2465668 | Insulin-like growth factor I (IGF-I, somatomedin C) was mapped by immunocytochemistry in the pancreas of normal and experimentally influenced rats. |
| 925 | 2465668 | D, A and B cells, while the levels of somatostatin, glucagon and insulin, respectively, remained unchanged. |
| 926 | 2465668 | Cysteamine pre-treatment reduced the normally intense IGF-I and somatostatin immunoreactivities in the D cells. |
| 927 | 2465668 | In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged. |
| 928 | 2465668 | Insulin-like growth factor I in the pancreas of normal and diabetic adult rats. |
| 929 | 2465668 | Insulin-like growth factor I (IGF-I, somatomedin C) was mapped by immunocytochemistry in the pancreas of normal and experimentally influenced rats. |
| 930 | 2465668 | D, A and B cells, while the levels of somatostatin, glucagon and insulin, respectively, remained unchanged. |
| 931 | 2465668 | Cysteamine pre-treatment reduced the normally intense IGF-I and somatostatin immunoreactivities in the D cells. |
| 932 | 2465668 | In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged. |
| 933 | 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). |
| 934 | 2467789 | It reacted with human insulin as well, but did not crossreact with other polypeptide hormones produced in the pancreatic islets such as glucagon, somatostatin and pancreatic polypeptide. |
| 935 | 2470628 | We conclude that in insulinopenic diabetes, tissue SLI and SmRNA accumulation undergo parallel changes; are increased in pancreas and upper gut, reflecting augmented somatostatin synthesis; are reciprocally related to insulin acting directly or indirectly on somatostatin-producing cells; and are unchanged in the lower gut and brain, suggesting tissue-specific regulation of somatostatin gene transcription in diabetes. |
| 936 | 2482123 | We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. |
| 937 | 2494027 | We previously reported that sulfonylurea treatment reduces insulin (IRI), glucagon (IRG) and somatostatin (SRIF) release following metabolic stimuli from the isolated perfused pancreas of normal rats and that a reduction in IRI, IRG and SRIF pancreatic content was also observed. |
| 938 | 2494093 | Islet grafts were removed in toto and analyzed for contents of insulin, glucagon, somatostatin, and DNA or rates of glucose-stimulated (pro)insulin biosynthesis. |
| 939 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 940 | 2498883 | IFN-gamma was 50% more potent than TNF-alpha; together, their effects were additive. |
| 941 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 942 | 2498883 | In contrast, infection with reovirus type 3 did not induce ICAM-1 on islet cells, although it stimulated the expression of class I MHC proteins. |
| 943 | 2498883 | By double-label indirect immunofluorescence microscopy, ICAM-1 expression was identified on both beta (insulin-secreting) and delta (somatostatin-secreting) islet cells. |
| 944 | 2498883 | Monoclonal antibody to ICAM-1 precipitated protein of Mr 97,000 from [35S]methionine-labeled islets exposed to IFN-gamma and TNF-alpha, but not from control islets. |
| 945 | 2504552 | Growth hormone (GH) secretion is mediated by hypothalamic factors, mainly growth hormone releasing factor (GRF) and somatostatin (SS). |
| 946 | 2513696 | Morphologically the transplanted islets in the renal subcapsular space appeared normal on hematoxylin-eosin staining and immunostaining with antisera directed against insulin, glucagon, somatostatin and chromogranin A/B. |
| 947 | 2518343 | When double immunohistochemical staining was used to demonstrate different endocrine cell types (insulin, glucagon and pancreatic polypeptide) and S-100 protein immunoreactive cells, the latter proved to be a distinct cell type. |
| 948 | 2518343 | Somatostatin-producing cells and S-100 protein-containing cells were usually also present as two distinct cell populations, but positive staining for both S-100 protein and somatostatin was occasionally observed within the same cells. |
| 949 | 2521554 | Cytochrome P450 in livers of diabetic rats: regulation by growth hormone and insulin. |
| 950 | 2521554 | However, the treatment of hypophysectomized rats with insulin had no effect, and treatment of diabetic rats with growth hormone or a suppressing agent of somatostatin, cysteamine, showed trivial effects on P450-male and P450b. |
| 951 | 2535825 | In contrast to the continually diminishing insulin responsiveness observed, hormone inhibition by somatostatin of insulin secretion and basal cAMP metabolism remained intact throughout the passages examined. |
| 952 | 2538376 | Plasma insulin and glucagon concentrations were maintained constant by infusion of somatostatin with insulin and glucagon replacements. |
| 953 | 2544774 | The 125I-ANF binding to retinal particulate preparations was not inhibited by 1 microM concentration of somatostatin, vasopressin, vasoactive intestinal peptide, adrenocorticotropin, thyrotropin releasing hormone, or leu-enkephalin. |
| 954 | 2564365 | Insulin- and non-insulin-mediated glucose uptake, estimated with somatostatin-induced suppression of endogenous insulin secretion, contributed almost equally to the excess glucose utilization observed in the obese children. |
| 955 | 2565915 | Suppression of ectopic adrenocorticotropin secretion by the long-acting somatostatin analog octreotide. |
| 956 | 2565915 | The long-acting somatostatin analog (octreotide) was administered to a 37-yr-old woman with the ectopic ACTH syndrome. |
| 957 | 2565915 | Suppression of ectopic adrenocorticotropin secretion by the long-acting somatostatin analog octreotide. |
| 958 | 2565915 | The long-acting somatostatin analog (octreotide) was administered to a 37-yr-old woman with the ectopic ACTH syndrome. |
| 959 | 2566332 | The volume density of insulin-positive cells was decreased in the fetal pancreas of diabetic BB rats compared to fetuses of nondiabetic rats, but the volume density of glucagon- and somatostatin-positive cells remained normal. |
| 960 | 2566332 | Plasma insulin levels were decreased while plasma glucagon and somatostatin concentrations were normal. |
| 961 | 2566332 | Metabolic characterization of the growth-retarded fetuses of diabetic rats revealed, besides lower plasma insulin concentrations, increased branched chain amino acid levels, and normal plasma Sm/IGF-I levels. |
| 962 | 2566332 | The volume density of insulin-positive cells was decreased in the fetal pancreas of diabetic BB rats compared to fetuses of nondiabetic rats, but the volume density of glucagon- and somatostatin-positive cells remained normal. |
| 963 | 2566332 | Plasma insulin levels were decreased while plasma glucagon and somatostatin concentrations were normal. |
| 964 | 2566332 | Metabolic characterization of the growth-retarded fetuses of diabetic rats revealed, besides lower plasma insulin concentrations, increased branched chain amino acid levels, and normal plasma Sm/IGF-I levels. |
| 965 | 2566459 | TMB-8 and TFP stimulated insulin, glucagon, and somatostatin release in a dose-dependent manner at a low glucose concentration (2.5 mM). |
| 966 | 2566459 | The addition of NE (10(-9) M) to the incubation medium increased insulin, glucagon, and somatostatin secretion by 20-30% over control levels (P less than 0.05). |
| 967 | 2566459 | TMB-8 and TFP stimulated insulin, glucagon, and somatostatin release in a dose-dependent manner at a low glucose concentration (2.5 mM). |
| 968 | 2566459 | The addition of NE (10(-9) M) to the incubation medium increased insulin, glucagon, and somatostatin secretion by 20-30% over control levels (P less than 0.05). |
| 969 | 2566546 | Dogs were studied during 150 min of exercise with saline infusion alone (C; n = 6) with the glucagon levels clamped at basal values (somatostatin infusion with basal glucagon replacement and the normal fall in insulin simulated; BG; n = 5) or with the normal exercise-induced rise in glucagon simulated (somatostatin infusion with the rise in glucagon and the fall in insulin simulated; SG; n = 5). |
| 970 | 2568667 | [Response of plasma and retinal somatostatin to insulin-induced hypoglycemia in diabetic and control rats]. |
| 971 | 2568667 | Changes in plasmatic levels and retinal content of somatostatin after insulin-induced hypoglycemia were investigated in three different groups of animals: Control group (C), Diabetic untreated group (D); and, Insulin-treated diabetic group (DI). |
| 972 | 2568667 | The somatostatin retinal content is similar in animals not subjected to hypoglycemia and in the C and DI groups after hypoglycemia, where the rats of the D groups showed significantly higher values than the remainder of the experimental groups, an effect that is also evident in nontreated diabetic animals, even if they are not subjected to hypoglycemia, Summing up, the plasmatic somatostatin response to insulin-induced hypoglycemia is impaired in diabetic rats. |
| 973 | 2568667 | [Response of plasma and retinal somatostatin to insulin-induced hypoglycemia in diabetic and control rats]. |
| 974 | 2568667 | Changes in plasmatic levels and retinal content of somatostatin after insulin-induced hypoglycemia were investigated in three different groups of animals: Control group (C), Diabetic untreated group (D); and, Insulin-treated diabetic group (DI). |
| 975 | 2568667 | The somatostatin retinal content is similar in animals not subjected to hypoglycemia and in the C and DI groups after hypoglycemia, where the rats of the D groups showed significantly higher values than the remainder of the experimental groups, an effect that is also evident in nontreated diabetic animals, even if they are not subjected to hypoglycemia, Summing up, the plasmatic somatostatin response to insulin-induced hypoglycemia is impaired in diabetic rats. |
| 976 | 2568667 | [Response of plasma and retinal somatostatin to insulin-induced hypoglycemia in diabetic and control rats]. |
| 977 | 2568667 | Changes in plasmatic levels and retinal content of somatostatin after insulin-induced hypoglycemia were investigated in three different groups of animals: Control group (C), Diabetic untreated group (D); and, Insulin-treated diabetic group (DI). |
| 978 | 2568667 | The somatostatin retinal content is similar in animals not subjected to hypoglycemia and in the C and DI groups after hypoglycemia, where the rats of the D groups showed significantly higher values than the remainder of the experimental groups, an effect that is also evident in nontreated diabetic animals, even if they are not subjected to hypoglycemia, Summing up, the plasmatic somatostatin response to insulin-induced hypoglycemia is impaired in diabetic rats. |
| 979 | 2571541 | Subjects were studied after 5 days of prednisone (60 mg/day) or no steroid treatment and were infused with somatostatin, glucagon, growth hormone, [3H]glucose, [14C]leucine, and insulin (0.1 or 0.2 mU.kg-1.min-1). |
| 980 | 2572125 | Insulin and pancreatic somatostatin secretions were studied after stimulation with an arginine infusion (5 mmol/l) in isolated perfused pancreata of adult streptozotocin-diabetic rats. |
| 981 | 2572125 | In the presence of 2.8 mmol/l glucose, arginine clearly stimulated insulin and somatostatin secretions in diabetic rats, whereas it was ineffective in normal rats. |
| 982 | 2572125 | Insulin and pancreatic somatostatin secretions were studied after stimulation with an arginine infusion (5 mmol/l) in isolated perfused pancreata of adult streptozotocin-diabetic rats. |
| 983 | 2572125 | In the presence of 2.8 mmol/l glucose, arginine clearly stimulated insulin and somatostatin secretions in diabetic rats, whereas it was ineffective in normal rats. |
| 984 | 2573553 | Effects of glucagonlike peptide I-(7-36) on release of insulin, glucagon, and somatostatin by rat pancreatic islet cell monolayer cultures. |
| 985 | 2573553 | To characterize its action on islet cells, the release of insulin, glucagon, and somatostatin by rat pancreatic islet monolayer cultures at varying concentrations of GLP-I-(7-36) was measured. |
| 986 | 2573553 | Effects of glucagonlike peptide I-(7-36) on release of insulin, glucagon, and somatostatin by rat pancreatic islet cell monolayer cultures. |
| 987 | 2573553 | To characterize its action on islet cells, the release of insulin, glucagon, and somatostatin by rat pancreatic islet monolayer cultures at varying concentrations of GLP-I-(7-36) was measured. |
| 988 | 2575447 | These studies suggest somatotrophs of diabetic rats have altered sensitivity in vitro to the controlling hormones growth hormone releasing factor and somatostatin. |
| 989 | 2575840 | In previous studies in C57BL/KsJ mdb/mdb mice, we observed alterations in glucose-induced insulin secretion in vitro, and a defective inhibitory effect of somatostatin on insulin secretion. |
| 990 | 2576005 | Infusion of propranolol did not prevent insulin resistance, whereas somatostatin partially prevented its appearance. |
| 991 | 2576005 | Somatostatin plus metyrapone completely normalized posthypoglycemic insulin resistance. |
| 992 | 2576005 | Infusion of propranolol did not prevent insulin resistance, whereas somatostatin partially prevented its appearance. |
| 993 | 2576005 | Somatostatin plus metyrapone completely normalized posthypoglycemic insulin resistance. |
| 994 | 2576774 | Immunohistochemical, morphometric, and ultrastructural investigations of the early development of insulin, somatostatin, glucagon, and PP cells in foetal human pancreas. |
| 995 | 2576774 | Fresh autopsy specimens of pancreas, taken from 18 human foetuses at the 10th (n = 4), 12th (n = 7), and 14th (n = 7) weeks of gestation, were analyzed immunohistochemically for the presence of islet parenchymal cells, immunoreactive with antisera raised against insulin (B cells), somatostatin (D cells), glucagon (A cells), and pancreatic polypeptide (PP cells). |
| 996 | 2576774 | Immunohistochemical, morphometric, and ultrastructural investigations of the early development of insulin, somatostatin, glucagon, and PP cells in foetal human pancreas. |
| 997 | 2576774 | Fresh autopsy specimens of pancreas, taken from 18 human foetuses at the 10th (n = 4), 12th (n = 7), and 14th (n = 7) weeks of gestation, were analyzed immunohistochemically for the presence of islet parenchymal cells, immunoreactive with antisera raised against insulin (B cells), somatostatin (D cells), glucagon (A cells), and pancreatic polypeptide (PP cells). |
| 998 | 2581286 | Never fibers containing somatostatin or gastrin/cholecystokinin could not be detected in any of the groups and somatostatin and gastrin/cholecystokinin could not be measured in extracts of the lower esophageal sphincter. |
| 999 | 2591607 | Immunohistochemical examination of the islets using anti-insulin, glucagon and somatostatin antibodies by ABC peroxidase method showed the selective disappearance of B cells in the islets. |
| 1000 | 2612718 | Intervention is possible as follows: A) hyperfiltration may be reduced by non-glycemic intervention such as a moderate reduction of protein intake, treatment with aldose reductase inhibitors (work in progress) or acute administration of a somatostatin analogue. |
| 1001 | 2642296 | Intravenous infusion of 50% glucose for 2 h was associated with a decrease in the blood-brain barrier permeability to sodium (5.4 +/- 1.2 X 10(5) ml/g/s), whereas rats treated with an inhibitor of insulin-secretion (SMS 201-995, a somatostatin-analogue) had normal sodium permeability (7.3 +/- 2.0 X 10(5) ml/g/s). |
| 1002 | 2646389 | Attention is thus directed towards factors which may be directly involved in the pathogenesis of diabetic microangiopathy: --Special sensitivity of vascular collagen to protein glycosylation which could be reflected in the involvement of tendon and aponeurotic collagen, --platelet abnormalities of which the exacerbating role appears to be confirmed by the significant efficacy of aspirin in the treatment of nonproliferative retinopathy in insulin-independent diabetics, --rheological abnormalities which might essentially be secondary to chronic hyperglycemia, --hormonal abnormalities, in particular hypersecretion of growth hormone and/or somatomedin C, whose role has long been suspected and could be established by therapeutic trials with new somatostatin analogues. |
| 1003 | 2655475 | Finally, induction of normoglycemic hyperinsulinemia by intravenous glucose-insulin infusion increased Jmax 1.8-fold, similar to hyperglycemic hyperinsulinemia, but induction of hyperglycemic normoinsulinemia by intravenous glucose-somatostatin infusion did not change Jmax. |
| 1004 | 2656340 | We evaluated the effectiveness of a more potent and longer-acting somatostatin analogue (SMS 201-995) as an adjunct to insulin therapy, in a double-blind placebo-controlled randomized study of 26 C-peptide-negative type I (insulin-dependent) diabetic patients (20 women, 6 men, aged 22-40 yr) on their conventional drug regimens for 12 wk. |
| 1005 | 2658456 | Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment. |
| 1006 | 2658456 | To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. |
| 1007 | 2658456 | The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. |
| 1008 | 2658456 | Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. |
| 1009 | 2658456 | A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. |
| 1010 | 2658456 | Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment. |
| 1011 | 2658456 | To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. |
| 1012 | 2658456 | The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. |
| 1013 | 2658456 | Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. |
| 1014 | 2658456 | A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. |
| 1015 | 2658456 | Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment. |
| 1016 | 2658456 | To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. |
| 1017 | 2658456 | The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. |
| 1018 | 2658456 | Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. |
| 1019 | 2658456 | A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. |
| 1020 | 2658456 | Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment. |
| 1021 | 2658456 | To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. |
| 1022 | 2658456 | The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. |
| 1023 | 2658456 | Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. |
| 1024 | 2658456 | A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. |
| 1025 | 2658456 | Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment. |
| 1026 | 2658456 | To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. |
| 1027 | 2658456 | The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. |
| 1028 | 2658456 | Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. |
| 1029 | 2658456 | A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. |
| 1030 | 2669517 | To examine the importance of first-phase insulin secretion on total body glucose homeostasis, six normal subjects (age, 24 +/- 1 yr; ideal body wt, 100 +/- 1%) received three hyperglycemic (+75 mg/100 ml) clamp studies in combination with [3-3H]glucose: study I, 150 min hyperglycemic clamp; study II, hyperglycemic clamp plus somatostatin (6 micrograms/min) plus basal glucagon replacement (0.4 ng.kg-1.min-1) plus an insulin infusion designed to mimic only the second phase of insulin secretion; and study III, hyperglycemic clamp plus somatostatin plus basal glucagon plus an insulin infusion designed to mimic both the first and second phase of insulin secretion. |
| 1031 | 2670104 | Slides were stained for insulin(B), glucagon(A), somatostatin(D), and pancreatic polypeptide (PP) producing cells using immunocytochemistry. |
| 1032 | 2671112 | Effects of a somatostatin derivative (SMS 201-995) on postprandial hyperglycemia in insulin-dependent diabetics studied by means of a closed-loop device. |
| 1033 | 2671112 | We studied the effects of a premeal sc injection of an analog of somatostatin (SMS 201-995, Sandoz) on the postprandial glycemic excursions, insulin requirement and hormone profiles (GH, glucagon and C-peptide) in 8 IDDM patients (diabetes duration 14.0 +/- 6.5 yr, daily insulin requirement 36 +/- 6.4 U) maintained normoglycemic by connecting them to a closed-loop insulin infusion system (Betalike, Genoa). |
| 1034 | 2671112 | Effects of a somatostatin derivative (SMS 201-995) on postprandial hyperglycemia in insulin-dependent diabetics studied by means of a closed-loop device. |
| 1035 | 2671112 | We studied the effects of a premeal sc injection of an analog of somatostatin (SMS 201-995, Sandoz) on the postprandial glycemic excursions, insulin requirement and hormone profiles (GH, glucagon and C-peptide) in 8 IDDM patients (diabetes duration 14.0 +/- 6.5 yr, daily insulin requirement 36 +/- 6.4 U) maintained normoglycemic by connecting them to a closed-loop insulin infusion system (Betalike, Genoa). |
| 1036 | 2680369 | During RIA, this Ab did not cross-react with glucagon, somatostatin or pancreatic polypeptide. |
| 1037 | 2687064 | Sandostatin, a new analogue of somatostatin, reduces the metabolic changes induced by the nocturnal interruption of continuous subcutaneous insulin infusion in type 1 (insulin-dependent) diabetic patients. |
| 1038 | 2687064 | With the aim of assessing a new somatostatin analogue to prevent the metabolic changes induced by a 6-h nocturnal arrest of an insulin pump, nine C-peptide negative Type 1 (insulin-dependent) diabetic patients were submitted blindly to two interruptions (from 23.00 to 05.00 hours) of their continuous s.c. insulin infusion, once after a single s.c. injection at 23.00 hours of 50 micrograms SMS 201-995 (Sandostatin, Sandoz) and once after 0.9% NaCl. |
| 1039 | 2687064 | Sandostatin, a new analogue of somatostatin, reduces the metabolic changes induced by the nocturnal interruption of continuous subcutaneous insulin infusion in type 1 (insulin-dependent) diabetic patients. |
| 1040 | 2687064 | With the aim of assessing a new somatostatin analogue to prevent the metabolic changes induced by a 6-h nocturnal arrest of an insulin pump, nine C-peptide negative Type 1 (insulin-dependent) diabetic patients were submitted blindly to two interruptions (from 23.00 to 05.00 hours) of their continuous s.c. insulin infusion, once after a single s.c. injection at 23.00 hours of 50 micrograms SMS 201-995 (Sandostatin, Sandoz) and once after 0.9% NaCl. |
| 1041 | 2689136 | Like endogenous somatostatin, it exerts a potent inhibitory effect on the release of anterior pituitary growth hormone and thyroid-stimulating hormone, and peptides of the gastroenteropancreatic endocrine system, while overcoming some of the shortcomings of exogenously administered somatostatin, namely a short duration of action, a need for intravenous administration and postinfusion rebound hypersecretion of hormone. |
| 1042 | 2689826 | Interleukin-1 induced increases in glucose utilization are insulin mediated. |
| 1043 | 2689826 | Interleukin-1 (IL-1) is known to modulate a variety of the acute-phase responses to infection. |
| 1044 | 2689826 | Human purified IL-1 was administered to chronically, catheterized conscious rats and increased the plasma insulin levels and the Rg in macrophage-rich tissues, including the lung, spleen, liver and skin. |
| 1045 | 2689826 | To eliminate the insulin-stimulated increase in Rg, somatostatin (SRIF) was infused 1 h prior to IL-1. |
| 1046 | 2689826 | SRIF prevented the IL-1 induced increase in insulin and tissue glucose utilization. |
| 1047 | 2689826 | These data suggest that the administration of IL-1 increases organ glucose utilization by insulin-dependent mechanisms. |
| 1048 | 2689969 | In basal conditions, 11 patients presented insulin insensitivity (as measured by the glucose-insulin-somatostatin technique) which was unaffected by the pharmacological treatment. |
| 1049 | 2747219 | Dystrophic axons contained substance P- and gastrin-releasing peptide (gastrin-releasing peptide/bombesin)-like staining but were not labeled by antisera directed against vasoactive intestinal peptide, dynorphin-B, somatostatin, leu- and met-enkephalin and neuropeptide tyrosine. |
| 1050 | 2747219 | Substance P and gastrin-releasing peptide/bombesin containing subpopulations of presynaptic elements in prevertebral sympathetic ganglia are thought to participate in local reflex control of bowel motility and lesions preferentially involving these elements may contribute to bowel dysfunction. |
| 1051 | 2753972 | As a group, serum insulin-like growth factor-I was lower in DM vs. non-DM individuals (P = 0.0014), although when separated by sex this difference did not reach statistical significance in women (P = 0.317). |
| 1052 | 2753972 | The altered frequency of GH pulses together with enhanced interpulse GH concentrations and an amplified circadian GH rhythm are compatible with hypothalamic dysfunction associated with dysregulation of somatostatin and/or GHRH secretion. |
| 1053 | 2759363 | Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats. |
| 1054 | 2759363 | In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. |
| 1055 | 2759363 | In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. |
| 1056 | 2759363 | The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. |
| 1057 | 2759363 | Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats. |
| 1058 | 2759363 | In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. |
| 1059 | 2759363 | In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. |
| 1060 | 2759363 | The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. |
| 1061 | 2759363 | Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats. |
| 1062 | 2759363 | In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. |
| 1063 | 2759363 | In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. |
| 1064 | 2759363 | The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. |
| 1065 | 2827061 | Insulin sensitivity, measured by the "steady state plasma glucose", obtained after a 150 min glucose-insulin-somatostatin infusion, improved in all patients but two. |
| 1066 | 2834942 | The fasting and incremental postprandial levels of insulin, C-peptide, glucagon, and somatostatin did not change, whereas the mean triglyceride concentrations were lower after the high-fiber diet. |
| 1067 | 2843409 | Using antisera to glucagon, insulin, and somatostatin, we found that less than 15% of the cells in any of these three islet cell lines contained immunopositive cells. |
| 1068 | 2857144 | Immunoperoxidase stains confirmed the presence of insulin, glucagon, and somatostatin within nests of islet cells. |
| 1069 | 2857668 | In contrast, treatment of alloxan-diabetic dogs (N = 3) by a GCIIS for 24 h revived some responsiveness of the glucagon, insulin, and somatostatin to glucose (1.3-11 mM) of the subsequently perfused pancreas. |
| 1070 | 2857669 | To study the effects of insulin on leucine turnover during fasting, acute insulin deficiency was induced by the simultaneous infusion of somatostatin and glucagon in conscious dogs fasted 18 h (N = 10) and 48 h (N = 11). |
| 1071 | 2857727 | The effect of insulin treatment on the rate of decline of plasma glucose concentration was determined in nine patients with hyperosmolar hyperglycemic nonketosis [HHNK; mean plasma glucose, 999 +/- 59 (+/- SEM) mg/dl] and in six normal subjects rendered hyperglycemic by a combined infusion of somatostatin and glucose (mean plasma glucose, 653 +/- 28 mg/dl). |
| 1072 | 2858423 | To determine the effects of prolonged hyperglycaemia on pancreatic islet A- and B-cell function, plasma glucose was clamped for 12 h at approximately 11 and 5 mmol/l in control experiments by infusing glucose and somatostatin along with replacement amounts of insulin, glucagon, and growth hormone in seven normal volunteers. |
| 1073 | 2861121 | Blood glucose, somatostatin and counterregulatory hormone responses to an i.v. bolus of insulin were studied in insulin-dependent diabetics with different degrees of autonomic neuropathy, after 24 hours of optimised control with an artificial pancreas. |
| 1074 | 2861121 | It is concluded that the glucagon response to insulin hypoglycaemia is reduced in all type 1 longstanding diabetics, whereas catecholamine and somatostatin responses are only abolished in those with autonomic neuropathy. |
| 1075 | 2861121 | Blood glucose, somatostatin and counterregulatory hormone responses to an i.v. bolus of insulin were studied in insulin-dependent diabetics with different degrees of autonomic neuropathy, after 24 hours of optimised control with an artificial pancreas. |
| 1076 | 2861121 | It is concluded that the glucagon response to insulin hypoglycaemia is reduced in all type 1 longstanding diabetics, whereas catecholamine and somatostatin responses are only abolished in those with autonomic neuropathy. |
| 1077 | 2861127 | The present study was designed to compare, in lean and obese nondiabetic subjects, basal and postprandial levels of peripheral venous plasma insulin, glucagon, gastrin, pancreatic polypeptide (PP), glucose, triglycerides, and somatostatin-like immunoreactivity (SLI) during the infusion of synthetic somatostatin-14 or saline. |
| 1078 | 2861127 | During the infusion of saline, basal peripheral vein levels of insulin, gastrin, and triglycerides were elevated in obese subjects, whereas basal plasma SLI levels were significantly lower compared with the lean controls. |
| 1079 | 2861127 | After the ingestion of the meal, augmented concentrations of insulin and gastrin were observed in the obese subjects, whereas postprandial SLI and PP levels were reduced. |
| 1080 | 2861127 | During the infusion of somatostatin, only basal insulin levels were significantly lower in the obese subjects, whereas no change of any basal hormone level was observed in the lean group. |
| 1081 | 2861127 | The present study was designed to compare, in lean and obese nondiabetic subjects, basal and postprandial levels of peripheral venous plasma insulin, glucagon, gastrin, pancreatic polypeptide (PP), glucose, triglycerides, and somatostatin-like immunoreactivity (SLI) during the infusion of synthetic somatostatin-14 or saline. |
| 1082 | 2861127 | During the infusion of saline, basal peripheral vein levels of insulin, gastrin, and triglycerides were elevated in obese subjects, whereas basal plasma SLI levels were significantly lower compared with the lean controls. |
| 1083 | 2861127 | After the ingestion of the meal, augmented concentrations of insulin and gastrin were observed in the obese subjects, whereas postprandial SLI and PP levels were reduced. |
| 1084 | 2861127 | During the infusion of somatostatin, only basal insulin levels were significantly lower in the obese subjects, whereas no change of any basal hormone level was observed in the lean group. |
| 1085 | 2861128 | We studied the effect of an acute reduction in glucose concentration on insulin and glucagon secretion in this model and contrasted the results with the effects of epinephrine and somatostatin using the in vitro isolated, perfused pancreas. |
| 1086 | 2861128 | Epinephrine (55 nM) and somatostatin (110 nM) caused similar decreases in insulin secretion in both groups. |
| 1087 | 2861128 | We studied the effect of an acute reduction in glucose concentration on insulin and glucagon secretion in this model and contrasted the results with the effects of epinephrine and somatostatin using the in vitro isolated, perfused pancreas. |
| 1088 | 2861128 | Epinephrine (55 nM) and somatostatin (110 nM) caused similar decreases in insulin secretion in both groups. |
| 1089 | 2861762 | Localization of insulin, glucagon and somatostatin-immunoreactive cells were demonstrated in all implants from the 1st to the 5th d. |
| 1090 | 2862565 | To study whether this is due to a direct effect on the endocrine pancreas, the effects of the thiazide hydroflumethiazide on the release of glucagon, insulin, and somatostatin from the isolated perfused pancreas of normal and alloxan diabetic dogs were examined. |
| 1091 | 2862565 | Hydroflumethiazide at concentrations ranging from 1 to 50 micrograms/mL stimulated the normal secretion of glucagon (P less than 0.001), insulin (P less than 0.001), and somatostatin (P less than 0.001) in a dose-dependent manner. |
| 1092 | 2862565 | The normal hormone responses evoked by 50 micrograms/mL of the thiazide were, however, modified by the prevailing glucose level: higher insulin (P less than 0.05) and somatostatin (P less than 0.05) and lower glucagon (P less than 0.05) were obtained at the high glucose concentration of 11 mmol/L rather than at the low glucose concentration of 1.3 mmol/L. |
| 1093 | 2862565 | The infusion of bumetanide at doses ranging from 0.5 to 3 micrograms/mL did not alter the release of glucagon, insulin, and somatostatin in the presence of 5.5 mmol/L glucose. |
| 1094 | 2862565 | To study whether this is due to a direct effect on the endocrine pancreas, the effects of the thiazide hydroflumethiazide on the release of glucagon, insulin, and somatostatin from the isolated perfused pancreas of normal and alloxan diabetic dogs were examined. |
| 1095 | 2862565 | Hydroflumethiazide at concentrations ranging from 1 to 50 micrograms/mL stimulated the normal secretion of glucagon (P less than 0.001), insulin (P less than 0.001), and somatostatin (P less than 0.001) in a dose-dependent manner. |
| 1096 | 2862565 | The normal hormone responses evoked by 50 micrograms/mL of the thiazide were, however, modified by the prevailing glucose level: higher insulin (P less than 0.05) and somatostatin (P less than 0.05) and lower glucagon (P less than 0.05) were obtained at the high glucose concentration of 11 mmol/L rather than at the low glucose concentration of 1.3 mmol/L. |
| 1097 | 2862565 | The infusion of bumetanide at doses ranging from 0.5 to 3 micrograms/mL did not alter the release of glucagon, insulin, and somatostatin in the presence of 5.5 mmol/L glucose. |
| 1098 | 2862565 | To study whether this is due to a direct effect on the endocrine pancreas, the effects of the thiazide hydroflumethiazide on the release of glucagon, insulin, and somatostatin from the isolated perfused pancreas of normal and alloxan diabetic dogs were examined. |
| 1099 | 2862565 | Hydroflumethiazide at concentrations ranging from 1 to 50 micrograms/mL stimulated the normal secretion of glucagon (P less than 0.001), insulin (P less than 0.001), and somatostatin (P less than 0.001) in a dose-dependent manner. |
| 1100 | 2862565 | The normal hormone responses evoked by 50 micrograms/mL of the thiazide were, however, modified by the prevailing glucose level: higher insulin (P less than 0.05) and somatostatin (P less than 0.05) and lower glucagon (P less than 0.05) were obtained at the high glucose concentration of 11 mmol/L rather than at the low glucose concentration of 1.3 mmol/L. |
| 1101 | 2862565 | The infusion of bumetanide at doses ranging from 0.5 to 3 micrograms/mL did not alter the release of glucagon, insulin, and somatostatin in the presence of 5.5 mmol/L glucose. |
| 1102 | 2862565 | To study whether this is due to a direct effect on the endocrine pancreas, the effects of the thiazide hydroflumethiazide on the release of glucagon, insulin, and somatostatin from the isolated perfused pancreas of normal and alloxan diabetic dogs were examined. |
| 1103 | 2862565 | Hydroflumethiazide at concentrations ranging from 1 to 50 micrograms/mL stimulated the normal secretion of glucagon (P less than 0.001), insulin (P less than 0.001), and somatostatin (P less than 0.001) in a dose-dependent manner. |
| 1104 | 2862565 | The normal hormone responses evoked by 50 micrograms/mL of the thiazide were, however, modified by the prevailing glucose level: higher insulin (P less than 0.05) and somatostatin (P less than 0.05) and lower glucagon (P less than 0.05) were obtained at the high glucose concentration of 11 mmol/L rather than at the low glucose concentration of 1.3 mmol/L. |
| 1105 | 2862565 | The infusion of bumetanide at doses ranging from 0.5 to 3 micrograms/mL did not alter the release of glucagon, insulin, and somatostatin in the presence of 5.5 mmol/L glucose. |
| 1106 | 2862717 | Insulin, glucagon and somatostatin content of the non-obese diabetic (NOD) mouse pancreas and plasma virus antibodies to Coxsackie B- and reoviruses. |
| 1107 | 2862717 | The amounts of insulin, glucagon and somatostatin in the pancreas of NOD mice were determined and the results were compared with those of normal ICR-strain mice, and plasma antibodies to Coxsackie B-3 and reovirus types 1, 2 and 3 were measured. |
| 1108 | 2862717 | Insulin, glucagon and somatostatin content of the non-obese diabetic (NOD) mouse pancreas and plasma virus antibodies to Coxsackie B- and reoviruses. |
| 1109 | 2862717 | The amounts of insulin, glucagon and somatostatin in the pancreas of NOD mice were determined and the results were compared with those of normal ICR-strain mice, and plasma antibodies to Coxsackie B-3 and reovirus types 1, 2 and 3 were measured. |
| 1110 | 2863188 | Endogenous insulin secretion was inhibited by somatostatin and plasma glucose level maintained at 180 mg/dl for 5. |
| 1111 | 2863282 | Insulin and somatostatin release were determined on culture day 3 or 4 when amylase measurements indicated an absence of functional exocrine cells. |
| 1112 | 2863282 | Glucose, alpha-ketoisocaproic acid, theophylline, glucagon, and tolbutamide each stimulated insulin release 2- to 3-fold and somatostatin release 1.5- to 2-fold. |
| 1113 | 2863282 | Epinephrine and somatostatin both inhibited glucose-stimulated insulin release. |
| 1114 | 2863282 | Of 15 sera from patients with newly diagnosed insulin-dependent diabetes mellitus 9 were ICSA positive, whereas all of 10 control sera were negative; in contrast, using rat insulinoma cells only 4 diabetic sera were positive, as well as 2 control sera. |
| 1115 | 2863282 | Insulin and somatostatin release were determined on culture day 3 or 4 when amylase measurements indicated an absence of functional exocrine cells. |
| 1116 | 2863282 | Glucose, alpha-ketoisocaproic acid, theophylline, glucagon, and tolbutamide each stimulated insulin release 2- to 3-fold and somatostatin release 1.5- to 2-fold. |
| 1117 | 2863282 | Epinephrine and somatostatin both inhibited glucose-stimulated insulin release. |
| 1118 | 2863282 | Of 15 sera from patients with newly diagnosed insulin-dependent diabetes mellitus 9 were ICSA positive, whereas all of 10 control sera were negative; in contrast, using rat insulinoma cells only 4 diabetic sera were positive, as well as 2 control sera. |
| 1119 | 2863282 | Insulin and somatostatin release were determined on culture day 3 or 4 when amylase measurements indicated an absence of functional exocrine cells. |
| 1120 | 2863282 | Glucose, alpha-ketoisocaproic acid, theophylline, glucagon, and tolbutamide each stimulated insulin release 2- to 3-fold and somatostatin release 1.5- to 2-fold. |
| 1121 | 2863282 | Epinephrine and somatostatin both inhibited glucose-stimulated insulin release. |
| 1122 | 2863282 | Of 15 sera from patients with newly diagnosed insulin-dependent diabetes mellitus 9 were ICSA positive, whereas all of 10 control sera were negative; in contrast, using rat insulinoma cells only 4 diabetic sera were positive, as well as 2 control sera. |
| 1123 | 2863913 | Increased peripheral venous somatostatin concentration and decreased glucagon response to arginine in patients with insulin dependent diabetes mellitus without residual B-cell function. |
| 1124 | 2864297 | The values from the standard FSIGT were then compared with direct measurements obtained from experiments in which the dynamic insulin response to glucose was suppressed with somatostatin (SRIF). |
| 1125 | 2865093 | Reduced postprandial hyperglycemia after subcutaneous injection of a somatostatin-analogue (SMS 201-995) in insulin-dependent diabetes mellitus. |
| 1126 | 2865093 | The effect of a new octapeptide analogue of somatostatin (SMS 201-995) on blood glucose and gut hormone levels was studied in 10 C-peptide-negative, insulin-dependent diabetic (IDDM) subjects. |
| 1127 | 2865093 | SMS abolished completely the postprandial increase in plasma gastrin and pancreatic polypeptide (PP) concentrations. |
| 1128 | 2865093 | Reduced postprandial hyperglycemia after subcutaneous injection of a somatostatin-analogue (SMS 201-995) in insulin-dependent diabetes mellitus. |
| 1129 | 2865093 | The effect of a new octapeptide analogue of somatostatin (SMS 201-995) on blood glucose and gut hormone levels was studied in 10 C-peptide-negative, insulin-dependent diabetic (IDDM) subjects. |
| 1130 | 2865093 | SMS abolished completely the postprandial increase in plasma gastrin and pancreatic polypeptide (PP) concentrations. |
| 1131 | 2865246 | To examine the beta-adrenergic effects of the catecholamines in poorly controlled diabetes, we have studied insulin-deprived alloxan-diabetic (A-D) dogs during 90 min of moderate exercise (100 m/min, 10-12 degrees) alone (C) or with propranolol (5 micrograms . kg-1 . min-1) (P) or combined P and somatostatin infusion (0.5 microgram . kg-1 . min-1) (P + St). |
| 1132 | 2865245 | To define the role of immunoreactive glucagon (IRG) during exercise in diabetes, 12 insulin-deprived alloxan-diabetic (A-D) dogs were run for 90 min (100 m/min, 12 degrees) with or without somatostatin (St 0.5 microgram . kg-1 . min-1). |
| 1133 | 2865274 | To accomplish this, the serum glucose was clamped at a desired level during a period of insulin deficiency induced by a somatostatin infusion (SRIF, 550 micrograms/h). |
| 1134 | 2866056 | The euglycaemic clamp, insulin sensitivity test with somatostatin, and insulin sensitivity test without somatostatin, were compared as in vivo methods of assessing insulin sensitivity. |
| 1135 | 2866056 | Somatostatin was not found to influence the assessment of insulin sensitivity by the insulin sensitivity test. |
| 1136 | 2866056 | The insulin sensitivity test without somatostatin thus provides a simple and economical tool for studying insulin sensitivity. |
| 1137 | 2866056 | The euglycaemic clamp, insulin sensitivity test with somatostatin, and insulin sensitivity test without somatostatin, were compared as in vivo methods of assessing insulin sensitivity. |
| 1138 | 2866056 | Somatostatin was not found to influence the assessment of insulin sensitivity by the insulin sensitivity test. |
| 1139 | 2866056 | The insulin sensitivity test without somatostatin thus provides a simple and economical tool for studying insulin sensitivity. |
| 1140 | 2866056 | The euglycaemic clamp, insulin sensitivity test with somatostatin, and insulin sensitivity test without somatostatin, were compared as in vivo methods of assessing insulin sensitivity. |
| 1141 | 2866056 | Somatostatin was not found to influence the assessment of insulin sensitivity by the insulin sensitivity test. |
| 1142 | 2866056 | The insulin sensitivity test without somatostatin thus provides a simple and economical tool for studying insulin sensitivity. |
| 1143 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1144 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1145 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1146 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1147 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1148 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1149 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1150 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1151 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1152 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1153 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1154 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1155 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1156 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1157 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1158 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1159 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1160 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1161 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1162 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1163 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1164 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1165 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1166 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1167 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1168 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1169 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1170 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1171 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1172 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1173 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 1174 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 1175 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 1176 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 1177 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 1178 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 1179 | 2866155 | Effect of twice daily subcutaneous administration of a long-acting somatostatin analog on 24-hour plasma glucose profiles in patients with insulin-dependent diabetes mellitus. |
| 1180 | 2866155 | To determine the effect of twice daily subcutaneous administration of a long-acting somatostatin analog on diabetic glycemic control, seven insulin-dependent diabetic subjects were treated with mixtures of insulin (regular and lente) given 30 minutes before breakfast and supper alone or along with WY-41, 747, a long-acting somatostatin analog. |
| 1181 | 2866155 | We conclude that administration of a long-acting somatostatin analog such as WY-41,747 twice daily along with insulin may permit some diabetic patients to achieve satisfactory glycemic control without having to inject insulin 3-4 times daily prior to each meal. |
| 1182 | 2866155 | Effect of twice daily subcutaneous administration of a long-acting somatostatin analog on 24-hour plasma glucose profiles in patients with insulin-dependent diabetes mellitus. |
| 1183 | 2866155 | To determine the effect of twice daily subcutaneous administration of a long-acting somatostatin analog on diabetic glycemic control, seven insulin-dependent diabetic subjects were treated with mixtures of insulin (regular and lente) given 30 minutes before breakfast and supper alone or along with WY-41, 747, a long-acting somatostatin analog. |
| 1184 | 2866155 | We conclude that administration of a long-acting somatostatin analog such as WY-41,747 twice daily along with insulin may permit some diabetic patients to achieve satisfactory glycemic control without having to inject insulin 3-4 times daily prior to each meal. |
| 1185 | 2866155 | Effect of twice daily subcutaneous administration of a long-acting somatostatin analog on 24-hour plasma glucose profiles in patients with insulin-dependent diabetes mellitus. |
| 1186 | 2866155 | To determine the effect of twice daily subcutaneous administration of a long-acting somatostatin analog on diabetic glycemic control, seven insulin-dependent diabetic subjects were treated with mixtures of insulin (regular and lente) given 30 minutes before breakfast and supper alone or along with WY-41, 747, a long-acting somatostatin analog. |
| 1187 | 2866155 | We conclude that administration of a long-acting somatostatin analog such as WY-41,747 twice daily along with insulin may permit some diabetic patients to achieve satisfactory glycemic control without having to inject insulin 3-4 times daily prior to each meal. |
| 1188 | 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. |
| 1189 | 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). |
| 1190 | 2866196 | Furthermore feedback insulin infusion enhanced GIP and decreased C-peptide responses, but did not affect the glucagon response to the meal. |
| 1191 | 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. |
| 1192 | 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. |
| 1193 | 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). |
| 1194 | 2866196 | Furthermore feedback insulin infusion enhanced GIP and decreased C-peptide responses, but did not affect the glucagon response to the meal. |
| 1195 | 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. |
| 1196 | 2866996 | GRF-40 produced a dose-dependent stimulation of insulin, glucagon, and somatostatin secretion. |
| 1197 | 2866996 | The responses to GRF-40 were modified by the prevailing glucose level: higher insulin and somatostatin and lower glucagon responses were obtained at high rather than low glucose. |
| 1198 | 2866996 | The findings reported here provide support that pancreatic insulin and glucagon are modulated by GRF-40 with somatostatin as its inhibitory counterpart. |
| 1199 | 2866996 | GRF-40 produced a dose-dependent stimulation of insulin, glucagon, and somatostatin secretion. |
| 1200 | 2866996 | The responses to GRF-40 were modified by the prevailing glucose level: higher insulin and somatostatin and lower glucagon responses were obtained at high rather than low glucose. |
| 1201 | 2866996 | The findings reported here provide support that pancreatic insulin and glucagon are modulated by GRF-40 with somatostatin as its inhibitory counterpart. |
| 1202 | 2866996 | GRF-40 produced a dose-dependent stimulation of insulin, glucagon, and somatostatin secretion. |
| 1203 | 2866996 | The responses to GRF-40 were modified by the prevailing glucose level: higher insulin and somatostatin and lower glucagon responses were obtained at high rather than low glucose. |
| 1204 | 2866996 | The findings reported here provide support that pancreatic insulin and glucagon are modulated by GRF-40 with somatostatin as its inhibitory counterpart. |
| 1205 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1206 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1207 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1208 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1209 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1210 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1211 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1212 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1213 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1214 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1215 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1216 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1217 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1218 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1219 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1220 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1221 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1222 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1223 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1224 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1225 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1226 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1227 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1228 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1229 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1230 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1231 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1232 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1233 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1234 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1235 | 2867847 | Somatostatin release from freshly isolated and cultured rat islets in response to rat insulin and to anti-insulin serum. |
| 1236 | 2867847 | This study deals with the influence insulin exerts upon pancreatic somatostatin release. |
| 1237 | 2867847 | No change in somatostatin release was caused by insulin (25 U/l) during perifusion of freshly isolated islets at 8.3 mmol/l glucose, whereas AIS showed an inhibitory effect. |
| 1238 | 2867847 | During a 42 hr culture period, somatostatin content of culture medium remained low in the presence of insulin but was elevated when AIS has been added. |
| 1239 | 2867847 | Precultivated islets responded to exogenous insulin with a decrease in somatostatin release in static incubations and in perifusion experiments. |
| 1240 | 2867847 | The inhibition of somatostatin release from freshly isolated islets observed during perifusion with AIS may be caused by anti-insulin receptor antibodies probably present in the anti-insulin serum. |
| 1241 | 2867944 | Insulin (approximately 14 microU/ml) and glucagon (approximately 70 pg/ml) were maintained constant on both occasions by an infusion of somatostatin and insulin. |
| 1242 | 2868453 | [Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. |
| 1243 | 2868453 | A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. |
| 1244 | 2868453 | [Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. |
| 1245 | 2868453 | A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. |
| 1246 | 2868708 | Ontogeny of cells containing insulin, glucagon, pancreatic polypeptide hormone and somatostatin in the bovine pancreas. |
| 1247 | 2868708 | Antibodies to insulin, glucagon, pancreatic polypeptide hormone (PP) and somatostatin were used in the immunofluorescence histochemical procedure to study the ontogeny of pancreatic endocrine cells containing the four hormones in the bovine fetus of approximately 100 days gestation to term. |
| 1248 | 2868708 | Immunoreactive cells staining for insulin, glucagon, PP and somatostatin were present in the pancreas of all fetuses studied. |
| 1249 | 2868708 | Ontogeny of cells containing insulin, glucagon, pancreatic polypeptide hormone and somatostatin in the bovine pancreas. |
| 1250 | 2868708 | Antibodies to insulin, glucagon, pancreatic polypeptide hormone (PP) and somatostatin were used in the immunofluorescence histochemical procedure to study the ontogeny of pancreatic endocrine cells containing the four hormones in the bovine fetus of approximately 100 days gestation to term. |
| 1251 | 2868708 | Immunoreactive cells staining for insulin, glucagon, PP and somatostatin were present in the pancreas of all fetuses studied. |
| 1252 | 2868708 | Ontogeny of cells containing insulin, glucagon, pancreatic polypeptide hormone and somatostatin in the bovine pancreas. |
| 1253 | 2868708 | Antibodies to insulin, glucagon, pancreatic polypeptide hormone (PP) and somatostatin were used in the immunofluorescence histochemical procedure to study the ontogeny of pancreatic endocrine cells containing the four hormones in the bovine fetus of approximately 100 days gestation to term. |
| 1254 | 2868708 | Immunoreactive cells staining for insulin, glucagon, PP and somatostatin were present in the pancreas of all fetuses studied. |
| 1255 | 2869846 | Intra-islet insulin-glucagon-somatostatin relationships. |
| 1256 | 2869995 | Modulatory effect of glucose, amino acids, and secretin on CCK-8-induced somatostatin and pancreatic polypeptide release in dogs. |
| 1257 | 2869995 | Protein- and fat-rich test meals elicit a strong stimulatory effect on postprandial somatostatin (SLI) and pancreatic polypeptide (PP) release, whereas carbohydrate-rich meals rather attenuate the response of both hormones. |
| 1258 | 2869995 | Pancreatic polypeptide (PP) levels rose 200-300 pg/ml during CCK plus saline. |
| 1259 | 2869995 | Modulatory effect of glucose, amino acids, and secretin on CCK-8-induced somatostatin and pancreatic polypeptide release in dogs. |
| 1260 | 2869995 | Protein- and fat-rich test meals elicit a strong stimulatory effect on postprandial somatostatin (SLI) and pancreatic polypeptide (PP) release, whereas carbohydrate-rich meals rather attenuate the response of both hormones. |
| 1261 | 2869995 | Pancreatic polypeptide (PP) levels rose 200-300 pg/ml during CCK plus saline. |
| 1262 | 2870077 | The effect of hyperglycemia per se on glucose uptake by muscle tissue was quantitated in six controls and six type II diabetics by the forearm technique, under conditions of insulin deficiency induced by somatostatin (SRIF) infusion (0.7 mg/h). |
| 1263 | 2871558 | The addition of subfraction "a" to insulin treatment resulted in a clear decrease of hyperglycemia and glycosuria accompanied by a reduction of the high plasma glucagon and somatostatin levels in diabetic dogs. |
| 1264 | 2872569 | Efficacy, pharmacokinetics and tolerability of a somatostatin analogue (L-363,586) in insulin-dependent diabetes mellitus. |
| 1265 | 2872569 | To assess the pharmacologic properties and possible use in the treatment of diabetes mellitus of a recently developed analogue somatostatin (L-363,586), the analogue (2, 5, 10 or 40 micrograms/hr), somatostatin (200 micrograms/hr), or placebo were infused intravenously for 5 hours in 6 insulin-dependent diabetic subjects who were given a standard meal containing xylose. |
| 1266 | 2872569 | We conclude that L-363,586 is a long-acting and potent analogue of somatostatin, which has the potential for use as an adjunct to insulin in the treatment of diabetes mellitus. |
| 1267 | 2872569 | Efficacy, pharmacokinetics and tolerability of a somatostatin analogue (L-363,586) in insulin-dependent diabetes mellitus. |
| 1268 | 2872569 | To assess the pharmacologic properties and possible use in the treatment of diabetes mellitus of a recently developed analogue somatostatin (L-363,586), the analogue (2, 5, 10 or 40 micrograms/hr), somatostatin (200 micrograms/hr), or placebo were infused intravenously for 5 hours in 6 insulin-dependent diabetic subjects who were given a standard meal containing xylose. |
| 1269 | 2872569 | We conclude that L-363,586 is a long-acting and potent analogue of somatostatin, which has the potential for use as an adjunct to insulin in the treatment of diabetes mellitus. |
| 1270 | 2872569 | Efficacy, pharmacokinetics and tolerability of a somatostatin analogue (L-363,586) in insulin-dependent diabetes mellitus. |
| 1271 | 2872569 | To assess the pharmacologic properties and possible use in the treatment of diabetes mellitus of a recently developed analogue somatostatin (L-363,586), the analogue (2, 5, 10 or 40 micrograms/hr), somatostatin (200 micrograms/hr), or placebo were infused intravenously for 5 hours in 6 insulin-dependent diabetic subjects who were given a standard meal containing xylose. |
| 1272 | 2872569 | We conclude that L-363,586 is a long-acting and potent analogue of somatostatin, which has the potential for use as an adjunct to insulin in the treatment of diabetes mellitus. |
| 1273 | 2873007 | This study was designed to assess the effect of Tris on insulin, glucagon and somatostatin release and insulin synthesis in pancreatic B cells by using isolated rat pancreatic islets. |
| 1274 | 2873007 | Tris suppressed glucose-induced insulin release, whereas it did not affect the glucagon and somatostatin release. |
| 1275 | 2873007 | This study was designed to assess the effect of Tris on insulin, glucagon and somatostatin release and insulin synthesis in pancreatic B cells by using isolated rat pancreatic islets. |
| 1276 | 2873007 | Tris suppressed glucose-induced insulin release, whereas it did not affect the glucagon and somatostatin release. |
| 1277 | 2873009 | Insulin, glucagon and somatostatin (SLI) in the pancreas and the gastrointestinal tissue of rats were measured following a high (300 mg/kg) or low (150 mg/kg) dose of cysteamine, given intermittently for 14 days. |
| 1278 | 2873028 | Plasma somatostatin-like immunoreactivity responses to a mixed meal and the heterogeneity in healthy and non-insulin-dependent (NIDDM) diabetics. |
| 1279 | 2873976 | Effect of composition of mixed meals--low- versus high-carbohydrate content--on insulin, glucagon, and somatostatin release in healthy humans and in patients with NIDDM. |
| 1280 | 2873976 | Effects of a low-carbohydrate high-fat meal (LCM) versus a high-carbohydrate low-fat meal (HCM) on insulin, glucagon, and somatostatin release in nonobese healthy volunteers and in subjects with mild non-insulin-dependent diabetes mellitus (NIDDM) were compared. |
| 1281 | 2873976 | Effect of composition of mixed meals--low- versus high-carbohydrate content--on insulin, glucagon, and somatostatin release in healthy humans and in patients with NIDDM. |
| 1282 | 2873976 | Effects of a low-carbohydrate high-fat meal (LCM) versus a high-carbohydrate low-fat meal (HCM) on insulin, glucagon, and somatostatin release in nonobese healthy volunteers and in subjects with mild non-insulin-dependent diabetes mellitus (NIDDM) were compared. |
| 1283 | 2874160 | The anatomical distribution and volume fractions of pancreatic A cells (glucagon), B cells (insulin) and D cells (somatostatin) were evaluated by an immunoperoxidase technique in 6 diabetic cats, 6 normoglycaemic glucose-intolerant cats and 6 normal control cats. |
| 1284 | 2874909 | Effects of furosemide and indapamide upon pancreatic insulin and somatostatin secretion in vitro. |
| 1285 | 2874909 | To study if this was due to a direct effect on the endocrine pancreas, we examined the effects of furosemide and indapamide on the release of insulin and somatostatin from the isolated perfused pancreas of normal dogs. |
| 1286 | 2874909 | Furosemide at concentrations ranging between 1-30 micrograms/ml inhibited insulin in a dose-dependent manner (2p less than 0.01) whereas the somatostatin secretion was left unchanged. |
| 1287 | 2874909 | Effects of furosemide and indapamide upon pancreatic insulin and somatostatin secretion in vitro. |
| 1288 | 2874909 | To study if this was due to a direct effect on the endocrine pancreas, we examined the effects of furosemide and indapamide on the release of insulin and somatostatin from the isolated perfused pancreas of normal dogs. |
| 1289 | 2874909 | Furosemide at concentrations ranging between 1-30 micrograms/ml inhibited insulin in a dose-dependent manner (2p less than 0.01) whereas the somatostatin secretion was left unchanged. |
| 1290 | 2874909 | Effects of furosemide and indapamide upon pancreatic insulin and somatostatin secretion in vitro. |
| 1291 | 2874909 | To study if this was due to a direct effect on the endocrine pancreas, we examined the effects of furosemide and indapamide on the release of insulin and somatostatin from the isolated perfused pancreas of normal dogs. |
| 1292 | 2874909 | Furosemide at concentrations ranging between 1-30 micrograms/ml inhibited insulin in a dose-dependent manner (2p less than 0.01) whereas the somatostatin secretion was left unchanged. |
| 1293 | 2875023 | Insulin dependence of the actions of growth hormone and somatostatin on splanchnic biogenic amines of the dog. |
| 1294 | 2875450 | The aim of the study was to evaluate the somatostatin response to a test meal in type I diabetics at the clinical onset of the disease and after two months of intensive insulin therapy. |
| 1295 | 2875745 | Effect of a 12-hour subcutaneous infusion of somatostatin-14 on blood glucose, insulin and glucagon levels in healthy subjects and insulin dependent diabetics. |
| 1296 | 2875745 | We compared the influence of a 12-hour subcutaneous infusion of somatostatin-14 on glucose homeostasis in two normal subjects and two insulin-dependent diabetics (IDD). |
| 1297 | 2875745 | Unexpected high levels of immunoreactive somatostatin were measured in insulin-dependent diabetic patients. |
| 1298 | 2875745 | Effect of a 12-hour subcutaneous infusion of somatostatin-14 on blood glucose, insulin and glucagon levels in healthy subjects and insulin dependent diabetics. |
| 1299 | 2875745 | We compared the influence of a 12-hour subcutaneous infusion of somatostatin-14 on glucose homeostasis in two normal subjects and two insulin-dependent diabetics (IDD). |
| 1300 | 2875745 | Unexpected high levels of immunoreactive somatostatin were measured in insulin-dependent diabetic patients. |
| 1301 | 2875745 | Effect of a 12-hour subcutaneous infusion of somatostatin-14 on blood glucose, insulin and glucagon levels in healthy subjects and insulin dependent diabetics. |
| 1302 | 2875745 | We compared the influence of a 12-hour subcutaneous infusion of somatostatin-14 on glucose homeostasis in two normal subjects and two insulin-dependent diabetics (IDD). |
| 1303 | 2875745 | Unexpected high levels of immunoreactive somatostatin were measured in insulin-dependent diabetic patients. |
| 1304 | 2875910 | Glucose disposal rate between the 2nd and 4th h of a euglycemic insulin clamp, developed through a constant infusion of insulin (0.77 mU X kg-1 X min-1) together with somatostatin (80 ng X kg-1 X min-1), was 2.5-fold higher in a DG-5128-treated group (P less than .01) than in a control group. |
| 1305 | 2875911 | In this study, an immunofluorescence and elution/restaining protocol is used to determine the distribution of GABA and either insulin, glucagon, or somatostatin in a tissue section. |
| 1306 | 2875912 | In a previous study in C57BL/KsJ (mdb) mice aged 12 to 90 days, we observed alterations in the secretion of insulin and somatostatin and in the inhibitory effect of the latter upon insulin secretion. |
| 1307 | 2875912 | The results demonstrate two distinct phases in the development of the syndrome: up to age 6 days, the perifused slices of pancreata of control animals present biphasic glucose-induced patterns of insulin and somatostatin secretion, whereas the diabetic animals show a diminished first peak of insulin secretion, but a similar pattern of somatostatin secretion, to that of the control animals; between ages 7 and 12 days, the pancreata of diabetic mice exhibit insulin hypersecretion in basal conditions, and an absence of the first secretion peak and insulin hypersecretion in the second phase in response to glucose stimulation. |
| 1308 | 2875912 | The results show that, in very early stages of the evolution of the diabetic syndrome in C57BL/KsJ (mdb) mice, there are already alterations in insulin and somatostatin secretion patterns and in the inhibitory effect of the latter on insulin secretion. |
| 1309 | 2875912 | In a previous study in C57BL/KsJ (mdb) mice aged 12 to 90 days, we observed alterations in the secretion of insulin and somatostatin and in the inhibitory effect of the latter upon insulin secretion. |
| 1310 | 2875912 | The results demonstrate two distinct phases in the development of the syndrome: up to age 6 days, the perifused slices of pancreata of control animals present biphasic glucose-induced patterns of insulin and somatostatin secretion, whereas the diabetic animals show a diminished first peak of insulin secretion, but a similar pattern of somatostatin secretion, to that of the control animals; between ages 7 and 12 days, the pancreata of diabetic mice exhibit insulin hypersecretion in basal conditions, and an absence of the first secretion peak and insulin hypersecretion in the second phase in response to glucose stimulation. |
| 1311 | 2875912 | The results show that, in very early stages of the evolution of the diabetic syndrome in C57BL/KsJ (mdb) mice, there are already alterations in insulin and somatostatin secretion patterns and in the inhibitory effect of the latter on insulin secretion. |
| 1312 | 2875912 | In a previous study in C57BL/KsJ (mdb) mice aged 12 to 90 days, we observed alterations in the secretion of insulin and somatostatin and in the inhibitory effect of the latter upon insulin secretion. |
| 1313 | 2875912 | The results demonstrate two distinct phases in the development of the syndrome: up to age 6 days, the perifused slices of pancreata of control animals present biphasic glucose-induced patterns of insulin and somatostatin secretion, whereas the diabetic animals show a diminished first peak of insulin secretion, but a similar pattern of somatostatin secretion, to that of the control animals; between ages 7 and 12 days, the pancreata of diabetic mice exhibit insulin hypersecretion in basal conditions, and an absence of the first secretion peak and insulin hypersecretion in the second phase in response to glucose stimulation. |
| 1314 | 2875912 | The results show that, in very early stages of the evolution of the diabetic syndrome in C57BL/KsJ (mdb) mice, there are already alterations in insulin and somatostatin secretion patterns and in the inhibitory effect of the latter on insulin secretion. |
| 1315 | 2876005 | Somatostatin analog SMS 201-995 and insulin needs in insulin-dependent diabetic patients studied by means of an artificial pancreas. |
| 1316 | 2876005 | SMS 201-995 is a new somatostatin analog which is 10-60 times more potent and specific than somatostatin as an inhibitor of GH and insulin release. |
| 1317 | 2876005 | Their average insulin doses ranged from 22-46 U/day, and hemoglobin A1c levels varied between 6.5-11.5%. |
| 1318 | 2876005 | In conclusion, the somatostatin analog SMS 201-995 has a potential value as an adjunct to insulin in the management of IDD patients. |
| 1319 | 2876005 | Somatostatin analog SMS 201-995 and insulin needs in insulin-dependent diabetic patients studied by means of an artificial pancreas. |
| 1320 | 2876005 | SMS 201-995 is a new somatostatin analog which is 10-60 times more potent and specific than somatostatin as an inhibitor of GH and insulin release. |
| 1321 | 2876005 | Their average insulin doses ranged from 22-46 U/day, and hemoglobin A1c levels varied between 6.5-11.5%. |
| 1322 | 2876005 | In conclusion, the somatostatin analog SMS 201-995 has a potential value as an adjunct to insulin in the management of IDD patients. |
| 1323 | 2876005 | Somatostatin analog SMS 201-995 and insulin needs in insulin-dependent diabetic patients studied by means of an artificial pancreas. |
| 1324 | 2876005 | SMS 201-995 is a new somatostatin analog which is 10-60 times more potent and specific than somatostatin as an inhibitor of GH and insulin release. |
| 1325 | 2876005 | Their average insulin doses ranged from 22-46 U/day, and hemoglobin A1c levels varied between 6.5-11.5%. |
| 1326 | 2876005 | In conclusion, the somatostatin analog SMS 201-995 has a potential value as an adjunct to insulin in the management of IDD patients. |
| 1327 | 2876501 | Native somatostatin has multiple actions, including inhibition of the secretion of insulin, glucagon, thyroid-stimulating hormone (TSH), and various gut hormones. |
| 1328 | 2878490 | To further study the elevated plasma somatostatin (SRIF)--and reduced plasma glucagon concentrations found in IDDM patients without residual B-cell function compared to normal controls, we investigated 39 such patients, randomly assigned to three different insulin treatment regimens; conventional therapy with two injections a day (CTh), insulin pump (CSII) and multiple injections (MI), for 1 year. |
| 1329 | 2878619 | Somatostatin potentiation of insulin-induced glucose uptake in normal individuals. |
| 1330 | 2878619 | The ability of somatostatin (SRIF) to enhance insulin-stimulated glucose uptake was evaluated during clamp studies in normal individuals and patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 1331 | 2878619 | Somatostatin potentiation of insulin-induced glucose uptake in normal individuals. |
| 1332 | 2878619 | The ability of somatostatin (SRIF) to enhance insulin-stimulated glucose uptake was evaluated during clamp studies in normal individuals and patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 1333 | 2878848 | Somatostatin does not increase insulin-stimulated glucose uptake in humans. |
| 1334 | 2878848 | Somatostatin (SRIF) has been widely used in the study of in vivo carbohydrate metabolism to suppress pancreatic hormone secretion and thereby interrupt the glucoregulatory feedback loops between insulin, glucagon, and glucose. |
| 1335 | 2878848 | Somatostatin does not increase insulin-stimulated glucose uptake in humans. |
| 1336 | 2878848 | Somatostatin (SRIF) has been widely used in the study of in vivo carbohydrate metabolism to suppress pancreatic hormone secretion and thereby interrupt the glucoregulatory feedback loops between insulin, glucagon, and glucose. |
| 1337 | 2878865 | Adrenalectomy restored the immunohistochemical appearance of the islets to normal when examined with anti-insulin, anti-glucagon and anti-somatostatin antisera. |
| 1338 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1339 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1340 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1341 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1342 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1343 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1344 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1345 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1346 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1347 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1348 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1349 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1350 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1351 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1352 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1353 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1354 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1355 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1356 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1357 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1358 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1359 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1360 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1361 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1362 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1363 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1364 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1365 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1366 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1367 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1368 | 2878938 | Relationship of glucagon suppression by insulin and somatostatin to the ambient glucose concentration. |
| 1369 | 2878938 | The glucagon-suppressing activity of insulin and somatostatin were compared at high and low glucose concentrations. |
| 1370 | 2878938 | In normal dogs made hyperglucagonemic by phloridzin pretreatment, insulin and somatostatin suppressed glucagon at rates of 47 +/- 8 and 35 +/- 8%/h (NS), respectively, despite profound hypoglycemia. |
| 1371 | 2878938 | In severely hyperglycemic alloxan-diabetic dogs, insulin and somatostatin suppressed glucagon at rates of 48 +/- 13 and 54 +/- 6%/h, respectively, not different from the nondiabetic dogs. |
| 1372 | 2878938 | After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively. |
| 1373 | 2878938 | We conclude that insulin and somatostatin suppress glucagon at similar rates irrespective of ambient glucose levels, and that diabetic hyperglucagonemia represents the summation of stimulation by insulin lack minus suppression by the associated hyperglycemia. |
| 1374 | 2879210 | In neither group was there any rise above basal in cortisol, prolactin, glucagon, or somatostatin (SRIH). |
| 1375 | 2879756 | Basal insulin and glucagon levels and their rate of release in response to 10 mM arginine, 11 mM glucose, 500 pg/ml somatostatin, or 500 pg/ml glucagon were similar under both conditions. |
| 1376 | 2879758 | Endogenous insulin and glucagon secretion were inhibited by somatostatin (0.8 micrograms X kg-1 X min-1), and intraportal replacement infusions of insulin (213 +/- 28 microU X kg-1 X min-1) and glucagon (0.65 ng X kg-1 X min-1) were given to maintain basal hormone concentrations for 2 h (12 +/- 2 microU/ml and 108 +/- 23 pg/ml, respectively). |
| 1377 | 2880702 | In Study B, endogenous secretion of IRI and IRG was suppressed by infusion of somatostatin (0.2 microgram/kg/min), while peripheral concentrations were maintained constant by replacing glucagon (0.65 ng/kg/min) and insulin (0.225 mU/kg/min). |
| 1378 | 2881482 | Effects of soy polysaccharide on postprandial plasma glucose, insulin, glucagon, pancreatic polypeptide, somatostatin, and triglyceride in obese diabetic patients. |
| 1379 | 2881482 | Postprandial concentrations of plasma insulin, glucagon, pancreatic polypeptide, and somatostatin were measured to explore the mechanism of action. |
| 1380 | 2881482 | Addition of soy polysaccharide had no effect on plasma insulin levels but appeared (p greater than 0.05) to lessen postprandial increases in glucagon and pancreatic polypeptide levels while it raised somatostatin levels. |
| 1381 | 2881482 | The changes in plasma glucagon, pancreatic polypeptide, and somatostatin levels may have been instrumental in the observed postprandial glucose and triglyceride effects. |
| 1382 | 2881482 | Effects of soy polysaccharide on postprandial plasma glucose, insulin, glucagon, pancreatic polypeptide, somatostatin, and triglyceride in obese diabetic patients. |
| 1383 | 2881482 | Postprandial concentrations of plasma insulin, glucagon, pancreatic polypeptide, and somatostatin were measured to explore the mechanism of action. |
| 1384 | 2881482 | Addition of soy polysaccharide had no effect on plasma insulin levels but appeared (p greater than 0.05) to lessen postprandial increases in glucagon and pancreatic polypeptide levels while it raised somatostatin levels. |
| 1385 | 2881482 | The changes in plasma glucagon, pancreatic polypeptide, and somatostatin levels may have been instrumental in the observed postprandial glucose and triglyceride effects. |
| 1386 | 2881482 | Effects of soy polysaccharide on postprandial plasma glucose, insulin, glucagon, pancreatic polypeptide, somatostatin, and triglyceride in obese diabetic patients. |
| 1387 | 2881482 | Postprandial concentrations of plasma insulin, glucagon, pancreatic polypeptide, and somatostatin were measured to explore the mechanism of action. |
| 1388 | 2881482 | Addition of soy polysaccharide had no effect on plasma insulin levels but appeared (p greater than 0.05) to lessen postprandial increases in glucagon and pancreatic polypeptide levels while it raised somatostatin levels. |
| 1389 | 2881482 | The changes in plasma glucagon, pancreatic polypeptide, and somatostatin levels may have been instrumental in the observed postprandial glucose and triglyceride effects. |
| 1390 | 2881482 | Effects of soy polysaccharide on postprandial plasma glucose, insulin, glucagon, pancreatic polypeptide, somatostatin, and triglyceride in obese diabetic patients. |
| 1391 | 2881482 | Postprandial concentrations of plasma insulin, glucagon, pancreatic polypeptide, and somatostatin were measured to explore the mechanism of action. |
| 1392 | 2881482 | Addition of soy polysaccharide had no effect on plasma insulin levels but appeared (p greater than 0.05) to lessen postprandial increases in glucagon and pancreatic polypeptide levels while it raised somatostatin levels. |
| 1393 | 2881482 | The changes in plasma glucagon, pancreatic polypeptide, and somatostatin levels may have been instrumental in the observed postprandial glucose and triglyceride effects. |
| 1394 | 2881511 | GH secretory bursts are due to the combination of a pulsatile GRF release and a decreased Somatostatin secretion in hypophysial portal blood. |
| 1395 | 2881944 | Renal response to intravenous somatostatin in insulin-dependent diabetic patients and normal subjects. |
| 1396 | 2881944 | The acute effects of iv somatostatin (SRIH; 100 micrograms/h) on the urinary flow (Uvol), effective renal plasma flow (RPF), and glomerular filtration rate (GFR) were compared with those of a control infusion of 0.15 M NaCl in nine insulin-dependent diabetic (IDD) patients of less than 10 yr disease duration and six normal subjects (NS). |
| 1397 | 2881944 | Renal response to intravenous somatostatin in insulin-dependent diabetic patients and normal subjects. |
| 1398 | 2881944 | The acute effects of iv somatostatin (SRIH; 100 micrograms/h) on the urinary flow (Uvol), effective renal plasma flow (RPF), and glomerular filtration rate (GFR) were compared with those of a control infusion of 0.15 M NaCl in nine insulin-dependent diabetic (IDD) patients of less than 10 yr disease duration and six normal subjects (NS). |
| 1399 | 2882748 | However, when insulin secretion was inhibited, either by the induction of streptozotocin-diabetes or by simultaneous infusion of somatostatin, glucagon treatment was able to depress the expressed activity of HMG-CoA reductase (i.e. it increased the phosphorylation of the enzyme). |
| 1400 | 2883057 | We have previously shown that a nonimmunoreactive analogue of somatostatin, (D-Ala5, D-Trp8)-somatostatin, differentially inhibits pancreatic somatostatin secretion without inhibiting insulin or glucagon secretion. |
| 1401 | 2883057 | During normoglycemia, suppression of pancreatic somatostatin with this analogue increases glucagon and insulin secretion, suggesting that pancreatic somatostatin tonically inhibits glucagon and insulin secretion by a paracrine mechanism. |
| 1402 | 2883057 | Pancreatic insulin output increased 10-fold, pancreatic somatostatin output increased from 1.2 +/- 0.3 to 3.0 +/- 0.8 ng/min, and pancreatic glucagon output was suppressed from 1.4 +/- 0.7 to 0.5 +/- 0.1 ng/min. |
| 1403 | 2883057 | After 2 h of glucose infusion, an infusion of the analogue (5.5 micrograms/min i.v.) reversed both the stimulation of somatostatin and the suppression of glucagon without significantly changing either the plasma glucose level or the pancreatic insulin output. |
| 1404 | 2883057 | We have previously shown that a nonimmunoreactive analogue of somatostatin, (D-Ala5, D-Trp8)-somatostatin, differentially inhibits pancreatic somatostatin secretion without inhibiting insulin or glucagon secretion. |
| 1405 | 2883057 | During normoglycemia, suppression of pancreatic somatostatin with this analogue increases glucagon and insulin secretion, suggesting that pancreatic somatostatin tonically inhibits glucagon and insulin secretion by a paracrine mechanism. |
| 1406 | 2883057 | Pancreatic insulin output increased 10-fold, pancreatic somatostatin output increased from 1.2 +/- 0.3 to 3.0 +/- 0.8 ng/min, and pancreatic glucagon output was suppressed from 1.4 +/- 0.7 to 0.5 +/- 0.1 ng/min. |
| 1407 | 2883057 | After 2 h of glucose infusion, an infusion of the analogue (5.5 micrograms/min i.v.) reversed both the stimulation of somatostatin and the suppression of glucagon without significantly changing either the plasma glucose level or the pancreatic insulin output. |
| 1408 | 2883057 | We have previously shown that a nonimmunoreactive analogue of somatostatin, (D-Ala5, D-Trp8)-somatostatin, differentially inhibits pancreatic somatostatin secretion without inhibiting insulin or glucagon secretion. |
| 1409 | 2883057 | During normoglycemia, suppression of pancreatic somatostatin with this analogue increases glucagon and insulin secretion, suggesting that pancreatic somatostatin tonically inhibits glucagon and insulin secretion by a paracrine mechanism. |
| 1410 | 2883057 | Pancreatic insulin output increased 10-fold, pancreatic somatostatin output increased from 1.2 +/- 0.3 to 3.0 +/- 0.8 ng/min, and pancreatic glucagon output was suppressed from 1.4 +/- 0.7 to 0.5 +/- 0.1 ng/min. |
| 1411 | 2883057 | After 2 h of glucose infusion, an infusion of the analogue (5.5 micrograms/min i.v.) reversed both the stimulation of somatostatin and the suppression of glucagon without significantly changing either the plasma glucose level or the pancreatic insulin output. |
| 1412 | 2883057 | We have previously shown that a nonimmunoreactive analogue of somatostatin, (D-Ala5, D-Trp8)-somatostatin, differentially inhibits pancreatic somatostatin secretion without inhibiting insulin or glucagon secretion. |
| 1413 | 2883057 | During normoglycemia, suppression of pancreatic somatostatin with this analogue increases glucagon and insulin secretion, suggesting that pancreatic somatostatin tonically inhibits glucagon and insulin secretion by a paracrine mechanism. |
| 1414 | 2883057 | Pancreatic insulin output increased 10-fold, pancreatic somatostatin output increased from 1.2 +/- 0.3 to 3.0 +/- 0.8 ng/min, and pancreatic glucagon output was suppressed from 1.4 +/- 0.7 to 0.5 +/- 0.1 ng/min. |
| 1415 | 2883057 | After 2 h of glucose infusion, an infusion of the analogue (5.5 micrograms/min i.v.) reversed both the stimulation of somatostatin and the suppression of glucagon without significantly changing either the plasma glucose level or the pancreatic insulin output. |
| 1416 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1417 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1418 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1419 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1420 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1421 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1422 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1423 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1424 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1425 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1426 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1427 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1428 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1429 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1430 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1431 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1432 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1433 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1434 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1435 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1436 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1437 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1438 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1439 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1440 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1441 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1442 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1443 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1444 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1445 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1446 | 2883058 | Somatostatin impairs clearance of exogenous insulin in humans. |
| 1447 | 2883058 | To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. |
| 1448 | 2883058 | Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). |
| 1449 | 2883058 | Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). |
| 1450 | 2883058 | When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. |
| 1451 | 2883058 | C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. |
| 1452 | 2883101 | Insulin, glucagon and somatostatin content in normal and diabetic duck pancreas. |
| 1453 | 2883807 | Insulin and somatostatin (SRIF) secretion induced by alloantigen were studied in genetically diabetic mice from the C57BL/KsJ mdb-mdb strain. |
| 1454 | 2884157 | Basal and meal-induced somatostatin-like immunoreactivity in healthy subjects and in IDDM and totally pancreatectomized patients. |
| 1455 | 2884157 | We investigated the impact of blood glucose normalization on plasma levels of somatostatin-like immunoreactivity (SLI) in subjects with C-peptide-negative insulin-dependent diabetes mellitus (IDDM) and in totally pancreatectomized patients. |
| 1456 | 2884157 | We conclude that in IDDM and in totally pancreatectomized patients, administration of insulin with subsequent normalization of blood glucose is accompanied by a decline in plasma levels of SLI in the fasted state, whereas the apparent response to a meal is enhanced. |
| 1457 | 2884157 | Basal and meal-induced somatostatin-like immunoreactivity in healthy subjects and in IDDM and totally pancreatectomized patients. |
| 1458 | 2884157 | We investigated the impact of blood glucose normalization on plasma levels of somatostatin-like immunoreactivity (SLI) in subjects with C-peptide-negative insulin-dependent diabetes mellitus (IDDM) and in totally pancreatectomized patients. |
| 1459 | 2884157 | We conclude that in IDDM and in totally pancreatectomized patients, administration of insulin with subsequent normalization of blood glucose is accompanied by a decline in plasma levels of SLI in the fasted state, whereas the apparent response to a meal is enhanced. |
| 1460 | 2884158 | We conclude that basal and stimulated gastric SLI release is increased in untreated BB rats and is suppressed with insulin therapy, gastric delta-cell hyperfunction accounts for portal vein hypersomatostatinemia characteristic of untreated diabetic BB rats, and somatostatin-14 is the main molecular form of SLI released from normal and diabetic stomachs. |
| 1461 | 2884159 | The animals received either a 420 min infusion of (1) somatostatin alone (0.3 microgram X kg-1 X min-1), (2) somatostatin with insulin replacement (100 microU X kg-1 X min-1) or (3) glucagon (6 ng X kg-1 X min-1) together with somatostatin and transient insulin replacement. |
| 1462 | 2884159 | When somatostatin was given alone, plasma glucagon (p less than 0.004) and insulin (p less than 0.0001) were suppressed. |
| 1463 | 2884159 | When insulin replacement was given during somatostatin infusion to correct for the small somatostatin-induced insulin suppression, there were similar changes in plasma glucagon, glucose concentrations and glucose kinetics as seen during the infusion of somatostatin alone. |
| 1464 | 2884159 | The animals received either a 420 min infusion of (1) somatostatin alone (0.3 microgram X kg-1 X min-1), (2) somatostatin with insulin replacement (100 microU X kg-1 X min-1) or (3) glucagon (6 ng X kg-1 X min-1) together with somatostatin and transient insulin replacement. |
| 1465 | 2884159 | When somatostatin was given alone, plasma glucagon (p less than 0.004) and insulin (p less than 0.0001) were suppressed. |
| 1466 | 2884159 | When insulin replacement was given during somatostatin infusion to correct for the small somatostatin-induced insulin suppression, there were similar changes in plasma glucagon, glucose concentrations and glucose kinetics as seen during the infusion of somatostatin alone. |
| 1467 | 2884159 | The animals received either a 420 min infusion of (1) somatostatin alone (0.3 microgram X kg-1 X min-1), (2) somatostatin with insulin replacement (100 microU X kg-1 X min-1) or (3) glucagon (6 ng X kg-1 X min-1) together with somatostatin and transient insulin replacement. |
| 1468 | 2884159 | When somatostatin was given alone, plasma glucagon (p less than 0.004) and insulin (p less than 0.0001) were suppressed. |
| 1469 | 2884159 | When insulin replacement was given during somatostatin infusion to correct for the small somatostatin-induced insulin suppression, there were similar changes in plasma glucagon, glucose concentrations and glucose kinetics as seen during the infusion of somatostatin alone. |
| 1470 | 2884179 | The effect on glucose homeostasis of a transient elevation of plasma growth hormone (GH) and cortisol was studied over 6 h in 14 male patients with insulin-dependent diabetes mellitus (IDDM) by using an i.v. somatostatin (100 micrograms/h) - insulin (0.4 mU/kg/min) glucose (3 mg/kg/min) - infusion test (SIGIT). |
| 1471 | 2884179 | It is concluded that an episodic increase in circulating GH-cortisol, resembling the responses of these hormones to an insulin-induced hypoglycemia, exerts a diabetogenic effect in IDDM-patients not deprived of insulin. |
| 1472 | 2885161 | Plasma immunoreactive somatostatin response to arginine after glycemic control with continuous subcutaneous insulin infusion in type I diabetics. |
| 1473 | 2885161 | The effects of 3 wk of near normoglycemia by continuous subcutaneous insulin infusion (CSII) on plasma immunoreactive somatostatin (IRS) responses to arginine (0.5 g X kg-1 X 30 min-1) in seven patients with insulin-dependent diabetes mellitus (IDDM) were compared with the same patients in poor glycemic control during conventional insulin therapy (CIT) and with seven normal controls. |
| 1474 | 2885161 | Plasma free-insulin levels in IDDM patients 30 min before a meal during CSII were significantly higher than those during CIT or in normal controls. |
| 1475 | 2885161 | Plasma immunoreactive somatostatin response to arginine after glycemic control with continuous subcutaneous insulin infusion in type I diabetics. |
| 1476 | 2885161 | The effects of 3 wk of near normoglycemia by continuous subcutaneous insulin infusion (CSII) on plasma immunoreactive somatostatin (IRS) responses to arginine (0.5 g X kg-1 X 30 min-1) in seven patients with insulin-dependent diabetes mellitus (IDDM) were compared with the same patients in poor glycemic control during conventional insulin therapy (CIT) and with seven normal controls. |
| 1477 | 2885161 | Plasma free-insulin levels in IDDM patients 30 min before a meal during CSII were significantly higher than those during CIT or in normal controls. |
| 1478 | 2886385 | Receptor-mediated adenylate cyclase-coupled mechanism for PGE2 inhibition of insulin secretion in HIT cells. |
| 1479 | 2886385 | These studies were performed with a clonal cell line of glucose-responsive beta-cells (HIT cells) to determine whether PGE2 effects on insulin secretion are receptor mediated and, if so, whether the postreceptor effects are mediated by inhibitory regulatory components (Ni) of adenylate cyclase. |
| 1480 | 2886385 | Maximum inhibition of glucose-induced insulin secretion was 26, 37, and 29% of control values for somatostatin, PGE2, and epinephrine, respectively. |
| 1481 | 2887504 | Suppression of growth hormone and somatomedin C by long-acting somatostatin analog SMS 201-995 in type I diabetes mellitus. |
| 1482 | 2887504 | Glucagon, somatomedin C (SM-C), triiodothyronine, thyroxine, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were also determined before and at the end of the therapy with SMS. |
| 1483 | 2887504 | Glucagon, triiodothyronine, thyroxine, LH, FSH and PRL showed no significant changes. |
| 1484 | 2888037 | The GH response to 2-min pulses of hGRF at concentrations of 1.56, 6.25, and 25 pM with and without somatostatin 10(-9) M was significantly greater in the diabetic group than in the control group. |
| 1485 | 2888547 | Effects of somatostatin analogue SMS 201-995 in non-insulin-dependent diabetes. |
| 1486 | 2888547 | The 24-h hormonal and metabolic profiles obtained in five non-insulin-dependent diabetics receiving twice daily s.c. injections of the long-acting somatostatin analogue SMS 201-995 (50 micrograms) have been compared with those obtained following placebo injection. |
| 1487 | 2888547 | Effects of somatostatin analogue SMS 201-995 in non-insulin-dependent diabetes. |
| 1488 | 2888547 | The 24-h hormonal and metabolic profiles obtained in five non-insulin-dependent diabetics receiving twice daily s.c. injections of the long-acting somatostatin analogue SMS 201-995 (50 micrograms) have been compared with those obtained following placebo injection. |
| 1489 | 2888696 | Human insulin and C-peptide were infused intraportally into conscious dogs (n = 11) at equimolar rates; endogenous insulin and C-peptide release were suppressed with somatostatin (0.8 micrograms . kg-1 . min-1). |
| 1490 | 2889641 | To study NIMGU, somatostatin (SRIF, 600 micrograms/h) was infused to suppress endogenous insulin secretion and create severe insulinopenia, and glucose turnover was measured isotopically while serum glucose was clamped at approximately 200 mg/dl for 240 min. |
| 1491 | 2889787 | Influence of streptozotocin-induced diabetes on the concentration of immunoreactive somatostatin in the retina and peripheral blood of the rat: effect of insulin treatment. |
| 1492 | 2890162 | The effect of pancreastatin on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. |
| 1493 | 2890162 | As expected, the glucose and the arginine augmented insulin and somatostatin release. |
| 1494 | 2890162 | Pancreastatin (1 and 10 nM) markedly suppressed the first phase of insulin release with both insulinogogues used, while the early somatostatin secretion was not significantly decreased. |
| 1495 | 2890162 | The effect of pancreastatin on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. |
| 1496 | 2890162 | As expected, the glucose and the arginine augmented insulin and somatostatin release. |
| 1497 | 2890162 | Pancreastatin (1 and 10 nM) markedly suppressed the first phase of insulin release with both insulinogogues used, while the early somatostatin secretion was not significantly decreased. |
| 1498 | 2890162 | The effect of pancreastatin on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. |
| 1499 | 2890162 | As expected, the glucose and the arginine augmented insulin and somatostatin release. |
| 1500 | 2890162 | Pancreastatin (1 and 10 nM) markedly suppressed the first phase of insulin release with both insulinogogues used, while the early somatostatin secretion was not significantly decreased. |
| 1501 | 2890212 | [Effects of exogenous and endogenous somatostatin on serum insulin concentration in streptozotocin diabetic mice]. |
| 1502 | 2890501 | The subjects underwent normoglycemic clamp studies and meal tests with determination of insulin, C-peptide, glucagon, somatostatin, and gastric inhibitory polypeptide in plasma. |
| 1503 | 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. |
| 1504 | 2890501 | The subjects underwent normoglycemic clamp studies and meal tests with determination of insulin, C-peptide, glucagon, somatostatin, and gastric inhibitory polypeptide in plasma. |
| 1505 | 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. |
| 1506 | 2890540 | Effects of arginine and arginine plus somatostatin infusion on insulin release in diabetic patients submitted to pancreas allotransplantation. |
| 1507 | 2890560 | Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin. |
| 1508 | 2890693 | In diabetic rats, pancreatic insulin levels were reduced to about 3.5% of control, whereas those of somatostatin (SRIF), PP and glucagon were elevated to 8.3, 2.7 and 1.4 times control, respectively. |
| 1509 | 2891015 | Designation of HIR and LIR was done on the basis of mathematical modeling of the insulin response to a glucose infusion test. |
| 1510 | 2891015 | Insulin sensitivity was determined by a somatostatin-insulin-glucose infusion test (SIGIT) according to which LIR were subdivided into groups with higher or lesser sensitivity. |
| 1511 | 2891235 | Glucose metabolism was studied by a somatostatin-insulin-glucose infusion test (SIGIT) for 8 h in 7 male patients with insulin-dependent diabetes mellitus. |
| 1512 | 2891470 | In anesthetized dogs (n = 6), during electromagnetic hepatic blood flow monitoring, endogenous insulin was suppressed with somatostatin, while equimolar proportions of porcine insulin and simian C-peptide (2.4 and 6.0 pmol/kg.min) were infused during two consecutive 45-min periods. |
| 1513 | 2892113 | Prevention of the Dawn phenomenon (early morning hyperglycemia) in insulin-dependent diabetes mellitus by bedtime intranasal administration of a long-acting somatostatin analog. |
| 1514 | 2892113 | We therefore assessed the effect of a long-acting somatostatin analog (L363,586) on overnight plasma glucose and growth hormone levels in six patients with insulin-dependent diabetes mellitus. |
| 1515 | 2892113 | Prevention of the Dawn phenomenon (early morning hyperglycemia) in insulin-dependent diabetes mellitus by bedtime intranasal administration of a long-acting somatostatin analog. |
| 1516 | 2892113 | We therefore assessed the effect of a long-acting somatostatin analog (L363,586) on overnight plasma glucose and growth hormone levels in six patients with insulin-dependent diabetes mellitus. |
| 1517 | 2892338 | SMS 201-995 (Sandostatin) is an octapeptide which differs in its action from native somatostatin in four ways: 1) it inhibits GH hormone secretion in preference to insulin secretion; 2) it can be administered subcutaneously or even orally; 3) it is long-acting (t1/2 after sc administration 113 min), and 4) there is no rebound hypersecretion of hormones when the effect of the analogue lingers off. |
| 1518 | 2892770 | In order to investigate the action of somatostatin-28 (SS-28) on the metabolic homeostasis of insulin-dependent diabetics, we compared its effects to those of somatostatin-14 (SS-14) in terms of insulin sparing, changes in dextrose demands, glucose fluctuations and behavior of growth hormone and glucagon secretion. |
| 1519 | 2894103 | Insulin, glucagon and somatostatin secretion by cultured islets from normal and diabetic hamsters. |
| 1520 | 2894750 | Insulin resistance was assessed after a hypoglycemia induced by insulin (1.5 mU X kg-1 X min-1) between 7 and 8 a.m. in 10 well-insulinized patients with insulin-dependent diabetes mellitus (IDDM). |
| 1521 | 2894750 | Blood glucose levels during a somatostatin (100 micrograms X h-1)-insulin (0.4 mU X kg-1 X min-1)-glucose (4.5 mg X kg-1)-infusion test (SIGIT) performed between 11 a.m. and 3 p.m. served as an indicator of total body insulin resistance. |
| 1522 | 2894750 | We conclude that hypoglycemia evokes a state of insulin resistance for several hours, as demonstrated by elevated blood glucose levels during a somatostatin-insulin-glucose-infusion test. |
| 1523 | 2894750 | Insulin resistance was assessed after a hypoglycemia induced by insulin (1.5 mU X kg-1 X min-1) between 7 and 8 a.m. in 10 well-insulinized patients with insulin-dependent diabetes mellitus (IDDM). |
| 1524 | 2894750 | Blood glucose levels during a somatostatin (100 micrograms X h-1)-insulin (0.4 mU X kg-1 X min-1)-glucose (4.5 mg X kg-1)-infusion test (SIGIT) performed between 11 a.m. and 3 p.m. served as an indicator of total body insulin resistance. |
| 1525 | 2894750 | We conclude that hypoglycemia evokes a state of insulin resistance for several hours, as demonstrated by elevated blood glucose levels during a somatostatin-insulin-glucose-infusion test. |
| 1526 | 2894751 | The effect of growth hormone (GH) on the glucose homeostasis following nocturnal hypoglycemia was studied between 4 a.m. and noon in eight male patients with insulin-dependent diabetes mellitus (IDDM) by a somatostatin (250 micrograms/h)-insulin (0.4 mU/kg/min)-glucose (6 mg/kg/min)-infusion test (SIGIT). |
| 1527 | 2894771 | After insulin-induced hypoglycemia, there was the greatest percent increase in somatostatin-28 and a doubling of somatostatin-14 and the void volume material. |
| 1528 | 2895013 | The ontogeny of insulin, glucagon, PP and somatostatin in the mammalian fetal pancreas has been examined in recent years largely by immunocytochemistry and in some instances by radioimmunoassay. |
| 1529 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 1530 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 1531 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 1532 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 1533 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 1534 | 2897274 | Insulin action was estimated by determination of the steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations during the last 60 min of a continuous 180-min intravenous infusion of somatostatin, crystalline insulin, and glucose. |
| 1535 | 2898427 | Postprandial glycaemic effects of a long-acting somatostatin analogue (octreotide) in non-insulin dependent diabetes mellitus. |
| 1536 | 2898427 | Postprandial changes in blood glucose, insulin and glucagon were examined in 7 non-insulin dependent diabetic patients, before and after 3 days' treatment with the somatostatin analogue, octreotide (50 ug injected subcutaneously thricedaily). |
| 1537 | 2898427 | Animal studies have suggested that octreotide inhibits growth hormone and glucagon secretion much more powerfully than native somatostatin, while relatively sparing insulin secretion. |
| 1538 | 2898427 | Postprandial glycaemic effects of a long-acting somatostatin analogue (octreotide) in non-insulin dependent diabetes mellitus. |
| 1539 | 2898427 | Postprandial changes in blood glucose, insulin and glucagon were examined in 7 non-insulin dependent diabetic patients, before and after 3 days' treatment with the somatostatin analogue, octreotide (50 ug injected subcutaneously thricedaily). |
| 1540 | 2898427 | Animal studies have suggested that octreotide inhibits growth hormone and glucagon secretion much more powerfully than native somatostatin, while relatively sparing insulin secretion. |
| 1541 | 2898427 | Postprandial glycaemic effects of a long-acting somatostatin analogue (octreotide) in non-insulin dependent diabetes mellitus. |
| 1542 | 2898427 | Postprandial changes in blood glucose, insulin and glucagon were examined in 7 non-insulin dependent diabetic patients, before and after 3 days' treatment with the somatostatin analogue, octreotide (50 ug injected subcutaneously thricedaily). |
| 1543 | 2898427 | Animal studies have suggested that octreotide inhibits growth hormone and glucagon secretion much more powerfully than native somatostatin, while relatively sparing insulin secretion. |
| 1544 | 2898855 | Somatostatin reduces posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. |
| 1545 | 2898855 | In order to study whether somatostatin reduces posthypoglycemic insulin resistance, hypoglycemia was induced between 7.00 and 8.00 h by an iv infusion of insulin with and without somatostatin (250 micrograms/h) in 6 male patients with insulin-dependent diabetes mellitus (IDDM). |
| 1546 | 2898855 | Insulin resistance was assessed by a somatostatin-insulin-infusion test (SIGIT) between 11.00 and 15.00 h. |
| 1547 | 2898855 | It is concluded that somatostatin reduces insulin resistance following hypoglycemia in patients with IDDM. |
| 1548 | 2898855 | Somatostatin reduces posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. |
| 1549 | 2898855 | In order to study whether somatostatin reduces posthypoglycemic insulin resistance, hypoglycemia was induced between 7.00 and 8.00 h by an iv infusion of insulin with and without somatostatin (250 micrograms/h) in 6 male patients with insulin-dependent diabetes mellitus (IDDM). |
| 1550 | 2898855 | Insulin resistance was assessed by a somatostatin-insulin-infusion test (SIGIT) between 11.00 and 15.00 h. |
| 1551 | 2898855 | It is concluded that somatostatin reduces insulin resistance following hypoglycemia in patients with IDDM. |
| 1552 | 2898855 | Somatostatin reduces posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. |
| 1553 | 2898855 | In order to study whether somatostatin reduces posthypoglycemic insulin resistance, hypoglycemia was induced between 7.00 and 8.00 h by an iv infusion of insulin with and without somatostatin (250 micrograms/h) in 6 male patients with insulin-dependent diabetes mellitus (IDDM). |
| 1554 | 2898855 | Insulin resistance was assessed by a somatostatin-insulin-infusion test (SIGIT) between 11.00 and 15.00 h. |
| 1555 | 2898855 | It is concluded that somatostatin reduces insulin resistance following hypoglycemia in patients with IDDM. |
| 1556 | 2898855 | Somatostatin reduces posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. |
| 1557 | 2898855 | In order to study whether somatostatin reduces posthypoglycemic insulin resistance, hypoglycemia was induced between 7.00 and 8.00 h by an iv infusion of insulin with and without somatostatin (250 micrograms/h) in 6 male patients with insulin-dependent diabetes mellitus (IDDM). |
| 1558 | 2898855 | Insulin resistance was assessed by a somatostatin-insulin-infusion test (SIGIT) between 11.00 and 15.00 h. |
| 1559 | 2898855 | It is concluded that somatostatin reduces insulin resistance following hypoglycemia in patients with IDDM. |
| 1560 | 2899369 | Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. |
| 1561 | 2899369 | In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. |
| 1562 | 2899369 | Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. |
| 1563 | 2899369 | In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. |
| 1564 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1565 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1566 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1567 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1568 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1569 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1570 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1571 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1572 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1573 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1574 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1575 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1576 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1577 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1578 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1579 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1580 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1581 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1582 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1583 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1584 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1585 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1586 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1587 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1588 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1589 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1590 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1591 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1592 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1593 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1594 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1595 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1596 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1597 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1598 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1599 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1600 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1601 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1602 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1603 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1604 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1605 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1606 | 2900090 | Somatostatin increases hepatic insulin extraction. |
| 1607 | 2900090 | Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. |
| 1608 | 2900090 | Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). |
| 1609 | 2900090 | Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). |
| 1610 | 2900090 | HIE was increased in the presence of insulin plus somatostatin infusion. |
| 1611 | 2900090 | HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). |
| 1612 | 2900090 | However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. |
| 1613 | 2900205 | The infusion of natural somatostatin (SRIF) has been able to partially correct postprandial hyperglycemic reactions in insulin-dependent diabetes mellitus (IDDM). |
| 1614 | 2900206 | Preliminary experience on treatment of insulin-dependent diabetes mellitus with a long-acting somatostatin analogue (L363,586). |
| 1615 | 2900755 | [Anti-insulin, proinsulin, pancreatic polypeptide, glucagon and somatostatin antibodies in patients with insulin-dependent diabetes mellitus treated with conventional insulin preparations]. |
| 1616 | 2901182 | Effect of insulin on basal pancreaticoduodenal output of somatostatin in normal and diabetic dogs. |
| 1617 | 2901329 | The effects of the somatostatin analogue SMS 201-995 on carbohydrate homeostasis of insulin-dependent diabetics as assessed by the artificial endocrine pancreas. |
| 1618 | 2901329 | On the basis of the inhibitory actions of the somatostatin analogue SMS 201-995 on growth hormone (GH) and glucagon (IRG) secretion we investigated its effects on carbohydrate metabolism of insulin-dependent diabetics. |
| 1619 | 2901329 | The effects of the somatostatin analogue SMS 201-995 on carbohydrate homeostasis of insulin-dependent diabetics as assessed by the artificial endocrine pancreas. |
| 1620 | 2901329 | On the basis of the inhibitory actions of the somatostatin analogue SMS 201-995 on growth hormone (GH) and glucagon (IRG) secretion we investigated its effects on carbohydrate metabolism of insulin-dependent diabetics. |
| 1621 | 2901377 | First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb). |
| 1622 | 2901377 | In a previous study in C57BL/KsJ mdb/mdb mice aged 4 to 12 days we observed a diminished first phase of glucose-induced insulin secretion in vitro, and alterations in the inhibitory effect of somatostatin on insulin secretion. |
| 1623 | 2901377 | This study explores, using perifused pancreatic slices, whether the reduced B-cell responsiveness to somatostatin in mdb/mdb mice can be overcome upon induction of a biphasic insulin release by using theophylline. |
| 1624 | 2901377 | Under these conditions our results show: (1) in mdb/mdb mice aged 4 to 6 days, the restoration of the first peak of insulin secretion overcomes the reduced B-cell sensitivity to somatostatin; and (2) in mdb/mdb mice aged 7 to 12 days, the addition of theophylline only causes a partial restoration of B-cell responsiveness to somatostatin, suggesting that other mechanisms could be involved in the progressive impairement of B-cell sensitivity to somatostatin inhibitory effect. |
| 1625 | 2901377 | First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb). |
| 1626 | 2901377 | In a previous study in C57BL/KsJ mdb/mdb mice aged 4 to 12 days we observed a diminished first phase of glucose-induced insulin secretion in vitro, and alterations in the inhibitory effect of somatostatin on insulin secretion. |
| 1627 | 2901377 | This study explores, using perifused pancreatic slices, whether the reduced B-cell responsiveness to somatostatin in mdb/mdb mice can be overcome upon induction of a biphasic insulin release by using theophylline. |
| 1628 | 2901377 | Under these conditions our results show: (1) in mdb/mdb mice aged 4 to 6 days, the restoration of the first peak of insulin secretion overcomes the reduced B-cell sensitivity to somatostatin; and (2) in mdb/mdb mice aged 7 to 12 days, the addition of theophylline only causes a partial restoration of B-cell responsiveness to somatostatin, suggesting that other mechanisms could be involved in the progressive impairement of B-cell sensitivity to somatostatin inhibitory effect. |
| 1629 | 2901377 | First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb). |
| 1630 | 2901377 | In a previous study in C57BL/KsJ mdb/mdb mice aged 4 to 12 days we observed a diminished first phase of glucose-induced insulin secretion in vitro, and alterations in the inhibitory effect of somatostatin on insulin secretion. |
| 1631 | 2901377 | This study explores, using perifused pancreatic slices, whether the reduced B-cell responsiveness to somatostatin in mdb/mdb mice can be overcome upon induction of a biphasic insulin release by using theophylline. |
| 1632 | 2901377 | Under these conditions our results show: (1) in mdb/mdb mice aged 4 to 6 days, the restoration of the first peak of insulin secretion overcomes the reduced B-cell sensitivity to somatostatin; and (2) in mdb/mdb mice aged 7 to 12 days, the addition of theophylline only causes a partial restoration of B-cell responsiveness to somatostatin, suggesting that other mechanisms could be involved in the progressive impairement of B-cell sensitivity to somatostatin inhibitory effect. |
| 1633 | 2901377 | First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb). |
| 1634 | 2901377 | In a previous study in C57BL/KsJ mdb/mdb mice aged 4 to 12 days we observed a diminished first phase of glucose-induced insulin secretion in vitro, and alterations in the inhibitory effect of somatostatin on insulin secretion. |
| 1635 | 2901377 | This study explores, using perifused pancreatic slices, whether the reduced B-cell responsiveness to somatostatin in mdb/mdb mice can be overcome upon induction of a biphasic insulin release by using theophylline. |
| 1636 | 2901377 | Under these conditions our results show: (1) in mdb/mdb mice aged 4 to 6 days, the restoration of the first peak of insulin secretion overcomes the reduced B-cell sensitivity to somatostatin; and (2) in mdb/mdb mice aged 7 to 12 days, the addition of theophylline only causes a partial restoration of B-cell responsiveness to somatostatin, suggesting that other mechanisms could be involved in the progressive impairement of B-cell sensitivity to somatostatin inhibitory effect. |
| 1637 | 2901737 | This analog may be useful as an adjunct to insulin in the treatment of diabetic patients, although caution should be exercised, to prevent hypoglycemia when using somatostatin analogs together with insulin. |
| 1638 | 2901899 | Two compartment pharmacodynamics of somatostatin in non-obese non-insulin-dependent diabetes. |
| 1639 | 2901949 | The effects of the diabetic state on the somatotroph's responsiveness to the secretagogues GRF and (Bu)2-cAMP and to the inhibitor somatostatin (SRIF) were evaluated in enzymatically dissociated rat adenohypophyseal cells in primary monolayer culture. |
| 1640 | 2903616 | Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. |
| 1641 | 2903616 | By using this method it was demonstrated that insulin resistance occurred for at least 12 hours after a hypoglycemic event in patients with IDDM, and that adrenaline caused immediate insulin resistance which, however, faded out within four to six hours, while GH exerted no immediate effect on insulin sensitivity but caused marked and sustained insulin resistance after a lag period of about four hours. |
| 1642 | 2903616 | It is possible that such prolonged insulin resistance may cause posthypoglycemic hyperglycemia in patients with IDDM. |
| 1643 | 2903616 | These studies therefore indicate that the GH suppressing hormone somatostatin may be of clinical value as an adjunct to insulin in the treatment of patients with insulin-dependent diabetes mellitus and labile blood glucose control. |
| 1644 | 2903616 | Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. |
| 1645 | 2903616 | By using this method it was demonstrated that insulin resistance occurred for at least 12 hours after a hypoglycemic event in patients with IDDM, and that adrenaline caused immediate insulin resistance which, however, faded out within four to six hours, while GH exerted no immediate effect on insulin sensitivity but caused marked and sustained insulin resistance after a lag period of about four hours. |
| 1646 | 2903616 | It is possible that such prolonged insulin resistance may cause posthypoglycemic hyperglycemia in patients with IDDM. |
| 1647 | 2903616 | These studies therefore indicate that the GH suppressing hormone somatostatin may be of clinical value as an adjunct to insulin in the treatment of patients with insulin-dependent diabetes mellitus and labile blood glucose control. |
| 1648 | 2903805 | The tumour was diagnosed preoperatively and metabolic studies demonstrated mild diabetes mellitus apparently due to suppression of insulin secretion by somatostatin, since oral glucose tolerance returned to normal post-operatively despite hemipancreatectomy. |
| 1649 | 2903836 | The embryogenesis of the pancreas suggests the existence of a common stem cell progenitor of the four islet cell types (insulin, glucagon, somatostatin, and pancreatic polypeptide). |
| 1650 | 2903836 | By analyses of RNA transcripts and immunoreactive peptides in four human insulinomas and one glucagonoma, we found that the insulin, somatostatin, and glucagon genes were coexpressed in all tumors. |
| 1651 | 2903836 | The embryogenesis of the pancreas suggests the existence of a common stem cell progenitor of the four islet cell types (insulin, glucagon, somatostatin, and pancreatic polypeptide). |
| 1652 | 2903836 | By analyses of RNA transcripts and immunoreactive peptides in four human insulinomas and one glucagonoma, we found that the insulin, somatostatin, and glucagon genes were coexpressed in all tumors. |
| 1653 | 2903837 | Anterograde (arterial) perfusion and retrograde (reversed or venous) perfusion of a segment of isolated dog pancreas with potent insulin antibodies yielded results similar to those found in the rat pancreas (anterograde, 158 +/- 44% increase in glucagon and 65 +/- 20% increase in somatostatin; retrograde, no change in glucagon or somatostatin). |
| 1654 | 2903837 | Anterograde infusion of glucagon antibody (no change in insulin, -33.5 +/- 3% decrease in somatostatin) or somatostatin antibody (no change in insulin or glucagon) also yielded the same results as in the rat pancreas. |
| 1655 | 2903837 | Anterograde infusion of 500 pg/ml glucagon caused a larger increase in insulin secretion (245 +/- 10%) than retrograde infusion (45 +/- 4%), whereas somatostatin was stimulated more retrogradely (339 +/- 17%) than anterogradely (121 +/- 9%). |
| 1656 | 2903837 | Anterograde infusion of somatostatin produced a larger decrease in insulin and glucagon than did retrograde perfusion (P less than .0001 for both comparisons). |
| 1657 | 2903837 | The results from the infusion of exogenous hormones suggest that the sensitivity of the alpha-, beta-, and delta-cells to insulin, glucagon, and somatostatin is determined by the beta----alpha----delta order of perfusion. |
| 1658 | 2903837 | Anterograde (arterial) perfusion and retrograde (reversed or venous) perfusion of a segment of isolated dog pancreas with potent insulin antibodies yielded results similar to those found in the rat pancreas (anterograde, 158 +/- 44% increase in glucagon and 65 +/- 20% increase in somatostatin; retrograde, no change in glucagon or somatostatin). |
| 1659 | 2903837 | Anterograde infusion of glucagon antibody (no change in insulin, -33.5 +/- 3% decrease in somatostatin) or somatostatin antibody (no change in insulin or glucagon) also yielded the same results as in the rat pancreas. |
| 1660 | 2903837 | Anterograde infusion of 500 pg/ml glucagon caused a larger increase in insulin secretion (245 +/- 10%) than retrograde infusion (45 +/- 4%), whereas somatostatin was stimulated more retrogradely (339 +/- 17%) than anterogradely (121 +/- 9%). |
| 1661 | 2903837 | Anterograde infusion of somatostatin produced a larger decrease in insulin and glucagon than did retrograde perfusion (P less than .0001 for both comparisons). |
| 1662 | 2903837 | The results from the infusion of exogenous hormones suggest that the sensitivity of the alpha-, beta-, and delta-cells to insulin, glucagon, and somatostatin is determined by the beta----alpha----delta order of perfusion. |
| 1663 | 2903837 | Anterograde (arterial) perfusion and retrograde (reversed or venous) perfusion of a segment of isolated dog pancreas with potent insulin antibodies yielded results similar to those found in the rat pancreas (anterograde, 158 +/- 44% increase in glucagon and 65 +/- 20% increase in somatostatin; retrograde, no change in glucagon or somatostatin). |
| 1664 | 2903837 | Anterograde infusion of glucagon antibody (no change in insulin, -33.5 +/- 3% decrease in somatostatin) or somatostatin antibody (no change in insulin or glucagon) also yielded the same results as in the rat pancreas. |
| 1665 | 2903837 | Anterograde infusion of 500 pg/ml glucagon caused a larger increase in insulin secretion (245 +/- 10%) than retrograde infusion (45 +/- 4%), whereas somatostatin was stimulated more retrogradely (339 +/- 17%) than anterogradely (121 +/- 9%). |
| 1666 | 2903837 | Anterograde infusion of somatostatin produced a larger decrease in insulin and glucagon than did retrograde perfusion (P less than .0001 for both comparisons). |
| 1667 | 2903837 | The results from the infusion of exogenous hormones suggest that the sensitivity of the alpha-, beta-, and delta-cells to insulin, glucagon, and somatostatin is determined by the beta----alpha----delta order of perfusion. |
| 1668 | 2903837 | Anterograde (arterial) perfusion and retrograde (reversed or venous) perfusion of a segment of isolated dog pancreas with potent insulin antibodies yielded results similar to those found in the rat pancreas (anterograde, 158 +/- 44% increase in glucagon and 65 +/- 20% increase in somatostatin; retrograde, no change in glucagon or somatostatin). |
| 1669 | 2903837 | Anterograde infusion of glucagon antibody (no change in insulin, -33.5 +/- 3% decrease in somatostatin) or somatostatin antibody (no change in insulin or glucagon) also yielded the same results as in the rat pancreas. |
| 1670 | 2903837 | Anterograde infusion of 500 pg/ml glucagon caused a larger increase in insulin secretion (245 +/- 10%) than retrograde infusion (45 +/- 4%), whereas somatostatin was stimulated more retrogradely (339 +/- 17%) than anterogradely (121 +/- 9%). |
| 1671 | 2903837 | Anterograde infusion of somatostatin produced a larger decrease in insulin and glucagon than did retrograde perfusion (P less than .0001 for both comparisons). |
| 1672 | 2903837 | The results from the infusion of exogenous hormones suggest that the sensitivity of the alpha-, beta-, and delta-cells to insulin, glucagon, and somatostatin is determined by the beta----alpha----delta order of perfusion. |
| 1673 | 2903837 | Anterograde (arterial) perfusion and retrograde (reversed or venous) perfusion of a segment of isolated dog pancreas with potent insulin antibodies yielded results similar to those found in the rat pancreas (anterograde, 158 +/- 44% increase in glucagon and 65 +/- 20% increase in somatostatin; retrograde, no change in glucagon or somatostatin). |
| 1674 | 2903837 | Anterograde infusion of glucagon antibody (no change in insulin, -33.5 +/- 3% decrease in somatostatin) or somatostatin antibody (no change in insulin or glucagon) also yielded the same results as in the rat pancreas. |
| 1675 | 2903837 | Anterograde infusion of 500 pg/ml glucagon caused a larger increase in insulin secretion (245 +/- 10%) than retrograde infusion (45 +/- 4%), whereas somatostatin was stimulated more retrogradely (339 +/- 17%) than anterogradely (121 +/- 9%). |
| 1676 | 2903837 | Anterograde infusion of somatostatin produced a larger decrease in insulin and glucagon than did retrograde perfusion (P less than .0001 for both comparisons). |
| 1677 | 2903837 | The results from the infusion of exogenous hormones suggest that the sensitivity of the alpha-, beta-, and delta-cells to insulin, glucagon, and somatostatin is determined by the beta----alpha----delta order of perfusion. |
| 1678 | 2905198 | Immunohistologic localization of tyrosine hydroxylase (TOH), dopamine-beta-hydroxylase (DBH) and selected neuropeptides (vasoactive intestinal polypeptide, gastrin-releasing peptide (GRP)/bombesin, substance P, Leu-enkephalin, Met-enkephalin, dynorphin B, neuropeptide Y (NPY), somatostatin) was used to investigate the innervation of the small bowel in a rat model of diabetic autonomic neuropathy. |
| 1679 | 2905691 | Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster. |
| 1680 | 2905691 | In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls. |
| 1681 | 2905691 | None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups. |
| 1682 | 2905691 | Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster. |
| 1683 | 2905691 | Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster. |
| 1684 | 2905691 | In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls. |
| 1685 | 2905691 | None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups. |
| 1686 | 2905691 | Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster. |
| 1687 | 2905691 | Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster. |
| 1688 | 2905691 | In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls. |
| 1689 | 2905691 | None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups. |
| 1690 | 2905691 | Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster. |
| 1691 | 2905942 | During the study endogenous insulin secretion was suppressed by somatostatin (300 micrograms h-1) and replaced by infusion of insulin (0.2 mU kg-1 min-1). |
| 1692 | 2906021 | The blood glucose level during a somatostatin (100 micrograms/h)-insulin (0.4 mU.kg-1.min-1)-glucose (4.5 mg.kg-1.min-1)-infusion-test performed between 10.30 and 14.30 hours served as an indicator of the total body insulin resistance. |
| 1693 | 2906021 | Furthermore, during the somatostatin-insulin-glucose infusion test the blood glucose rose significantly (p less than 0.05) over the initial 2 h; thereafter no significant differences between the two studies were seen. |
| 1694 | 2906021 | The blood glucose level during a somatostatin (100 micrograms/h)-insulin (0.4 mU.kg-1.min-1)-glucose (4.5 mg.kg-1.min-1)-infusion-test performed between 10.30 and 14.30 hours served as an indicator of the total body insulin resistance. |
| 1695 | 2906021 | Furthermore, during the somatostatin-insulin-glucose infusion test the blood glucose rose significantly (p less than 0.05) over the initial 2 h; thereafter no significant differences between the two studies were seen. |
| 1696 | 2907780 | [Behavior of intraluminal gastrin and somatostatin in subjects with type II diabetes mellitus]. |
| 1697 | 2916380 | The response to GH releasing hormone (GHRH 1-29) and 24-h serum GH and IGF-I levels were measured in 9 insulin-dependent diabetics with retinopathy and 6 normal volunteers before and after different treatment regimens with octreotide, a long-acting somatostatin analogue. |
| 1698 | 2981750 | The enzyme is inactive at pHs below 6.0, indicating that it is not lysosomal, is completely inhibited by N-ethylmaleimide, and exhibits apparent competitive inhibition constants (microM) for the following peptides: desoctapeptide insulin, 0.043; guinea pig insulin, 0.048; proinsulin, 0.64; insulin B-chain, 1.17; glucagon, 7.0; and cyclic somatostatin, 8.6. |
| 1699 | 3004244 | Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. |
| 1700 | 3004244 | The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. |
| 1701 | 3005153 | After glucose administration, abnormal insulin release accompanied by glucose intolerance were observed, whereas the high glucagon circulating levels were only partially blocked after glucose or somatostatin infusion. |
| 1702 | 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. |
| 1703 | 3028898 | Whereas the calcium-pentagastrin test provoked a markedly elevated plasma somatostatin level in association with a depressed plasma neurotensin level, the tolbutamide test surprisingly did not. |
| 1704 | 3042030 | The morphological data correlate well with the previously reported evolution of plasma and pancreatic hormone concentration after surgery, and suggest that the normal inhibitory control of glucagon and insulin secretion by the local release of somatostatin might be reduced or suppressed during transient diabetes in subtotally depancreatized ducks. |
| 1705 | 3049768 | Effect of a new long-acting somatostatin analogue (SMS 201-995) on glycemic and hormonal profiles in insulin-treated type II diabetic patients. |
| 1706 | 3049768 | Five type II diabetic patients were studied after secondary failure of oral agents, with and without the addition of the new long-acting somatostatin analogue SMS 201-995 to an intermediate-acting insulin regimen. |
| 1707 | 3049768 | Effect of a new long-acting somatostatin analogue (SMS 201-995) on glycemic and hormonal profiles in insulin-treated type II diabetic patients. |
| 1708 | 3049768 | Five type II diabetic patients were studied after secondary failure of oral agents, with and without the addition of the new long-acting somatostatin analogue SMS 201-995 to an intermediate-acting insulin regimen. |
| 1709 | 3065203 | Severe hypoglycemia as a short-term side-effect of the somatostatin analog SMS 201-995 in insulin-dependent diabetes mellitus. |
| 1710 | 3065203 | We report on a case of severe hypoglycemia observed after injection of the somatostatin analog SMS 201-995 in an insulin-dependent diabetic patient connected to an artificial pancreas (Biostator GCIIS). |
| 1711 | 3065203 | Severe hypoglycemia as a short-term side-effect of the somatostatin analog SMS 201-995 in insulin-dependent diabetes mellitus. |
| 1712 | 3065203 | We report on a case of severe hypoglycemia observed after injection of the somatostatin analog SMS 201-995 in an insulin-dependent diabetic patient connected to an artificial pancreas (Biostator GCIIS). |
| 1713 | 3106122 | However, when diabetic rats had been treated with insulin for 6-7 days, glibenclamide suppressed glucagon release at low calcium levels in the absence of stimulated insulin and somatostatin release. |
| 1714 | 3113971 | Pancreatic response was measured by sequential injection of 0.1, 0.3 and 0.9 g kg-1 glucose; peripheral sensitivity to insulin was determined from the rate of clearance (Kgluc) of 0.3 g glucose injected sequentially together with 25, 50 and 100 mU insulin kg-1 or with 0, 12.5 and 50 mU kg-1, under somatostatin infusion. |
| 1715 | 3159965 | Some of the T cells were "activated" (positive for HLA-DR antigen, and the interleukin-2 receptor). |
| 1716 | 3159965 | Increased expression of Class I (HLA-A, B, and C) molecules was observed in the affected islet cells, and in damaged islets showing scant lymphocytic infiltration, some beta cells (still producing insulin), but not glucagon or somatostatin cells, were HLA-DR positive. |
| 1717 | 3276206 | Immunolocalization of islet amyloid polypeptide (IAPP) in pancreatic beta cells by means of peroxidase-antiperoxidase (PAP) and protein A-gold techniques. |
| 1718 | 3276206 | A novel putative polypeptide hormone identified as islet amyloid polypeptide (IAPP) was recently purified from islet amyloid (IA) of diabetic humans and cats, and also from amyloid of a human insulinoma. |
| 1719 | 3276206 | In the present investigation, the authors utilized antisera to insulin, glucagon, somatostatin, pancreatic polypeptide, synthetic human CGRP, and a synthetic human IAPP (7-17) undecapeptide to immunohistochemically (PAP technique) document the presence of IAPP immunoreactive cells in the islets of the cat, dog, mouse, and rat, but not in the islets of the horse or calf. |
| 1720 | 3286166 | Endogenous secretion of insulin was inhibited by concomitant administration of somatostatin (300 micrograms/h). |
| 1721 | 3286166 | This at least applies to peripheral, short-term insulin administration in somatostatin-treated normal man, during an euglycemic clamp. |
| 1722 | 3286166 | Endogenous secretion of insulin was inhibited by concomitant administration of somatostatin (300 micrograms/h). |
| 1723 | 3286166 | This at least applies to peripheral, short-term insulin administration in somatostatin-treated normal man, during an euglycemic clamp. |
| 1724 | 3289997 | Hypothalamic concentrations of the other six peptides examined (bombesin, galanin, neuromedin B, substance P, somatostatin, and vasoactive intestinal peptide) did not differ significantly between STZ-D and control groups at any time. |
| 1725 | 3301157 | An insulin-producing cell line, Clone-16, of hamster origin, was characterized for islet hormone production and for reactivity with islet cell surface (ICSA) and islet cell cytoplasmic (ICA) antibodies in sera from children with newly diagnosed insulin-dependent (Type 1) diabetes mellitus (IDDM). |
| 1726 | 3301157 | The cells produced 63 +/- 3 ng (mean +/- SD) immunoreactive insulin and 9.4 +/- 0.3 ng immunoreactive glucagon per day per 10(6) cells, while somatostatin (SRIF) and pancreatic polypeptide (PP) were undetectable. |
| 1727 | 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. |
| 1728 | 3322915 | No significant differences were obtained between HLA-identical, HLA-haplo-identical siblings and HLA-non-identical siblings in insulin response using an i.v. glucose infusion test even when the insulin sensitivity as estimated by the somatostatin-insulin-glucose infusion test was taken into account. |
| 1729 | 3329722 | We report an immunohistochemical and semiquantitative study of hypertrophic islet cells in 14 infants with neonatal hypoglycemia (10 with documented persistent neonatal hypoglycemia and 4 with probable persistent neonatal hypoglycemia) and 6 infants born to diabetic mothers (IDM), using an indirect immunoperoxidase methods for the demonstration of insulin, somatostatin, and glucagon. |
| 1730 | 3329722 | Polyploid cells were positive for insulin and somatostatin but negative for glucagon; insulin-positive cells outnumbered somatostatin-positive cells in both groups. |
| 1731 | 3329722 | We report an immunohistochemical and semiquantitative study of hypertrophic islet cells in 14 infants with neonatal hypoglycemia (10 with documented persistent neonatal hypoglycemia and 4 with probable persistent neonatal hypoglycemia) and 6 infants born to diabetic mothers (IDM), using an indirect immunoperoxidase methods for the demonstration of insulin, somatostatin, and glucagon. |
| 1732 | 3329722 | Polyploid cells were positive for insulin and somatostatin but negative for glucagon; insulin-positive cells outnumbered somatostatin-positive cells in both groups. |
| 1733 | 3434945 | There was no diabetes mellitus, but an oral glucose tolerance test and a somatostatin insulin glucose test elicited definite resistance to insulin. |
| 1734 | 3516750 | We have determined peripheral venous somatostatin like immunoreactivity (SLI) levels in 11 normal subjects (blood glucose--BG--: 4.4 +/- 0.1 mM; ketone bodies--KB--: 90 +/- 12 microM; plasma free fatty acids--FFA --: 340 +/- 42 microM), 4 Biostator controlled insulin dependent diabetics (BG: 5.4 +/- 0.2 mM; FFA: 418 +/- 38 microM; KB: 226 +/- 41 microM) and 7 poorly controlled ketotic diabetics (BG: 10.8 +/- 1.3 mM; FFA: 915 +/- 19 microM; KB: 2490 +/- 576 microM). |
| 1735 | 3522319 | In our study the ability of each component of insulin release to counter the effects of the glucagon on gluconeogenesis and alanine metabolism was assessed by mimicking first- and/or second-phase insulin release with infusions of somatostatin and intraportal insulin. |
| 1736 | 3530862 | Somatostatin (0.25 mg/h) and insulin (0.3 mU X kg-1 X min-1) were infused from 22.00-02.30 hours on one occasion, and from 04.00-08.30 hours on the other. |
| 1737 | 3542647 | In vivo insulin action was measured during a 3-insulin-step, hyperglycemic (approximately 310 mg/dl) clamp with somatostatin (250 micrograms/h). |
| 1738 | 3542647 | The discrepancy between in vivo and in vitro results suggests that the adipocyte may not always reflect in vivo insulin action. |
| 1739 | 3545944 | Out of 57 women with previous histories of gestational diabetes (GD), 23 were of normal weight postpartum and willing to participate in three studies characterizing oral glucose tolerance (OGTT), insulin responsiveness to intravenous glucose (glucose infusion test, GIT), and insulin sensitivity (somatostatin, insulin, and glucose infusion test, SIGIT). |
| 1740 | 3552822 | Insulin, glucagon, somatostatin and pancreatic polypeptide cells were quantified after immunoperoxidase staining in sections of pancreases obtained from nine control subjects and seven diabetic patients with primary or secondary iron overload. |
| 1741 | 3552824 | Double staining with anti-insulin, glucagon, somatostatin or pancreatic polypeptide antibodies revealed that I-A positive cells corresponded with insulin cells, while other types of pancreatic islet cells were virtually negative for I-A. |
| 1742 | 3552828 | Synthesized [LeuA3] insulin showed 0.14% of receptor binding activity on rat adipocytes and a 10-fold prolonged half-life in a somatostatin-infused dog compared with human insulin. |
| 1743 | 3886459 | Plasma insulin and glucagon levels were maintained constant by means of a somatostatin infusion (0.8 microgram/kg-min) and intraportal replacement infusions of insulin and glucagon. |
| 1744 | 3891786 | To determine if the enhanced glycemic response to epinephrine in patients with insulin-dependent diabetes mellitus (IDDM) is the result of increased adrenergic sensitivity per se, increased glucagon secretion, decreased insulin secretion, or a combination of these, plasma epinephrine concentration-response curves were determined in insulin-infused (initially euglycemic) patients with IDDM and nondiabetic subjects on two occasions: once when insulin and glucagon were free to change (control study), and again when insulin and glucagon were held constant (islet clamp study). |
| 1745 | 3891786 | During the islet clamp study (somatostatin infusion with insulin and glucagon replacement at fixed rates), the heightened glycemic response was unaltered in the patients with IDDM, but the nondiabetic subjects exhibited an enhanced glycemic response to epinephrine indistinguishable from that of patients with IDDM. |
| 1746 | 3891786 | Enhanced glycemic responsiveness of patients with IDDM to epinephrine is not the result of increased sensitivity of adrenergic receptor-effector mechanisms per se nor of their increased glucagon secretory response; rather, it is the result of their inability to augment insulin secretion. |
| 1747 | 4430415 | Inhibition of pancreatic glucagon responses to arginine by somatostatin in normal man and in insulin-dependent diabetics. |
| 1748 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1749 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1750 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1751 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1752 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1753 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1754 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1755 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1756 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1757 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1758 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1759 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1760 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1761 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1762 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1763 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1764 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1765 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1766 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1767 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1768 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1769 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1770 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1771 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1772 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1773 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1774 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1775 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1776 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1777 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1778 | 4436439 | Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs. |
| 1779 | 4436439 | In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. |
| 1780 | 4436439 | In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. |
| 1781 | 4436439 | Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. |
| 1782 | 4436439 | It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. |
| 1783 | 4436439 | Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. |
| 1784 | 6084513 | Somatostatin, as an adjunct to insulin in the treatment of poorly controlled type 1 diabetes, has been recently suggested. |
| 1785 | 6084513 | To answer these questions, the plasma levels of proaggregatory thromboxane A2 and of B-thromboglobulin, marker of the platelet activation, were studied in nine control subjects and in thirteen insulin dependent diabetic patients before and during the endovenous injection, for three hours, of somatostatin (250 micrograms in bolus followed by infusion of 100 micrograms/h). |
| 1786 | 6084513 | Somatostatin, as an adjunct to insulin in the treatment of poorly controlled type 1 diabetes, has been recently suggested. |
| 1787 | 6084513 | To answer these questions, the plasma levels of proaggregatory thromboxane A2 and of B-thromboglobulin, marker of the platelet activation, were studied in nine control subjects and in thirteen insulin dependent diabetic patients before and during the endovenous injection, for three hours, of somatostatin (250 micrograms in bolus followed by infusion of 100 micrograms/h). |
| 1788 | 6092332 | Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. |
| 1789 | 6092332 | Previously, we reported that pancreatic acini have specific receptors for the insulin-like growth factors (IGF) I and II. |
| 1790 | 6092332 | We now report that the binding of 125I-labeled IGF II to mouse pancreatic acini is maximally increased by 100 nM insulin (51%) and is maximally reduced by 10 nM cholecystokinin octapeptide (CCK8) (34%), but is not affected by other regulatory peptides such as somatostatin or glucagon. |
| 1791 | 6100886 | Although the histologic structure of the tumor was indistinguishable from that of most islet cell tumors of adults, immunofluorescence revealed that the four islet cell hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide) were all present in the tumor. |
| 1792 | 6103853 | Somatostatin concentration responds to arginine in portal plasma: effects of fasting, streptozotocin diabetes, and insulin administration in diabetic rats. |
| 1793 | 6103853 | Changes of somatostatin concentration in response to a single i.v. injection of arginine (400 mg/kg body weight) were examined in extracted portal plasma of normal and diabetic rats in the fully fed state and after 24 h or fasting, as well as in diabetic rats treated with insulin for one week. |
| 1794 | 6103853 | When compared with intact rats, diabetic animals were shown to have increased levels of somatostatin before and after arginine administration, both of which were attenuated by insulin replacement therapy. |
| 1795 | 6103853 | Somatostatin concentration responds to arginine in portal plasma: effects of fasting, streptozotocin diabetes, and insulin administration in diabetic rats. |
| 1796 | 6103853 | Changes of somatostatin concentration in response to a single i.v. injection of arginine (400 mg/kg body weight) were examined in extracted portal plasma of normal and diabetic rats in the fully fed state and after 24 h or fasting, as well as in diabetic rats treated with insulin for one week. |
| 1797 | 6103853 | When compared with intact rats, diabetic animals were shown to have increased levels of somatostatin before and after arginine administration, both of which were attenuated by insulin replacement therapy. |
| 1798 | 6103853 | Somatostatin concentration responds to arginine in portal plasma: effects of fasting, streptozotocin diabetes, and insulin administration in diabetic rats. |
| 1799 | 6103853 | Changes of somatostatin concentration in response to a single i.v. injection of arginine (400 mg/kg body weight) were examined in extracted portal plasma of normal and diabetic rats in the fully fed state and after 24 h or fasting, as well as in diabetic rats treated with insulin for one week. |
| 1800 | 6103853 | When compared with intact rats, diabetic animals were shown to have increased levels of somatostatin before and after arginine administration, both of which were attenuated by insulin replacement therapy. |
| 1801 | 6103855 | The magnitude and dynamics of somatostatin, glucagon, and insulin responses during stimulation with 5 mM calcium were identical whether or not the duodenal remnant was excluded from the perfusion by clamping. |
| 1802 | 6103856 | Streptozotocin diabetes in the monkey: plasma levels of glucose, insulin, glucagon, and somatostatin, with corresponding morphometric analysis of islet endocrine cells. |
| 1803 | 6103856 | Fasting somatostatin levels were also significantly elevated in insulin-dependent animals when compared with controls. |
| 1804 | 6103856 | Streptozotocin diabetes in the monkey: plasma levels of glucose, insulin, glucagon, and somatostatin, with corresponding morphometric analysis of islet endocrine cells. |
| 1805 | 6103856 | Fasting somatostatin levels were also significantly elevated in insulin-dependent animals when compared with controls. |
| 1806 | 6104595 | These results suggest that an abrupt deprivation of insulin from islets results in an elevation of pancreatic somatostatin concentration, and that glucagon in the pancreas plays a minor role in determining pancreatic somatostatin concentration in rats with insulin-deprived diabetes of short duration. |
| 1807 | 6104627 | Beside a 50-fold IRG excess, the tumour concentrations of insulin and somatostatin were 4 to 150 times increased. |
| 1808 | 6104680 | Effect of the somatostatin analog D-Trp8,D-Cys14 on glucose insulin, pancreatic glucagon and growth hormone plasma levels in acromegalics and mild diabetics. |
| 1809 | 6104680 | The effect of the somatostatin analog (GHRIH-A) D-Trp8, D-Cys14 on plasma levels of growth hormone, pancreatic glucagon, insulin and glucose was studied in four acromegalic patients and in four maturity-onset mild diabetics. |
| 1810 | 6104680 | Our data suggest that this somatostatin analog may be potentially useful only when GH suppression is the main therapeutic goal to be reached, as in acromegaly and in severe diabetic retinopathy, but not in metabolic control of mild diabetic patients with a good residual insulin secretion. |
| 1811 | 6104680 | Effect of the somatostatin analog D-Trp8,D-Cys14 on glucose insulin, pancreatic glucagon and growth hormone plasma levels in acromegalics and mild diabetics. |
| 1812 | 6104680 | The effect of the somatostatin analog (GHRIH-A) D-Trp8, D-Cys14 on plasma levels of growth hormone, pancreatic glucagon, insulin and glucose was studied in four acromegalic patients and in four maturity-onset mild diabetics. |
| 1813 | 6104680 | Our data suggest that this somatostatin analog may be potentially useful only when GH suppression is the main therapeutic goal to be reached, as in acromegaly and in severe diabetic retinopathy, but not in metabolic control of mild diabetic patients with a good residual insulin secretion. |
| 1814 | 6104680 | Effect of the somatostatin analog D-Trp8,D-Cys14 on glucose insulin, pancreatic glucagon and growth hormone plasma levels in acromegalics and mild diabetics. |
| 1815 | 6104680 | The effect of the somatostatin analog (GHRIH-A) D-Trp8, D-Cys14 on plasma levels of growth hormone, pancreatic glucagon, insulin and glucose was studied in four acromegalic patients and in four maturity-onset mild diabetics. |
| 1816 | 6104680 | Our data suggest that this somatostatin analog may be potentially useful only when GH suppression is the main therapeutic goal to be reached, as in acromegaly and in severe diabetic retinopathy, but not in metabolic control of mild diabetic patients with a good residual insulin secretion. |
| 1817 | 6106057 | The endocrine pancreas of birds contains 3 islet types and releases glucagon, insulin, somatostatin and avian pancreatic polypeptide (APP). |
| 1818 | 6106342 | Effect of a somatostatin analog on insulin requirement and hormone levels in 6 insulin-dependent juvenile-onset diabetics subjected to artificial pancreas. |
| 1819 | 6106342 | This study was performed in order to investigate the effect of a 12-h infusion of the somatostatin selective analog D-Trp8, D-Cys14 Serono, (SRIF-A), on insuli requirement and C-peptide (CP), growth hormone (GH) and glucagon (IRG) levels in 6 insulin-dependent diabetics submitted to 60-h artificial pancreas (Biostator Miles) metabolic control from 2000 of the first day to 0800 of the fourth day. |
| 1820 | 6106342 | Effect of a somatostatin analog on insulin requirement and hormone levels in 6 insulin-dependent juvenile-onset diabetics subjected to artificial pancreas. |
| 1821 | 6106342 | This study was performed in order to investigate the effect of a 12-h infusion of the somatostatin selective analog D-Trp8, D-Cys14 Serono, (SRIF-A), on insuli requirement and C-peptide (CP), growth hormone (GH) and glucagon (IRG) levels in 6 insulin-dependent diabetics submitted to 60-h artificial pancreas (Biostator Miles) metabolic control from 2000 of the first day to 0800 of the fourth day. |
| 1822 | 6106923 | Somatostatin is know to inhibit insulin and glucagon secretion. |
| 1823 | 6108269 | The pancreatic somatostatin content increased in proportion to the dose of STZ (I, 189 +/- 31; II, 222 +/- 20, III, 343 +/- 4; IV, 515 +/- 36 ng/g wet wt), while graded reductions of insulin content were observed. |
| 1824 | 6108269 | Pancreatic somatostatin release increased during arginine infusion (19.2 mM) dose dependently, (I, 543 +/- 36; II, 946 +/- 64; III, 1229 +/- 55; IV, 2186 +/- 150 pg/15 min), and it correlated with the graded decreases of insulin release. |
| 1825 | 6108269 | These results indicate that pancreatic somatostatin content and release increased in STZ-diabetic rats in proportion to the degree of insulin deficiency. |
| 1826 | 6108269 | The pancreatic somatostatin content increased in proportion to the dose of STZ (I, 189 +/- 31; II, 222 +/- 20, III, 343 +/- 4; IV, 515 +/- 36 ng/g wet wt), while graded reductions of insulin content were observed. |
| 1827 | 6108269 | Pancreatic somatostatin release increased during arginine infusion (19.2 mM) dose dependently, (I, 543 +/- 36; II, 946 +/- 64; III, 1229 +/- 55; IV, 2186 +/- 150 pg/15 min), and it correlated with the graded decreases of insulin release. |
| 1828 | 6108269 | These results indicate that pancreatic somatostatin content and release increased in STZ-diabetic rats in proportion to the degree of insulin deficiency. |
| 1829 | 6108269 | The pancreatic somatostatin content increased in proportion to the dose of STZ (I, 189 +/- 31; II, 222 +/- 20, III, 343 +/- 4; IV, 515 +/- 36 ng/g wet wt), while graded reductions of insulin content were observed. |
| 1830 | 6108269 | Pancreatic somatostatin release increased during arginine infusion (19.2 mM) dose dependently, (I, 543 +/- 36; II, 946 +/- 64; III, 1229 +/- 55; IV, 2186 +/- 150 pg/15 min), and it correlated with the graded decreases of insulin release. |
| 1831 | 6108269 | These results indicate that pancreatic somatostatin content and release increased in STZ-diabetic rats in proportion to the degree of insulin deficiency. |
| 1832 | 6108274 | To investigate the pancreatic endocrine function in streptozotocin-diabetic rats before and after the whole pancreas was transplanted, pancreatic insulin, glucagon, and somatostatin content and release were measured. |
| 1833 | 6108274 | Studies in vitro using the isolated perfused rat pancreas revealed a significant increase of somatostatin release from the diabetic pancreas, with a marked reduction of insulin release and almost normal glucagon release. |
| 1834 | 6108274 | In the transplanted rats, on the other hand, arginine-induced somatostatin release from the host pancreas was reduced to normal without a significant change in insulin or glucagon release. |
| 1835 | 6108274 | Pancreatic somatostatin release, thus, appears to be effected by changes in circulating insulin, since pancreatic transplantation effectively corrects the circulating insulin level. |
| 1836 | 6108274 | To investigate the pancreatic endocrine function in streptozotocin-diabetic rats before and after the whole pancreas was transplanted, pancreatic insulin, glucagon, and somatostatin content and release were measured. |
| 1837 | 6108274 | Studies in vitro using the isolated perfused rat pancreas revealed a significant increase of somatostatin release from the diabetic pancreas, with a marked reduction of insulin release and almost normal glucagon release. |
| 1838 | 6108274 | In the transplanted rats, on the other hand, arginine-induced somatostatin release from the host pancreas was reduced to normal without a significant change in insulin or glucagon release. |
| 1839 | 6108274 | Pancreatic somatostatin release, thus, appears to be effected by changes in circulating insulin, since pancreatic transplantation effectively corrects the circulating insulin level. |
| 1840 | 6108274 | To investigate the pancreatic endocrine function in streptozotocin-diabetic rats before and after the whole pancreas was transplanted, pancreatic insulin, glucagon, and somatostatin content and release were measured. |
| 1841 | 6108274 | Studies in vitro using the isolated perfused rat pancreas revealed a significant increase of somatostatin release from the diabetic pancreas, with a marked reduction of insulin release and almost normal glucagon release. |
| 1842 | 6108274 | In the transplanted rats, on the other hand, arginine-induced somatostatin release from the host pancreas was reduced to normal without a significant change in insulin or glucagon release. |
| 1843 | 6108274 | Pancreatic somatostatin release, thus, appears to be effected by changes in circulating insulin, since pancreatic transplantation effectively corrects the circulating insulin level. |
| 1844 | 6108274 | To investigate the pancreatic endocrine function in streptozotocin-diabetic rats before and after the whole pancreas was transplanted, pancreatic insulin, glucagon, and somatostatin content and release were measured. |
| 1845 | 6108274 | Studies in vitro using the isolated perfused rat pancreas revealed a significant increase of somatostatin release from the diabetic pancreas, with a marked reduction of insulin release and almost normal glucagon release. |
| 1846 | 6108274 | In the transplanted rats, on the other hand, arginine-induced somatostatin release from the host pancreas was reduced to normal without a significant change in insulin or glucagon release. |
| 1847 | 6108274 | Pancreatic somatostatin release, thus, appears to be effected by changes in circulating insulin, since pancreatic transplantation effectively corrects the circulating insulin level. |
| 1848 | 6108275 | Glucose stimulation of somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1849 | 6108275 | Insulin and somatostatin release from the isolated perfused rat pancreas was studied under conditions of 50 and 300 mg/dl glucose as well as a linear 50-300 mg/dl glucose gradient. |
| 1850 | 6108275 | The glucose-stimulated response profile of somatostatin was nearly parallel to that of insulin in both the acute and gradient dose experiments. |
| 1851 | 6108275 | In spite of the marked, fifteenfold stimulation of somatostatin release (1.5 x 10-10 M in the perfusate effluent) by glucose, the concentration of somatostatin was insufficient to significantly alter glucose-stimulated insulin release in the isolated perfused rat pancreas. |
| 1852 | 6108275 | Glucose stimulation of somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1853 | 6108275 | Insulin and somatostatin release from the isolated perfused rat pancreas was studied under conditions of 50 and 300 mg/dl glucose as well as a linear 50-300 mg/dl glucose gradient. |
| 1854 | 6108275 | The glucose-stimulated response profile of somatostatin was nearly parallel to that of insulin in both the acute and gradient dose experiments. |
| 1855 | 6108275 | In spite of the marked, fifteenfold stimulation of somatostatin release (1.5 x 10-10 M in the perfusate effluent) by glucose, the concentration of somatostatin was insufficient to significantly alter glucose-stimulated insulin release in the isolated perfused rat pancreas. |
| 1856 | 6108275 | Glucose stimulation of somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1857 | 6108275 | Insulin and somatostatin release from the isolated perfused rat pancreas was studied under conditions of 50 and 300 mg/dl glucose as well as a linear 50-300 mg/dl glucose gradient. |
| 1858 | 6108275 | The glucose-stimulated response profile of somatostatin was nearly parallel to that of insulin in both the acute and gradient dose experiments. |
| 1859 | 6108275 | In spite of the marked, fifteenfold stimulation of somatostatin release (1.5 x 10-10 M in the perfusate effluent) by glucose, the concentration of somatostatin was insufficient to significantly alter glucose-stimulated insulin release in the isolated perfused rat pancreas. |
| 1860 | 6108275 | Glucose stimulation of somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1861 | 6108275 | Insulin and somatostatin release from the isolated perfused rat pancreas was studied under conditions of 50 and 300 mg/dl glucose as well as a linear 50-300 mg/dl glucose gradient. |
| 1862 | 6108275 | The glucose-stimulated response profile of somatostatin was nearly parallel to that of insulin in both the acute and gradient dose experiments. |
| 1863 | 6108275 | In spite of the marked, fifteenfold stimulation of somatostatin release (1.5 x 10-10 M in the perfusate effluent) by glucose, the concentration of somatostatin was insufficient to significantly alter glucose-stimulated insulin release in the isolated perfused rat pancreas. |
| 1864 | 6108276 | Immunoreactive somatostatin (IRS) was measured in extracted plasma obtained from the hepatic portal vein (PV) and inferior vena cava (IVC) of acute, untreated, spontaneously diabetic Wistar rats (BBL), insulin-treated diabetic rats, and nondiabetic controls. |
| 1865 | 6108887 | Somatostatin, in addition to depressing insulin, produced a slight but significant (P < 0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). |
| 1866 | 6108887 | Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. |
| 1867 | 6108887 | Somatostatin, in addition to depressing insulin, produced a slight but significant (P < 0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). |
| 1868 | 6108887 | Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. |
| 1869 | 6109733 | Peripheral plasma somatostatin-like immunoreactive responses to insulin hypoglycemia and a mixed meal in healthy subjects and in noninsulin-dependent maturity-onset diabetics. |
| 1870 | 6110160 | The aim of the present study was to further evaluate the significance of circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1871 | 6110160 | Eight insulin-dependent diabetics and eight normals were infused with somatostatin at increasing doses (250, 500, and 750 microgram/h), each dose for 30 min. |
| 1872 | 6110160 | The aim of the present study was to further evaluate the significance of circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1873 | 6110160 | Eight insulin-dependent diabetics and eight normals were infused with somatostatin at increasing doses (250, 500, and 750 microgram/h), each dose for 30 min. |
| 1874 | 6110570 | Circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1875 | 6110570 | The present study was undertaken to reevaluate the influence of somatostatin on platelet function in insulin-dependent diabetics and in normal subjects. |
| 1876 | 6110570 | In in vivo studies, nine insulin-requiring diabetics were infused with cyclic somatostatin (250 microgram/hour) for 120 minutes or with saline, in randomized order. |
| 1877 | 6110570 | This dose of somatostatin, sufficient to depress the basal concentrations of plasma glucose, glucagon and C-peptide, resulted in no significant change of platelet aggregation response to either ADP or collagen. |
| 1878 | 6110570 | Circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1879 | 6110570 | The present study was undertaken to reevaluate the influence of somatostatin on platelet function in insulin-dependent diabetics and in normal subjects. |
| 1880 | 6110570 | In in vivo studies, nine insulin-requiring diabetics were infused with cyclic somatostatin (250 microgram/hour) for 120 minutes or with saline, in randomized order. |
| 1881 | 6110570 | This dose of somatostatin, sufficient to depress the basal concentrations of plasma glucose, glucagon and C-peptide, resulted in no significant change of platelet aggregation response to either ADP or collagen. |
| 1882 | 6110570 | Circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1883 | 6110570 | The present study was undertaken to reevaluate the influence of somatostatin on platelet function in insulin-dependent diabetics and in normal subjects. |
| 1884 | 6110570 | In in vivo studies, nine insulin-requiring diabetics were infused with cyclic somatostatin (250 microgram/hour) for 120 minutes or with saline, in randomized order. |
| 1885 | 6110570 | This dose of somatostatin, sufficient to depress the basal concentrations of plasma glucose, glucagon and C-peptide, resulted in no significant change of platelet aggregation response to either ADP or collagen. |
| 1886 | 6110570 | Circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. |
| 1887 | 6110570 | The present study was undertaken to reevaluate the influence of somatostatin on platelet function in insulin-dependent diabetics and in normal subjects. |
| 1888 | 6110570 | In in vivo studies, nine insulin-requiring diabetics were infused with cyclic somatostatin (250 microgram/hour) for 120 minutes or with saline, in randomized order. |
| 1889 | 6110570 | This dose of somatostatin, sufficient to depress the basal concentrations of plasma glucose, glucagon and C-peptide, resulted in no significant change of platelet aggregation response to either ADP or collagen. |
| 1890 | 6110595 | A possible deficiency of somatostatin, one of the factors controlling insulin release, has only recently been considered. |
| 1891 | 6110595 | Pancreatic tissue from five babies with severe hypoglycemia, hyperinsulinemia, and nesidioblastosis was examined for insulin, somatostatin, and glucagon by immunocytochemistry and radioimmunoassay. |
| 1892 | 6110595 | A possible deficiency of somatostatin, one of the factors controlling insulin release, has only recently been considered. |
| 1893 | 6110595 | Pancreatic tissue from five babies with severe hypoglycemia, hyperinsulinemia, and nesidioblastosis was examined for insulin, somatostatin, and glucagon by immunocytochemistry and radioimmunoassay. |
| 1894 | 6110594 | Glucose stimulates somatostatin release from perifused pancreatic islets of diabetic rats 42-47 days after the induction of diabetes, and 48 h after withdrawal of insulin replacement therapy. |
| 1895 | 6110596 | Specific binding to somatostatin, glucagon, and insulin was measured in the three fractions. |
| 1896 | 6110596 | Binding of glucagon and insulin to the L fraction was very low while, in contrast, somatostatin binding was substantial and linear with lymphocyte number. |
| 1897 | 6110596 | Specific binding to somatostatin, glucagon, and insulin was measured in the three fractions. |
| 1898 | 6110596 | Binding of glucagon and insulin to the L fraction was very low while, in contrast, somatostatin binding was substantial and linear with lymphocyte number. |
| 1899 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1900 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1901 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1902 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1903 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1904 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1905 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1906 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1907 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1908 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1909 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1910 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1911 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1912 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1913 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1914 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1915 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1916 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1917 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1918 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1919 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1920 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1921 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1922 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1923 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1924 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1925 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1926 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1927 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1928 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1929 | 6110597 | Effect of muscimol on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1930 | 6110597 | This study examines the effect of muscimol, a high affinity, specific gamma-aminobutyric acid (GABA) agonist, on glucose-stimulated somatostatin and insulin release from the isolated, perfused rat pancreas. |
| 1931 | 6110597 | High glucose (300 mg/dl) conditions stimulated somatostatin and insulin release. |
| 1932 | 6110597 | Steady-state levels of somatostatin and insulin release under high glucose conditions were 425 +/- 12 pg/ml and 419 +/- 18 microU/ml, respectively. |
| 1933 | 6110597 | Perfusion with medium containing 1 microM muscimol inhibited glucose-stimulated somatostatin release by 38%, whereas the course of glucose-stimulated insulin release was unaffected. |
| 1934 | 6110597 | Tentative conclusions from this study are (1) that GABA is potentially a modulator of islet somatostatin but not insulin release, and (2) the fact that somatostatin, an inhibitor of insulin, can be suppressed 38% without coincidental increase in insulin release seems to indicate that, under high glucose conditions, somatostatin is without a significant paracrine effect on the beta-cells. |
| 1935 | 6110598 | To answer these questions, conscious overnight-fasted dogs were given somatostatin (0.8 microgram/kg . min) plus basal intraportal replacement amounts of insulin (273 microU/kg . min) and glucagon (0.65 ng/kg . min) for 2 h, after which the rate of glucagon infusion was increased fourfold for 3 h and then returned to basal for 1.5 h. |
| 1936 | 6110600 | Both of the trioses stimulated B- and inhibited A-cell secretion. (3) Mannoheptulose (5 mM) attenuated somatostatin and insulin secretion to 8.3 mM glucose, while it augmented glucagon output. |
| 1937 | 6110600 | In contrast, mannoheptulose (5 mM) did not affect D-, A-, or B-cell responses to glyceraldehyde (5 mM) in the absence of glucose. (4) The somatostatin, insulin, and glucagon release remained unchanged when 8.3 mM of either galactose, fructose, or ribose was added. |
| 1938 | 6110600 | Both of the trioses stimulated B- and inhibited A-cell secretion. (3) Mannoheptulose (5 mM) attenuated somatostatin and insulin secretion to 8.3 mM glucose, while it augmented glucagon output. |
| 1939 | 6110600 | In contrast, mannoheptulose (5 mM) did not affect D-, A-, or B-cell responses to glyceraldehyde (5 mM) in the absence of glucose. (4) The somatostatin, insulin, and glucagon release remained unchanged when 8.3 mM of either galactose, fructose, or ribose was added. |
| 1940 | 6110602 | Pancreatic specimens from 34 infants of diabetic mothers (IDM) and 32 control infants of gestational ages 26-44 wk were examined histologically using immunocytochemical stains for insulin, glucagon, somatostatin, and pancreatic polypeptide (PP). |
| 1941 | 6110603 | High plasma levels of free fatty acids (FFA) stimulate the secretion of splanchnic somatostatin, and both are elevated in insulin deficiency. |
| 1942 | 6110603 | To determine if the hypersomatostatinemia of insulin deficiency is secondary to high FFA levels, plasma somatostatin-like immunoreactivity (SLI) was measured in a group of insulin-deprived alloxan-diabetic dogs during nicotinic acid-induced lowering of their elevated plasma FFA to normal, and in a group of nondiabetic dogs during nicotinic acid-induced lowering of their FFA to subnormal values. |
| 1943 | 6110603 | High plasma levels of free fatty acids (FFA) stimulate the secretion of splanchnic somatostatin, and both are elevated in insulin deficiency. |
| 1944 | 6110603 | To determine if the hypersomatostatinemia of insulin deficiency is secondary to high FFA levels, plasma somatostatin-like immunoreactivity (SLI) was measured in a group of insulin-deprived alloxan-diabetic dogs during nicotinic acid-induced lowering of their elevated plasma FFA to normal, and in a group of nondiabetic dogs during nicotinic acid-induced lowering of their FFA to subnormal values. |
| 1945 | 6110604 | Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation. |
| 1946 | 6110604 | The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. |
| 1947 | 6110604 | A 10 min 0.625 mmol/l alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. |
| 1948 | 6110604 | Addition of 1 microgram/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. |
| 1949 | 6110604 | Streptozotocin treatment 90 min prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. |
| 1950 | 6110604 | Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation. |
| 1951 | 6110604 | The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. |
| 1952 | 6110604 | A 10 min 0.625 mmol/l alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. |
| 1953 | 6110604 | Addition of 1 microgram/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. |
| 1954 | 6110604 | Streptozotocin treatment 90 min prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. |
| 1955 | 6110604 | Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation. |
| 1956 | 6110604 | The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. |
| 1957 | 6110604 | A 10 min 0.625 mmol/l alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. |
| 1958 | 6110604 | Addition of 1 microgram/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. |
| 1959 | 6110604 | Streptozotocin treatment 90 min prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. |
| 1960 | 6110604 | Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation. |
| 1961 | 6110604 | The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. |
| 1962 | 6110604 | A 10 min 0.625 mmol/l alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. |
| 1963 | 6110604 | Addition of 1 microgram/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. |
| 1964 | 6110604 | Streptozotocin treatment 90 min prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. |
| 1965 | 6110604 | Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation. |
| 1966 | 6110604 | The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. |
| 1967 | 6110604 | A 10 min 0.625 mmol/l alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. |
| 1968 | 6110604 | Addition of 1 microgram/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. |
| 1969 | 6110604 | Streptozotocin treatment 90 min prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. |
| 1970 | 6111018 | The antiketogenic effect of adding glucagon was due to an eventual breakthrough of the somatostatin blockade on insulin secretion, the latter gradually returning toward preinfusion levels. |
| 1971 | 6111018 | Inclusion of exogenous insulin with the somatostatin-glucagon infusion immediately lowered free fatty acids and ketoacids. |
| 1972 | 6111018 | The antiketogenic effect of adding glucagon was due to an eventual breakthrough of the somatostatin blockade on insulin secretion, the latter gradually returning toward preinfusion levels. |
| 1973 | 6111018 | Inclusion of exogenous insulin with the somatostatin-glucagon infusion immediately lowered free fatty acids and ketoacids. |
| 1974 | 6111219 | Somatostatin, a tetradecapeptide originally isolated from the hypothalamus on the basis of its ability to inhibit the secretion of growth hormone, is now known to be widely distributed in various endocrine and gastrointestinal tissues and to have diverse actions, including inhibition of insulin and glucagon secretion. |
| 1975 | 6111219 | The location of somatostatin in pancreatic islet D cells suggests that it may act as a local regulator of insulin and glucagon secretion. |
| 1976 | 6111219 | Somatostatin, a tetradecapeptide originally isolated from the hypothalamus on the basis of its ability to inhibit the secretion of growth hormone, is now known to be widely distributed in various endocrine and gastrointestinal tissues and to have diverse actions, including inhibition of insulin and glucagon secretion. |
| 1977 | 6111219 | The location of somatostatin in pancreatic islet D cells suggests that it may act as a local regulator of insulin and glucagon secretion. |
| 1978 | 6111928 | Endogenous hyperglycemia restores insulin release impaired by somatostatin analogue. |
| 1979 | 6111928 | These studies assessed the ability of des-Asn5-[D-Trp8-D-Ser13]-somatostatin (d-ATS-SS) to selectively inhibit insulin release and produce a hyperglycemia sufficient to compensate for the original impairment. d-ATS-SS at 0.017 micrograms/min inhibited basal insulin output (delta = -38 +/- 6%, P less than 0.005) and increased basal pancreatic glucagon output (delta - +21 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.17 micrograms/min markedly inhibited insulin output (delta = -84 +/- 4%, P less than 0.0005) and slightly inhibited glucagon output (delta = -14 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.055 micrograms/min decreased basal and stimulated insulin release but not basal nor stimulated glucagon release. |
| 1980 | 6111928 | Endogenous hyperglycemia restores insulin release impaired by somatostatin analogue. |
| 1981 | 6111928 | These studies assessed the ability of des-Asn5-[D-Trp8-D-Ser13]-somatostatin (d-ATS-SS) to selectively inhibit insulin release and produce a hyperglycemia sufficient to compensate for the original impairment. d-ATS-SS at 0.017 micrograms/min inhibited basal insulin output (delta = -38 +/- 6%, P less than 0.005) and increased basal pancreatic glucagon output (delta - +21 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.17 micrograms/min markedly inhibited insulin output (delta = -84 +/- 4%, P less than 0.0005) and slightly inhibited glucagon output (delta = -14 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.055 micrograms/min decreased basal and stimulated insulin release but not basal nor stimulated glucagon release. |
| 1982 | 6112177 | Despite a marked reduction of pancreatic insulin content observed during development, there was little effect upon glucagon or somatostatin content. |
| 1983 | 6112181 | To determine this, somatostatin was infused along with basal replacement amounts of glucagon (0.65 ng/mg x min) and insulin (228 microU/kg x min) into five postabsorptive conscious dogs. |
| 1984 | 6112233 | Antibodies to insulin, pancreatic polypeptide, glucagon, and somatostatin in insulin-treated diabetics. |
| 1985 | 6112233 | Connaught insulins contained 62 +/- 10 ng pancreatic polypeptide (PP)/100 U insulin, 11 +/- 2 ng glucagon/100 U, and 56 +/- 16 pg somatostatin (SRIF)/100 U. |
| 1986 | 6112233 | Antibodies to insulin, pancreatic polypeptide, glucagon, and somatostatin in insulin-treated diabetics. |
| 1987 | 6112233 | Connaught insulins contained 62 +/- 10 ng pancreatic polypeptide (PP)/100 U insulin, 11 +/- 2 ng glucagon/100 U, and 56 +/- 16 pg somatostatin (SRIF)/100 U. |
| 1988 | 6112234 | Clinical significance of altered insulin sensitivity in diabetes mellitus assessed by glucose, insulin, and somatostatin infusion. |
| 1989 | 6112234 | Insulin sensitivity has been determined in primary nonobese diabetics and subjects with borderline glucose intolerance by a newly devised technique using glucose, insulin, and somatostatin infusion. |
| 1990 | 6112234 | Clinical significance of altered insulin sensitivity in diabetes mellitus assessed by glucose, insulin, and somatostatin infusion. |
| 1991 | 6112234 | Insulin sensitivity has been determined in primary nonobese diabetics and subjects with borderline glucose intolerance by a newly devised technique using glucose, insulin, and somatostatin infusion. |
| 1992 | 6112718 | On the basis of our findings it might be suggested, therefore, that in the subjects, who are genetically pre disposed to developing diabetes mellitus, insulin does not suppress pancreatic glucagon secretion or owing to a functional disorder among alpha- beta- and delta-cells, somatostatin secretion is deficient or slow with following hyperinsulinemia and hyperglucagonemia. |
| 1993 | 6112741 | [Relation between blood somatostatin concentration and somatotropin, insulin and glucagon secretion in endocrine diseases]. |
| 1994 | 6112741 | Comparative analysis of somatostatin, somatotropin, glucagon and immunoreactive insulin content in the blood of patients with different endocrine disturbances was carried out. |
| 1995 | 6112741 | An increase in the blood somatostatin concentration of patients with diabetes mellitus, Icenko-Cushing's disease and obesity was accompanied by a fall in somatotropin and glucagon secretion and a rise in the blood insulin level. |
| 1996 | 6112741 | [Relation between blood somatostatin concentration and somatotropin, insulin and glucagon secretion in endocrine diseases]. |
| 1997 | 6112741 | Comparative analysis of somatostatin, somatotropin, glucagon and immunoreactive insulin content in the blood of patients with different endocrine disturbances was carried out. |
| 1998 | 6112741 | An increase in the blood somatostatin concentration of patients with diabetes mellitus, Icenko-Cushing's disease and obesity was accompanied by a fall in somatotropin and glucagon secretion and a rise in the blood insulin level. |
| 1999 | 6112741 | [Relation between blood somatostatin concentration and somatotropin, insulin and glucagon secretion in endocrine diseases]. |
| 2000 | 6112741 | Comparative analysis of somatostatin, somatotropin, glucagon and immunoreactive insulin content in the blood of patients with different endocrine disturbances was carried out. |
| 2001 | 6112741 | An increase in the blood somatostatin concentration of patients with diabetes mellitus, Icenko-Cushing's disease and obesity was accompanied by a fall in somatotropin and glucagon secretion and a rise in the blood insulin level. |
| 2002 | 6114006 | Insulin and glucagon breakthrough of somatostatin suppression: importance of portal vein hormone measurements. |
| 2003 | 6114888 | Insulin inhibits somatostatin-like immunoreactivity release stimulated by intragastric HCl. |
| 2004 | 6114888 | To determine the effect of an increase in insulin levels within the range occurring under physiologic conditions on the protein- and acid-induced release of splanchnic somatostatin, insulin was infused in dogs for 1 h following the intragastric instillation of a neutral protein load (20% liver extract at pH 7), a weak stimulus of somatostatin-like immunoreactivity (SLI), and after an intragastric HCl, a strong stimulus of SLI release, instilled 30 min later. |
| 2005 | 6114888 | Prevention of the insulin-induced hypoglycemia and the secondary rise in glucagon, a known stimulus of pancreatic somatostatin secretion, by means of a concomitant infusion of glucose, did not modify the reduction in acid-induced increase in plasma SLI concentration associated with hyperinsulinemia. |
| 2006 | 6114888 | Insulin inhibits somatostatin-like immunoreactivity release stimulated by intragastric HCl. |
| 2007 | 6114888 | To determine the effect of an increase in insulin levels within the range occurring under physiologic conditions on the protein- and acid-induced release of splanchnic somatostatin, insulin was infused in dogs for 1 h following the intragastric instillation of a neutral protein load (20% liver extract at pH 7), a weak stimulus of somatostatin-like immunoreactivity (SLI), and after an intragastric HCl, a strong stimulus of SLI release, instilled 30 min later. |
| 2008 | 6114888 | Prevention of the insulin-induced hypoglycemia and the secondary rise in glucagon, a known stimulus of pancreatic somatostatin secretion, by means of a concomitant infusion of glucose, did not modify the reduction in acid-induced increase in plasma SLI concentration associated with hyperinsulinemia. |
| 2009 | 6114888 | Insulin inhibits somatostatin-like immunoreactivity release stimulated by intragastric HCl. |
| 2010 | 6114888 | To determine the effect of an increase in insulin levels within the range occurring under physiologic conditions on the protein- and acid-induced release of splanchnic somatostatin, insulin was infused in dogs for 1 h following the intragastric instillation of a neutral protein load (20% liver extract at pH 7), a weak stimulus of somatostatin-like immunoreactivity (SLI), and after an intragastric HCl, a strong stimulus of SLI release, instilled 30 min later. |
| 2011 | 6114888 | Prevention of the insulin-induced hypoglycemia and the secondary rise in glucagon, a known stimulus of pancreatic somatostatin secretion, by means of a concomitant infusion of glucose, did not modify the reduction in acid-induced increase in plasma SLI concentration associated with hyperinsulinemia. |
| 2012 | 6114891 | Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system. |
| 2013 | 6114891 | When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). |
| 2014 | 6114891 | Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled. |
| 2015 | 6114891 | Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system. |
| 2016 | 6114891 | When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). |
| 2017 | 6114891 | Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled. |
| 2018 | 6114891 | Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system. |
| 2019 | 6114891 | When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). |
| 2020 | 6114891 | Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled. |
| 2021 | 6114915 | Somatostatin and insulin infusion in the management of diabetic ketoacidosis. |
| 2022 | 6114915 | The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). |
| 2023 | 6114915 | During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. |
| 2024 | 6114915 | The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced. |
| 2025 | 6114915 | Somatostatin and insulin infusion in the management of diabetic ketoacidosis. |
| 2026 | 6114915 | The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). |
| 2027 | 6114915 | During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. |
| 2028 | 6114915 | The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced. |
| 2029 | 6114915 | Somatostatin and insulin infusion in the management of diabetic ketoacidosis. |
| 2030 | 6114915 | The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). |
| 2031 | 6114915 | During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. |
| 2032 | 6114915 | The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced. |
| 2033 | 6114915 | Somatostatin and insulin infusion in the management of diabetic ketoacidosis. |
| 2034 | 6114915 | The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). |
| 2035 | 6114915 | During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. |
| 2036 | 6114915 | The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced. |
| 2037 | 6114914 | To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. |
| 2038 | 6114914 | During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). |
| 2039 | 6114914 | With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). |
| 2040 | 6114914 | It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. |
| 2041 | 6114914 | To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. |
| 2042 | 6114914 | During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). |
| 2043 | 6114914 | With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). |
| 2044 | 6114914 | It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. |
| 2045 | 6114914 | To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. |
| 2046 | 6114914 | During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). |
| 2047 | 6114914 | With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). |
| 2048 | 6114914 | It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. |
| 2049 | 6114914 | To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. |
| 2050 | 6114914 | During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). |
| 2051 | 6114914 | With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). |
| 2052 | 6114914 | It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. |
| 2053 | 6115783 | The insulin-, glucagon-, and somatostatin-positive cell populations of the islets were identified by immunocytochemical staining, and their volumes were determined by linear scanning. |
| 2054 | 6115785 | To test this assumption, the relationship between glucose concentration and disposal rate was studied in man during infusion of somatostatin +/- exogenous insulin to achieve fixed plasma insulin levels of 1, 18, and 46 microM/ml on separate days. |
| 2055 | 6115786 | The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. |
| 2056 | 6115786 | Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. |
| 2057 | 6115786 | In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone. |
| 2058 | 6115786 | The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. |
| 2059 | 6115786 | Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. |
| 2060 | 6115786 | In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone. |
| 2061 | 6115786 | The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. |
| 2062 | 6115786 | Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. |
| 2063 | 6115786 | In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone. |
| 2064 | 6116366 | The content and the distribution of insulin, glucagon and somatostatin were studied in normoglycemic and hyperglycemic rodents by immunohistochemical techniques. |
| 2065 | 6118255 | Insulin-, glucagon-, and somatostatin-reactive cells in the pancreas. |
| 2066 | 6120875 | Results were compared with those obtained in control and in insulin-dependent diabetic subjects, and in pancreatectomized subjects receiving a combined infusion of glucagon and arginine or somatostatin and arginine. |
| 2067 | 6120949 | The responses of pancreatic hormones (i.e. glucagon, pancreatic polypeptide, and somatostatin) to insulin-induced hypoglycemia were investigated in 18 insulin-dependent diabetics without residual beta-cell function and in 6 normal subjects. |
| 2068 | 6124374 | For instance, cholecystokinin and human pancreatic polypeptide (hPP) may be importantly involved in the regulation of appetite and satiety control and the development of obesity whereas somatostatin, "endorphins", and neurotensin may directly or indirectly modulate islet hormone secretion. |
| 2069 | 6125480 | Somatostatin-reduced tumor proliferation is accompanied by the strong suppression of insulin and SICRI levels, respectively; this effect is completely abolished by the administration of modest doses of crystalline insulin. |
| 2070 | 6125480 | It is concluded that somatostatin retards tumor growth by diminution of plasma levels of insulin and SICRI, respectively. |
| 2071 | 6125480 | Somatostatin-reduced tumor proliferation is accompanied by the strong suppression of insulin and SICRI levels, respectively; this effect is completely abolished by the administration of modest doses of crystalline insulin. |
| 2072 | 6125480 | It is concluded that somatostatin retards tumor growth by diminution of plasma levels of insulin and SICRI, respectively. |
| 2073 | 6125526 | Basal somatostatin levels (mean = 14.0 +/- 0.4 pg/ml) for nonobese (BMI less than 30, n = 10) were not different from values (mean = 13.3 +/- 0.7 pg/ml) observed for the obese group (BMI greater than 35, n = 17) nor from the values (n = 8, x = 15.4 +/- 1.2 pg/ml) obtained for subjects with non-insulin dependent diabetes mellitus. |
| 2074 | 6126426 | Alterations in the somatostatin (SRIF)-, insulin- and glucagon-containing cells were examined in two strains of spontaneously diabetic mice, KK and newly inbred non-obese diabetic (NOD) mice, using radioimmunoassay and immunohistochemical methods. |
| 2075 | 6126608 | Endocrine function of pancreas transplant: insulin, glucagon and somatostatin release from rat pancreatic isograft. |
| 2076 | 6126608 | The release of insulin, glucagon and somatostatin by the pancreatic grafts were examined and compared with those in normal rats with or without syngenic pancreas transplantation, using in vivo and in vitro systems. |
| 2077 | 6126608 | These studies demonstrate that the grafted pancreas maintained normal insulin, glucagon and somatostatin secretion after transplantation. |
| 2078 | 6126608 | Endocrine function of pancreas transplant: insulin, glucagon and somatostatin release from rat pancreatic isograft. |
| 2079 | 6126608 | The release of insulin, glucagon and somatostatin by the pancreatic grafts were examined and compared with those in normal rats with or without syngenic pancreas transplantation, using in vivo and in vitro systems. |
| 2080 | 6126608 | These studies demonstrate that the grafted pancreas maintained normal insulin, glucagon and somatostatin secretion after transplantation. |
| 2081 | 6126608 | Endocrine function of pancreas transplant: insulin, glucagon and somatostatin release from rat pancreatic isograft. |
| 2082 | 6126608 | The release of insulin, glucagon and somatostatin by the pancreatic grafts were examined and compared with those in normal rats with or without syngenic pancreas transplantation, using in vivo and in vitro systems. |
| 2083 | 6126608 | These studies demonstrate that the grafted pancreas maintained normal insulin, glucagon and somatostatin secretion after transplantation. |
| 2084 | 6129168 | Radioimmunoassay of hormone content in cell fractions collected across the the two peaks showed that glucagon-containing cells were concentrated towards the left side of the left peak and somatostatin-containing cells were concentrated towards the right side of the left peak, whereas insulin-containing cells were clearly enriched in the right peak. |
| 2085 | 6129185 | The metabolic effects of Somatostatin (SRIF) added to insulin were studied in five diabetic subjects with ketonuria induced by insulin withdrawal. |
| 2086 | 6129185 | Finally the prolactin plasma levels fell considerably when combined treatment was given but not when just insulin was administered. |
| 2087 | 6130016 | Effects of synthetic human pancreatic polypeptide, synthetic bovine pancreatic polypeptide, and the C-terminal hexapeptide on pancreatic somatostatin and glucagon secretion in the rat. |
| 2088 | 6130016 | Synthetic human pancreatic polypeptide stimulated pancreatic somatostatin secretion by isolated rat islets and by the isolated perfused rat pancreas. |
| 2089 | 6130016 | In contrast, synthetic bovine pancreatic polypeptide and the C-terminal hexapeptide had no effect on somatostatin secretion. |
| 2090 | 6130016 | Effects of synthetic human pancreatic polypeptide, synthetic bovine pancreatic polypeptide, and the C-terminal hexapeptide on pancreatic somatostatin and glucagon secretion in the rat. |
| 2091 | 6130016 | Synthetic human pancreatic polypeptide stimulated pancreatic somatostatin secretion by isolated rat islets and by the isolated perfused rat pancreas. |
| 2092 | 6130016 | In contrast, synthetic bovine pancreatic polypeptide and the C-terminal hexapeptide had no effect on somatostatin secretion. |
| 2093 | 6130016 | Effects of synthetic human pancreatic polypeptide, synthetic bovine pancreatic polypeptide, and the C-terminal hexapeptide on pancreatic somatostatin and glucagon secretion in the rat. |
| 2094 | 6130016 | Synthetic human pancreatic polypeptide stimulated pancreatic somatostatin secretion by isolated rat islets and by the isolated perfused rat pancreas. |
| 2095 | 6130016 | In contrast, synthetic bovine pancreatic polypeptide and the C-terminal hexapeptide had no effect on somatostatin secretion. |
| 2096 | 6130017 | The secretion of insulin, somatostatin, and glucagon by the cells was monitored by radioimmunoassays. |
| 2097 | 6130017 | Increasing glucose concentrations in the superfusion medium increased the release of insulin and somatostatin (SS), whereas glucagon secretory rates remained constant or decreased. |
| 2098 | 6130017 | Various secretagogues such as IBMX, 8-bromo cyclic AMP, and L-arginine increased insulin, somatostatin, and glucagon secretory rates in an expected manner. |
| 2099 | 6130017 | The secretion of insulin, somatostatin, and glucagon by the cells was monitored by radioimmunoassays. |
| 2100 | 6130017 | Increasing glucose concentrations in the superfusion medium increased the release of insulin and somatostatin (SS), whereas glucagon secretory rates remained constant or decreased. |
| 2101 | 6130017 | Various secretagogues such as IBMX, 8-bromo cyclic AMP, and L-arginine increased insulin, somatostatin, and glucagon secretory rates in an expected manner. |
| 2102 | 6130017 | The secretion of insulin, somatostatin, and glucagon by the cells was monitored by radioimmunoassays. |
| 2103 | 6130017 | Increasing glucose concentrations in the superfusion medium increased the release of insulin and somatostatin (SS), whereas glucagon secretory rates remained constant or decreased. |
| 2104 | 6130017 | Various secretagogues such as IBMX, 8-bromo cyclic AMP, and L-arginine increased insulin, somatostatin, and glucagon secretory rates in an expected manner. |
| 2105 | 6131002 | The application of immunofluorescence technique with anti-insulin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide (PP) antisera to sections of precisely sampled regions of the human pancreas allowed the quantitative evaluation of the total content of these four endocrine cell populations in 13 nondiabetics, in 2 insulin-dependent diabetics (IDDM), and in 2 non-insulin-dependent diabetic subjects (NIDDM) of various age and sex. |
| 2106 | 6131002 | In diabetic subjects, the only marked difference as compared with nondiabetics is the reduction of insulin cell volume in IDDM. |
| 2107 | 6131002 | The qualitative changes of islet structure accompanying insulin cell reduction in IDDM were not considered in the present study. |
| 2108 | 6131006 | Conversely, insulin treatment in vivo did not restore a priming effect of glucose on somatostatin secretion. |
| 2109 | 6131006 | Other effects noted were failure of 27.7 mmol/l glucose to stimulate, during its presence, the release of somatostatin from pancreases of the diabetic rats whether untreated or insulin-treated. |
| 2110 | 6131006 | Furthermore, insulin treatment abolished the arginine-induced somatostatin secretion observed in pancreases from untreated rats. |
| 2111 | 6131006 | Conversely, insulin treatment in vivo did not restore a priming effect of glucose on somatostatin secretion. |
| 2112 | 6131006 | Other effects noted were failure of 27.7 mmol/l glucose to stimulate, during its presence, the release of somatostatin from pancreases of the diabetic rats whether untreated or insulin-treated. |
| 2113 | 6131006 | Furthermore, insulin treatment abolished the arginine-induced somatostatin secretion observed in pancreases from untreated rats. |
| 2114 | 6131006 | Conversely, insulin treatment in vivo did not restore a priming effect of glucose on somatostatin secretion. |
| 2115 | 6131006 | Other effects noted were failure of 27.7 mmol/l glucose to stimulate, during its presence, the release of somatostatin from pancreases of the diabetic rats whether untreated or insulin-treated. |
| 2116 | 6131006 | Furthermore, insulin treatment abolished the arginine-induced somatostatin secretion observed in pancreases from untreated rats. |
| 2117 | 6131079 | The loss of insulin inhibition of glucagon-mediated somatostatin secretion may account for the hypersomatostatinemia of severe diabetes. |
| 2118 | 6131815 | In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). |
| 2119 | 6131815 | In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased. |
| 2120 | 6131815 | In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). |
| 2121 | 6131815 | In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased. |
| 2122 | 6131849 | The immunofluorescent cell content of the pancreas of 8--40-wk fetuses and of 1.5--5-mo Caucasian infants was quantitatively evaluated using anti-insulin, anti-glicentin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide antisera. |
| 2123 | 6131849 | This cell population decreases and disappears in later stages and is replaced by the adult type glucagon/glicentin immunoreactive cell; (2) the pancreatic polypeptide-rich region shows a lower relative endocrine cell content as compared with the glucagon-rich region and its islets appear smaller; (3) in the total pancreas, the relative (volume density) and absolute (microliter) insulin cell content increases regularly with age, while the relative volume of glucagon cells peaks in fetal life (wk 17--20) to decrease in infants, although remaining at higher levels than in adults; the relative and absolute volumes of somatostatin cells are elevated in fetal and infant stages studied where they represent the second most abundant cell type, while pancreatic polypeptide cells appear to least abundant cells during prenatal and infant life. |
| 2124 | 6131849 | The immunofluorescent cell content of the pancreas of 8--40-wk fetuses and of 1.5--5-mo Caucasian infants was quantitatively evaluated using anti-insulin, anti-glicentin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide antisera. |
| 2125 | 6131849 | This cell population decreases and disappears in later stages and is replaced by the adult type glucagon/glicentin immunoreactive cell; (2) the pancreatic polypeptide-rich region shows a lower relative endocrine cell content as compared with the glucagon-rich region and its islets appear smaller; (3) in the total pancreas, the relative (volume density) and absolute (microliter) insulin cell content increases regularly with age, while the relative volume of glucagon cells peaks in fetal life (wk 17--20) to decrease in infants, although remaining at higher levels than in adults; the relative and absolute volumes of somatostatin cells are elevated in fetal and infant stages studied where they represent the second most abundant cell type, while pancreatic polypeptide cells appear to least abundant cells during prenatal and infant life. |
| 2126 | 6131850 | Cysteamine blocks somatostatin secretion without altering the course of insulin or glucagon release. |
| 2127 | 6131850 | Cysteamine (300 mg/kg) administered subcutaneously depletes pancreatic somatostatin to 36% of control levels, but does not alter pancreatic insulin or glucagon content. |
| 2128 | 6131850 | Cysteamine blocks somatostatin secretion without altering the course of insulin or glucagon release. |
| 2129 | 6131850 | Cysteamine (300 mg/kg) administered subcutaneously depletes pancreatic somatostatin to 36% of control levels, but does not alter pancreatic insulin or glucagon content. |
| 2130 | 6132848 | To investigate the hypothesis that in Type 1 (insulin-dependent) diabetes the increase in plasma potassium during decompensation may be due to a rise in glucagon concentrations, we have measured plasma glucose, potassium and glucagon levels in five diabetic patients during two tests with 0.154 mol/l saline or somatostatin (500 micrograms/h) performed on two successive days. |
| 2131 | 6133449 | There were a few glucagon-containing cells, but pancreatic polypeptide-labeled and somatostatin-labeled cells were rarely seen. |
| 2132 | 6133710 | Although the incremental plasma insulin values achieved with the two insulins were similar in the two studies, the hypoglycemic effect was accentuated in the presence of somatostatin, with a delayed recovery toward normoglycemia. |
| 2133 | 6133743 | Effect of tolbutamide on insulin, glucagon, and somatostatin release from the diabetic rat pancreas with special reference to glucose concentration. |
| 2134 | 6133743 | The effects of tolbutamide on insulin, glucagon, and somatostatin secretion were investigated in the isolated perfused pancreas from normal and diabetic rats under low (30 mg/dl), normal (100 mg/dl), and high (300 mg/dl) glucose conditions. |
| 2135 | 6133743 | In the diabetic rat pancreas, insulin release was diminished and tolbutamide-induced somatostatin release was enhanced with increasing glucose concentrations. |
| 2136 | 6133743 | Effect of tolbutamide on insulin, glucagon, and somatostatin release from the diabetic rat pancreas with special reference to glucose concentration. |
| 2137 | 6133743 | The effects of tolbutamide on insulin, glucagon, and somatostatin secretion were investigated in the isolated perfused pancreas from normal and diabetic rats under low (30 mg/dl), normal (100 mg/dl), and high (300 mg/dl) glucose conditions. |
| 2138 | 6133743 | In the diabetic rat pancreas, insulin release was diminished and tolbutamide-induced somatostatin release was enhanced with increasing glucose concentrations. |
| 2139 | 6133743 | Effect of tolbutamide on insulin, glucagon, and somatostatin release from the diabetic rat pancreas with special reference to glucose concentration. |
| 2140 | 6133743 | The effects of tolbutamide on insulin, glucagon, and somatostatin secretion were investigated in the isolated perfused pancreas from normal and diabetic rats under low (30 mg/dl), normal (100 mg/dl), and high (300 mg/dl) glucose conditions. |
| 2141 | 6133743 | In the diabetic rat pancreas, insulin release was diminished and tolbutamide-induced somatostatin release was enhanced with increasing glucose concentrations. |
| 2142 | 6133785 | The eventual appearance of an extra-pancreatic source of insulin and the effect of pancreatectomy on somatostatin containing cells of the intestine were also investigated. |
| 2143 | 6133785 | The size of the somatostatin cells from the gizzard-duodenum junction was negatively related to the magnitude of the glucose-induced insulin release, which suggests an increase in somatostatin cell activity in true insulin-deficient depancreatized chickens as observed in insulin deficient diabetic mammals. |
| 2144 | 6133785 | The eventual appearance of an extra-pancreatic source of insulin and the effect of pancreatectomy on somatostatin containing cells of the intestine were also investigated. |
| 2145 | 6133785 | The size of the somatostatin cells from the gizzard-duodenum junction was negatively related to the magnitude of the glucose-induced insulin release, which suggests an increase in somatostatin cell activity in true insulin-deficient depancreatized chickens as observed in insulin deficient diabetic mammals. |
| 2146 | 6134649 | The relative hypoglycemic effects of pulsatile versus steadily infused insulin have been examined in six normal subjects in whom pancreatic insulin output was suppressed by somatostatin-14. |
| 2147 | 6134650 | In man a small dose of somatostatin (50 micrograms/h) suppressed moderately basal insulin (5 microU/ml) and glucagon (40 pg/ml) levels. |
| 2148 | 6134651 | Free-insulin, pancreatic glucagon, and growth hormone concentrations were measured after both oral and intravenous glucose tolerance tests, and following tolbutamide, arginine and arginine plus somatostatin infusions. |
| 2149 | 6134651 | Somatostatin was less effective in diabetic patients than in control subjects in suppressing insulin and glucagon release. |
| 2150 | 6134651 | Free-insulin, pancreatic glucagon, and growth hormone concentrations were measured after both oral and intravenous glucose tolerance tests, and following tolbutamide, arginine and arginine plus somatostatin infusions. |
| 2151 | 6134651 | Somatostatin was less effective in diabetic patients than in control subjects in suppressing insulin and glucagon release. |
| 2152 | 6134660 | In the present study effect of guar intake (12 g) on plasma somatostatin-like immunoreactivity (SRIF-LI) was studied in non-insulin dependent diabetes (NIDDM) and in insulin-dependent diabetes (IDDM) to see if somatostatin plays a role in reducing postprandial glucose. |
| 2153 | 6135136 | Somatostatin-like immunoreactivity (SLI), glucagon, and insulin were measured in extracted plasma obtained from the hepatic portal vein (PV) and inferior vena cava (IVC) of acutely diabetic untreated rats, insulin-treated diabetic rats and nondiabetic controls. |
| 2154 | 6135137 | Unstable diabetic rats demonstrate a reduction in the concentration of pancreatic immunoreactive glucagon and somatostatin, suggesting that alpha and delta cells also sustain injury in this model of insulin-dependent diabetes mellitus. |
| 2155 | 6135634 | Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans. |
| 2156 | 6135634 | Dynorphin-induced insulin secretion from islets was blocked by verapamil (5 microM) or by chlorpropamide (72 microM), but not by a mu opiate receptor antagonist, naloxone (0.11 microM), or by ICI 154129, a specific antagonist for the delta receptor (0.25 microM). |
| 2157 | 6135634 | Dynorphin had no effect on islet somatostatin secretion, under conditions in which insulin secretion was greatly stimulated. |
| 2158 | 6135634 | Glucose (20 mM) and glyceraldehyde (6 and 12 mM) significantly increased both insulin and somatostatin secretion. |
| 2159 | 6135634 | These results suggest that (1) dynorphin is a very potent stimulus for insulin secretion; (2) dynorphin does not affect somatostatin secretion in static incubations of islets, in the same way as does glucose and glyceraldehyde; (3) dynorphin's effects may involve increased calcium ion movement and can be blocked by verapamil; (4) dynorphin can also increase islet c-AMP, and could thereby modulate the responsiveness of other secretagogues; (5) the actions of dynorphin on insulin secretion are not mediated by delta or mu opiate receptors in islets. |
| 2160 | 6135634 | Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans. |
| 2161 | 6135634 | Dynorphin-induced insulin secretion from islets was blocked by verapamil (5 microM) or by chlorpropamide (72 microM), but not by a mu opiate receptor antagonist, naloxone (0.11 microM), or by ICI 154129, a specific antagonist for the delta receptor (0.25 microM). |
| 2162 | 6135634 | Dynorphin had no effect on islet somatostatin secretion, under conditions in which insulin secretion was greatly stimulated. |
| 2163 | 6135634 | Glucose (20 mM) and glyceraldehyde (6 and 12 mM) significantly increased both insulin and somatostatin secretion. |
| 2164 | 6135634 | These results suggest that (1) dynorphin is a very potent stimulus for insulin secretion; (2) dynorphin does not affect somatostatin secretion in static incubations of islets, in the same way as does glucose and glyceraldehyde; (3) dynorphin's effects may involve increased calcium ion movement and can be blocked by verapamil; (4) dynorphin can also increase islet c-AMP, and could thereby modulate the responsiveness of other secretagogues; (5) the actions of dynorphin on insulin secretion are not mediated by delta or mu opiate receptors in islets. |
| 2165 | 6135634 | Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans. |
| 2166 | 6135634 | Dynorphin-induced insulin secretion from islets was blocked by verapamil (5 microM) or by chlorpropamide (72 microM), but not by a mu opiate receptor antagonist, naloxone (0.11 microM), or by ICI 154129, a specific antagonist for the delta receptor (0.25 microM). |
| 2167 | 6135634 | Dynorphin had no effect on islet somatostatin secretion, under conditions in which insulin secretion was greatly stimulated. |
| 2168 | 6135634 | Glucose (20 mM) and glyceraldehyde (6 and 12 mM) significantly increased both insulin and somatostatin secretion. |
| 2169 | 6135634 | These results suggest that (1) dynorphin is a very potent stimulus for insulin secretion; (2) dynorphin does not affect somatostatin secretion in static incubations of islets, in the same way as does glucose and glyceraldehyde; (3) dynorphin's effects may involve increased calcium ion movement and can be blocked by verapamil; (4) dynorphin can also increase islet c-AMP, and could thereby modulate the responsiveness of other secretagogues; (5) the actions of dynorphin on insulin secretion are not mediated by delta or mu opiate receptors in islets. |
| 2170 | 6135634 | Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans. |
| 2171 | 6135634 | Dynorphin-induced insulin secretion from islets was blocked by verapamil (5 microM) or by chlorpropamide (72 microM), but not by a mu opiate receptor antagonist, naloxone (0.11 microM), or by ICI 154129, a specific antagonist for the delta receptor (0.25 microM). |
| 2172 | 6135634 | Dynorphin had no effect on islet somatostatin secretion, under conditions in which insulin secretion was greatly stimulated. |
| 2173 | 6135634 | Glucose (20 mM) and glyceraldehyde (6 and 12 mM) significantly increased both insulin and somatostatin secretion. |
| 2174 | 6135634 | These results suggest that (1) dynorphin is a very potent stimulus for insulin secretion; (2) dynorphin does not affect somatostatin secretion in static incubations of islets, in the same way as does glucose and glyceraldehyde; (3) dynorphin's effects may involve increased calcium ion movement and can be blocked by verapamil; (4) dynorphin can also increase islet c-AMP, and could thereby modulate the responsiveness of other secretagogues; (5) the actions of dynorphin on insulin secretion are not mediated by delta or mu opiate receptors in islets. |
| 2175 | 6136893 | Effects of a long-acting somatostatin analogue on postprandial hyperglycemia in insulin-dependent diabetes mellitus. |
| 2176 | 6136893 | To determine whether an agent such as WY-41,747, a long-acting somatostatin analogue, could be useful as an adjunct to insulin in the treatment of diabetes mellitus, postprandial plasma glucose concentrations were determined in subjects with insulin-dependent diabetes rendered euglycemic with the Biostator insulin infusion device under four conditions: (1) subcutaneous minipump infusion of insulin alone (13 +/- 1 units) over 30 minutes beginning 30 minutes before ingestion of a meal using insulin doses determined by the Biostator; (2) the same conditions as 1 but beginning immediately before meal ingestion; (3) the same conditions as 1 but with less insulin (7 +/- 1 units) accompanied by the analogue (0.01-0.05 mg/kg); (4) the same conditions as 2 but with the analogue and less insulin (11 +/- 1 units). |
| 2177 | 6136893 | Administration of the somatostatin analogue increased the effectiveness of insulin in controlling postprandial hyperglycemia and permitted satisfactory postprandial glycemic control when the insulin infusion was initiated immediately before meal ingestion. |
| 2178 | 6136893 | These results suggest that subcutaneous administration of a long-acting somatostatin analogue such as WY-41,747 along with insulin may be clinically useful in the treatment of diabetes mellitus. |
| 2179 | 6136893 | Effects of a long-acting somatostatin analogue on postprandial hyperglycemia in insulin-dependent diabetes mellitus. |
| 2180 | 6136893 | To determine whether an agent such as WY-41,747, a long-acting somatostatin analogue, could be useful as an adjunct to insulin in the treatment of diabetes mellitus, postprandial plasma glucose concentrations were determined in subjects with insulin-dependent diabetes rendered euglycemic with the Biostator insulin infusion device under four conditions: (1) subcutaneous minipump infusion of insulin alone (13 +/- 1 units) over 30 minutes beginning 30 minutes before ingestion of a meal using insulin doses determined by the Biostator; (2) the same conditions as 1 but beginning immediately before meal ingestion; (3) the same conditions as 1 but with less insulin (7 +/- 1 units) accompanied by the analogue (0.01-0.05 mg/kg); (4) the same conditions as 2 but with the analogue and less insulin (11 +/- 1 units). |
| 2181 | 6136893 | Administration of the somatostatin analogue increased the effectiveness of insulin in controlling postprandial hyperglycemia and permitted satisfactory postprandial glycemic control when the insulin infusion was initiated immediately before meal ingestion. |
| 2182 | 6136893 | These results suggest that subcutaneous administration of a long-acting somatostatin analogue such as WY-41,747 along with insulin may be clinically useful in the treatment of diabetes mellitus. |
| 2183 | 6136893 | Effects of a long-acting somatostatin analogue on postprandial hyperglycemia in insulin-dependent diabetes mellitus. |
| 2184 | 6136893 | To determine whether an agent such as WY-41,747, a long-acting somatostatin analogue, could be useful as an adjunct to insulin in the treatment of diabetes mellitus, postprandial plasma glucose concentrations were determined in subjects with insulin-dependent diabetes rendered euglycemic with the Biostator insulin infusion device under four conditions: (1) subcutaneous minipump infusion of insulin alone (13 +/- 1 units) over 30 minutes beginning 30 minutes before ingestion of a meal using insulin doses determined by the Biostator; (2) the same conditions as 1 but beginning immediately before meal ingestion; (3) the same conditions as 1 but with less insulin (7 +/- 1 units) accompanied by the analogue (0.01-0.05 mg/kg); (4) the same conditions as 2 but with the analogue and less insulin (11 +/- 1 units). |
| 2185 | 6136893 | Administration of the somatostatin analogue increased the effectiveness of insulin in controlling postprandial hyperglycemia and permitted satisfactory postprandial glycemic control when the insulin infusion was initiated immediately before meal ingestion. |
| 2186 | 6136893 | These results suggest that subcutaneous administration of a long-acting somatostatin analogue such as WY-41,747 along with insulin may be clinically useful in the treatment of diabetes mellitus. |
| 2187 | 6136893 | Effects of a long-acting somatostatin analogue on postprandial hyperglycemia in insulin-dependent diabetes mellitus. |
| 2188 | 6136893 | To determine whether an agent such as WY-41,747, a long-acting somatostatin analogue, could be useful as an adjunct to insulin in the treatment of diabetes mellitus, postprandial plasma glucose concentrations were determined in subjects with insulin-dependent diabetes rendered euglycemic with the Biostator insulin infusion device under four conditions: (1) subcutaneous minipump infusion of insulin alone (13 +/- 1 units) over 30 minutes beginning 30 minutes before ingestion of a meal using insulin doses determined by the Biostator; (2) the same conditions as 1 but beginning immediately before meal ingestion; (3) the same conditions as 1 but with less insulin (7 +/- 1 units) accompanied by the analogue (0.01-0.05 mg/kg); (4) the same conditions as 2 but with the analogue and less insulin (11 +/- 1 units). |
| 2189 | 6136893 | Administration of the somatostatin analogue increased the effectiveness of insulin in controlling postprandial hyperglycemia and permitted satisfactory postprandial glycemic control when the insulin infusion was initiated immediately before meal ingestion. |
| 2190 | 6136893 | These results suggest that subcutaneous administration of a long-acting somatostatin analogue such as WY-41,747 along with insulin may be clinically useful in the treatment of diabetes mellitus. |
| 2191 | 6137295 | Plasma somatostatin increases during hypoglycaemia in insulin-dependent patients with and without B-cell function. |
| 2192 | 6137295 | Responses of somatostatin-like immunoreactivity (SLI) to hypoglycaemia were investigated in seven type 1 (insulin-dependent) patients with residual B-cell function, eight patients without B-cell function, and six healthy controls. |
| 2193 | 6137295 | Plasma somatostatin increases during hypoglycaemia in insulin-dependent patients with and without B-cell function. |
| 2194 | 6137295 | Responses of somatostatin-like immunoreactivity (SLI) to hypoglycaemia were investigated in seven type 1 (insulin-dependent) patients with residual B-cell function, eight patients without B-cell function, and six healthy controls. |
| 2195 | 6137430 | Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. |
| 2196 | 6137430 | Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. |
| 2197 | 6137430 | In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. |
| 2198 | 6137430 | First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. |
| 2199 | 6137430 | In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. |
| 2200 | 6137430 | Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. |
| 2201 | 6137430 | Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. |
| 2202 | 6137430 | In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. |
| 2203 | 6137430 | First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. |
| 2204 | 6137430 | In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. |
| 2205 | 6137430 | Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. |
| 2206 | 6137430 | Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. |
| 2207 | 6137430 | In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. |
| 2208 | 6137430 | First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. |
| 2209 | 6137430 | In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. |
| 2210 | 6137430 | Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. |
| 2211 | 6137430 | Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. |
| 2212 | 6137430 | In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. |
| 2213 | 6137430 | First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. |
| 2214 | 6137430 | In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. |
| 2215 | 6137430 | Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. |
| 2216 | 6137430 | Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. |
| 2217 | 6137430 | In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. |
| 2218 | 6137430 | First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. |
| 2219 | 6137430 | In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. |
| 2220 | 6137431 | The lowest concentration of secretin, a level which is within the physiologic range, significantly suppressed glucagon release and stimulated somatostatin release but was without significant effect on insulin release. |
| 2221 | 6137926 | Insulin sensitivity was also measured by computer analysis of GIT (parameter KG) and, in a limited group of subjects, by a somatostatin infusion test. |
| 2222 | 6137957 | To determine the effectiveness of glucagon suppression in improving glucose homeostasis in diabetes, tracer-determined glucose kinetics were measured during a 6-h somatostatin infusion in six alloxan-diabetic dogs (moderately severe diabetes) and five depancreatized dogs deprived of insulin treatment for 3 days (prolonged severe diabetes). |
| 2223 | 6138289 | Dissociation of glucose stimulation of somatostatin and insulin release from glucose inhibition of glucagon release in the isolated perfused rat pancreas. |
| 2224 | 6138289 | This study investigated the modulating role of glucose on 5 mM arginine stimulation of insulin, somatostatin, and glucagon release from the isolated perfused rat pancreas. |
| 2225 | 6138289 | As glucose increased above 80 mg/dl, somatostatin and insulin release was initiated and they continued to increase in a nearly parallel fashion during the glucose gradient (300 mg/dl). |
| 2226 | 6138289 | Dissociation of glucose stimulation of somatostatin and insulin release from glucose inhibition of glucagon release in the isolated perfused rat pancreas. |
| 2227 | 6138289 | This study investigated the modulating role of glucose on 5 mM arginine stimulation of insulin, somatostatin, and glucagon release from the isolated perfused rat pancreas. |
| 2228 | 6138289 | As glucose increased above 80 mg/dl, somatostatin and insulin release was initiated and they continued to increase in a nearly parallel fashion during the glucose gradient (300 mg/dl). |
| 2229 | 6138289 | Dissociation of glucose stimulation of somatostatin and insulin release from glucose inhibition of glucagon release in the isolated perfused rat pancreas. |
| 2230 | 6138289 | This study investigated the modulating role of glucose on 5 mM arginine stimulation of insulin, somatostatin, and glucagon release from the isolated perfused rat pancreas. |
| 2231 | 6138289 | As glucose increased above 80 mg/dl, somatostatin and insulin release was initiated and they continued to increase in a nearly parallel fashion during the glucose gradient (300 mg/dl). |
| 2232 | 6138852 | Several studies demonstrating a tight interaction between somatostatin and insulin indicate that insulin is another important factor in the regulation of basal and postprandial somatostatin release. |
| 2233 | 6138852 | The role of somatostatin in pathophysiological states such as peptic ulceration and diabetes mellitus is not entirely clear but the present evidence indicates that alterations of tissue somatostatin content or plasma somatostatin levels are secondary to changes of other factors (increased gastric acid secretion, insulin deficiency) rather than representing the primary cause for the underlying disease. |
| 2234 | 6138852 | Several studies demonstrating a tight interaction between somatostatin and insulin indicate that insulin is another important factor in the regulation of basal and postprandial somatostatin release. |
| 2235 | 6138852 | The role of somatostatin in pathophysiological states such as peptic ulceration and diabetes mellitus is not entirely clear but the present evidence indicates that alterations of tissue somatostatin content or plasma somatostatin levels are secondary to changes of other factors (increased gastric acid secretion, insulin deficiency) rather than representing the primary cause for the underlying disease. |
| 2236 | 6139144 | High, vasopressin-reversible, immunoreactive somatostatin in specific hypothalamic nuclei of rats with diabetes insipidus (Brattleboro rats). |
| 2237 | 6139272 | Somatostatin (SRIF) acts as a physiological regulator of insulin and glucagon secretion. |
| 2238 | 6139319 | Somatostatin infused at a rate of 50 micrograms X h-1 X kg-1 body weight inhibited glucose-induced insulin secretion by 33%. |
| 2239 | 6139329 | Dissociated effects of somatostatin analogs on arginine-induced insulin, glucagon and growth hormone release in acromegalic patients. |
| 2240 | 6139329 | Under the same conditions the two somatostatin analogs induced a much smaller inhibition of insulin (33 +/- 13% and 44 +/- 18%) and glucagon (28 +/- 10% and 45 +/- 17%, respectively) release than somatostatin did. |
| 2241 | 6139329 | Dissociated effects of somatostatin analogs on arginine-induced insulin, glucagon and growth hormone release in acromegalic patients. |
| 2242 | 6139329 | Under the same conditions the two somatostatin analogs induced a much smaller inhibition of insulin (33 +/- 13% and 44 +/- 18%) and glucagon (28 +/- 10% and 45 +/- 17%, respectively) release than somatostatin did. |
| 2243 | 6140199 | We studied the release of insulin, glucagon, and somatostatin in response to glucose, glyceraldehyde (GA), and alpha-ketoisocaproate (KIC) from rat kidneys containing transplanted insulinomas. |
| 2244 | 6140199 | The insulin content of the tumor-containing kidney ranged from 40 to 679 micrograms; the glucagon and somatostatin concentrations ranged from undetectable levels to 3.7 micrograms and 248 ng, respectively. |
| 2245 | 6140199 | We studied the release of insulin, glucagon, and somatostatin in response to glucose, glyceraldehyde (GA), and alpha-ketoisocaproate (KIC) from rat kidneys containing transplanted insulinomas. |
| 2246 | 6140199 | The insulin content of the tumor-containing kidney ranged from 40 to 679 micrograms; the glucagon and somatostatin concentrations ranged from undetectable levels to 3.7 micrograms and 248 ng, respectively. |
| 2247 | 6140806 | To study the role of somatostatin in the pathophysiology of glucose intolerance in man, plasma somatostatin-like immunoreactivity (SLI) was measured in 8 normal subjects, 6 patients with insulin dependent diabetes mellitus (IDDM), 13 with non-insulin dependent diabetes mellitus (NIDDM), and 9 with hyperthyroidism, by extraction of plasma SLI and radioimmunoassay. |
| 2248 | 6141177 | We conclude that prolonged mild selective insulin deficiency produced by infusion of somatostatin with glucagon replacement in normal men causes an elevation of the fasting plasma glucose level, which is maintained by glucose overproduction rather than by glucose underutilization. |
| 2249 | 6141989 | Insulin sensitivity in pancreatitis, liver diseases, steroid treatment and hyperthyroidism assessed by glucose, insulin and somatostatin infusion. |
| 2250 | 6143233 | We now report structure-activity studies which optimize the potency of this cyclic hexapeptide series with the synthesis of cyclo (N-Me-Ala-Tyr-D-Trp-Lys-Val-Phe), II, which is 50-100 times more potent than somatostatin for the inhibition of insulin, glucagon and growth hormone release. |
| 2251 | 6143305 | The present study was designed to determine the effect of naloxone, a specific opiate receptor antagonist, on postprandial levels of insulin, glucagon, pancreatic polypeptide (PP), somatostatin-like immunoreactivity (SLI) and gastrin in response to carbohydrate and fat-rich test meals in a group of 6 healthy volunteers. |
| 2252 | 6143305 | The addition of naloxone to a meal consisting of 50 g sucrose dissolved in 200 ml water augmented the rise of plasma insulin levels significantly during the first 30 min after its ingestion and reduced the rise in plasma insulin and pancreatic polypeptide and elevated glucagon levels during the last 30 min of the experimental period. |
| 2253 | 6143305 | These data raise the possibility that endogenous opiates participate in the regulation of postprandial insulin, glucagon, somatostatin and pancreatic polypeptide release not only in certain disease states as demonstrated recently for insulin secretion in type II diabetes mellitus but endogenous opiates may also be of importance under physiological conditions. |
| 2254 | 6143305 | The present study was designed to determine the effect of naloxone, a specific opiate receptor antagonist, on postprandial levels of insulin, glucagon, pancreatic polypeptide (PP), somatostatin-like immunoreactivity (SLI) and gastrin in response to carbohydrate and fat-rich test meals in a group of 6 healthy volunteers. |
| 2255 | 6143305 | The addition of naloxone to a meal consisting of 50 g sucrose dissolved in 200 ml water augmented the rise of plasma insulin levels significantly during the first 30 min after its ingestion and reduced the rise in plasma insulin and pancreatic polypeptide and elevated glucagon levels during the last 30 min of the experimental period. |
| 2256 | 6143305 | These data raise the possibility that endogenous opiates participate in the regulation of postprandial insulin, glucagon, somatostatin and pancreatic polypeptide release not only in certain disease states as demonstrated recently for insulin secretion in type II diabetes mellitus but endogenous opiates may also be of importance under physiological conditions. |
| 2257 | 6143553 | The production of insulin and somatostatin by foetal mouse brain cells in culture suggests that they may be a useful model system for studies of neuropeptide biosynthesis. |
| 2258 | 6143702 | During somatostatin-induced acute insulin deficiency (n = 7), growth hormone enhanced the increase in total ketone body production observed in six subjects receiving somatostatin alone (8.4 +/- 0.8 versus 4.1 +/- 0.7 mumol X kg-1 X min-1, p less than 0.01). |
| 2259 | 6144228 | The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. |
| 2260 | 6144228 | Since exogenous insulin is known to inhibit glucose-induced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. |
| 2261 | 6144228 | In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). |
| 2262 | 6144228 | However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. |
| 2263 | 6144228 | Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucose-stimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. |
| 2264 | 6144228 | The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. |
| 2265 | 6144228 | Since exogenous insulin is known to inhibit glucose-induced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. |
| 2266 | 6144228 | In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). |
| 2267 | 6144228 | However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. |
| 2268 | 6144228 | Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucose-stimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. |
| 2269 | 6144228 | The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. |
| 2270 | 6144228 | Since exogenous insulin is known to inhibit glucose-induced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. |
| 2271 | 6144228 | In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). |
| 2272 | 6144228 | However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. |
| 2273 | 6144228 | Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucose-stimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. |
| 2274 | 6144228 | The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. |
| 2275 | 6144228 | Since exogenous insulin is known to inhibit glucose-induced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. |
| 2276 | 6144228 | In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). |
| 2277 | 6144228 | However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. |
| 2278 | 6144228 | Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucose-stimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. |
| 2279 | 6144228 | The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. |
| 2280 | 6144228 | Since exogenous insulin is known to inhibit glucose-induced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. |
| 2281 | 6144228 | In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). |
| 2282 | 6144228 | However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur. |
| 2283 | 6144228 | Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucose-stimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. |
| 2284 | 6145549 | Immunoreactive somatostatin (IRS) in the pancreatic juice of the nondiabetic subjects ranged from 43 to 97 pg/ml, in non-insulin-dependent diabetics from 5 to 3872, and in the insulin-dependent diabetics from 0 to 2093. |
| 2285 | 6146545 | Effect of epinephrine and somatostatin-induced insulin deficiency on ketone body kinetics and lipolysis in man. |
| 2286 | 6146545 | To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 micrograms/kg/h). |
| 2287 | 6146545 | The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P less than 0.01). |
| 2288 | 6146545 | Effect of epinephrine and somatostatin-induced insulin deficiency on ketone body kinetics and lipolysis in man. |
| 2289 | 6146545 | To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 micrograms/kg/h). |
| 2290 | 6146545 | The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P less than 0.01). |
| 2291 | 6146545 | Effect of epinephrine and somatostatin-induced insulin deficiency on ketone body kinetics and lipolysis in man. |
| 2292 | 6146545 | To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 micrograms/kg/h). |
| 2293 | 6146545 | The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P less than 0.01). |
| 2294 | 6147095 | Somatostatin, glucagon, and insulin secretion from perfused pancreas of BB rats. |
| 2295 | 6147095 | We reported previously that pancreatic somatostatin and glucagon content and D and A cells are reduced in spontaneously diabetic BB rats while portal plasma levels of these hormones are elevated but normalized by insulin therapy. |
| 2296 | 6147095 | A theophylline-induced paradoxical inhibition of somatostatin secretion that was normalized by insulin was found in insulin-openic diabetic rats. |
| 2297 | 6147095 | Somatostatin, glucagon, and insulin secretion from perfused pancreas of BB rats. |
| 2298 | 6147095 | We reported previously that pancreatic somatostatin and glucagon content and D and A cells are reduced in spontaneously diabetic BB rats while portal plasma levels of these hormones are elevated but normalized by insulin therapy. |
| 2299 | 6147095 | A theophylline-induced paradoxical inhibition of somatostatin secretion that was normalized by insulin was found in insulin-openic diabetic rats. |
| 2300 | 6147095 | Somatostatin, glucagon, and insulin secretion from perfused pancreas of BB rats. |
| 2301 | 6147095 | We reported previously that pancreatic somatostatin and glucagon content and D and A cells are reduced in spontaneously diabetic BB rats while portal plasma levels of these hormones are elevated but normalized by insulin therapy. |
| 2302 | 6147095 | A theophylline-induced paradoxical inhibition of somatostatin secretion that was normalized by insulin was found in insulin-openic diabetic rats. |
| 2303 | 6147819 | The two studies with glucose administration designed to demonstrate the release of insulin, VIP, somatostatin into plasma as modified by enteric signals (represented by the difference of plasma peptide concentration during OGT minus peptide concentration during IV glucose) revealed the following: (1) basal plasma glucose, insulin, VIP, somatostatin did not differ between Sham and Occ dogs; (2) after OGT in Occ dogs the plasma glucose was elevated, whereas plasma insulin was markedly reduced, and VIP, somatostatin were largely unchanged; (3) the integrated output of insulin only was impaired when considering the so-called entero-insulin axis, while integrated VIP, somatostatin were unaltered. |
| 2304 | 6147819 | It was concluded (a) the Occ procedure in the dog has the capacity to subtotal destruction of the pancreatic acinar tissue, and of the entero-insular axis of insulin, the latter through yet unknown pathways, (b) the Occ technique may be a useful tool for investigation of the nature of "incretin," (c) VIP and somatostatin do not respond to elevated blood glucose and may have no role in the "incretin" concept of enteric modulation of the B-cell. |
| 2305 | 6147819 | The two studies with glucose administration designed to demonstrate the release of insulin, VIP, somatostatin into plasma as modified by enteric signals (represented by the difference of plasma peptide concentration during OGT minus peptide concentration during IV glucose) revealed the following: (1) basal plasma glucose, insulin, VIP, somatostatin did not differ between Sham and Occ dogs; (2) after OGT in Occ dogs the plasma glucose was elevated, whereas plasma insulin was markedly reduced, and VIP, somatostatin were largely unchanged; (3) the integrated output of insulin only was impaired when considering the so-called entero-insulin axis, while integrated VIP, somatostatin were unaltered. |
| 2306 | 6147819 | It was concluded (a) the Occ procedure in the dog has the capacity to subtotal destruction of the pancreatic acinar tissue, and of the entero-insular axis of insulin, the latter through yet unknown pathways, (b) the Occ technique may be a useful tool for investigation of the nature of "incretin," (c) VIP and somatostatin do not respond to elevated blood glucose and may have no role in the "incretin" concept of enteric modulation of the B-cell. |
| 2307 | 6148021 | Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. |
| 2308 | 6149971 | Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster. |
| 2309 | 6149971 | We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). |
| 2310 | 6149971 | Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. |
| 2311 | 6149971 | At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. |
| 2312 | 6149971 | Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster. |
| 2313 | 6149971 | We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). |
| 2314 | 6149971 | Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. |
| 2315 | 6149971 | At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. |
| 2316 | 6149971 | Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster. |
| 2317 | 6149971 | We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). |
| 2318 | 6149971 | Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. |
| 2319 | 6149971 | At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. |
| 2320 | 6149971 | Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster. |
| 2321 | 6149971 | We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). |
| 2322 | 6149971 | Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. |
| 2323 | 6149971 | At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. |
| 2324 | 6150716 | The results show that the infusion test of somatostatin is fitted to measure a steady state of blood glucose and insulin and that it is possible by this technique to quantify a changed utilisation of blood glucose induced by specific therapy. |
| 2325 | 6151111 | We conclude that such a somatostatin analog in zinc phosphate suspension may have a sufficient duration of action to be useful as an adjunct to insulin in the treatment of diabetes mellitus. |
| 2326 | 6160072 | Antisomatostatin gamma globulin augments secretion of both insulin and glucagon in vitro: evidence for a physiologic role for endogenous somatostatin in the regulation of pancreatic A- and B-cell function. |
| 2327 | 6160072 | To assess the effects of endogenous somatostatin on pancreatic islet A- and B-cell function, isolated rat islets were incubated in antisomatostatin gamma-globulin to bind endogenously released somatostatin, and the insulin and glucagon secretion of these islets was compared with that of islets incubated in gamma-globulin isolated from nonimmune serum. |
| 2328 | 6160072 | These results provide evidence that endogenous somatostatin may act as a physiologic local regulator of both insulin and glucagon secretion and that its effect on insulin and glucagon secretion is dependent on the prevailing glucose concentration. |
| 2329 | 6160072 | Antisomatostatin gamma globulin augments secretion of both insulin and glucagon in vitro: evidence for a physiologic role for endogenous somatostatin in the regulation of pancreatic A- and B-cell function. |
| 2330 | 6160072 | To assess the effects of endogenous somatostatin on pancreatic islet A- and B-cell function, isolated rat islets were incubated in antisomatostatin gamma-globulin to bind endogenously released somatostatin, and the insulin and glucagon secretion of these islets was compared with that of islets incubated in gamma-globulin isolated from nonimmune serum. |
| 2331 | 6160072 | These results provide evidence that endogenous somatostatin may act as a physiologic local regulator of both insulin and glucagon secretion and that its effect on insulin and glucagon secretion is dependent on the prevailing glucose concentration. |
| 2332 | 6160072 | Antisomatostatin gamma globulin augments secretion of both insulin and glucagon in vitro: evidence for a physiologic role for endogenous somatostatin in the regulation of pancreatic A- and B-cell function. |
| 2333 | 6160072 | To assess the effects of endogenous somatostatin on pancreatic islet A- and B-cell function, isolated rat islets were incubated in antisomatostatin gamma-globulin to bind endogenously released somatostatin, and the insulin and glucagon secretion of these islets was compared with that of islets incubated in gamma-globulin isolated from nonimmune serum. |
| 2334 | 6160072 | These results provide evidence that endogenous somatostatin may act as a physiologic local regulator of both insulin and glucagon secretion and that its effect on insulin and glucagon secretion is dependent on the prevailing glucose concentration. |
| 2335 | 6162696 | Immunofluorescence staining with insulin, glucagon, and somatostatin antisera revealed different immunoreactive cell types in the pancreatic islets of the ratfish. |
| 2336 | 6164586 | Glucose and cyclic AMP as stimulators of somatostatin and insulin secretion from the isolated, perfused rat pancreas: a quantitative study. |
| 2337 | 6164586 | Insulin release was stimulated 50-fold and somatostatin (SRIF) secretion twofold when the glucose concentration was increased from 100 mg/dl to 300 mg/dl. |
| 2338 | 6164586 | Glucose and cyclic AMP as stimulators of somatostatin and insulin secretion from the isolated, perfused rat pancreas: a quantitative study. |
| 2339 | 6164586 | Insulin release was stimulated 50-fold and somatostatin (SRIF) secretion twofold when the glucose concentration was increased from 100 mg/dl to 300 mg/dl. |
| 2340 | 6168508 | Abnormalities of pancreatic somatostatin secretion corrected by in vivo insulin treatment of streptozotocin-diabetic rats. |
| 2341 | 6168508 | By contrast, in vivo insulin treatment restored the glucose sensitivity of the somatostatin secreting cells. |
| 2342 | 6168508 | In addition, in vivo insulin treatment resulted in a lowering of the high basal somatostatin secretion rate found in islets from untreated diabetic rats. |
| 2343 | 6168508 | Abnormalities of pancreatic somatostatin secretion corrected by in vivo insulin treatment of streptozotocin-diabetic rats. |
| 2344 | 6168508 | By contrast, in vivo insulin treatment restored the glucose sensitivity of the somatostatin secreting cells. |
| 2345 | 6168508 | In addition, in vivo insulin treatment resulted in a lowering of the high basal somatostatin secretion rate found in islets from untreated diabetic rats. |
| 2346 | 6168508 | Abnormalities of pancreatic somatostatin secretion corrected by in vivo insulin treatment of streptozotocin-diabetic rats. |
| 2347 | 6168508 | By contrast, in vivo insulin treatment restored the glucose sensitivity of the somatostatin secreting cells. |
| 2348 | 6168508 | In addition, in vivo insulin treatment resulted in a lowering of the high basal somatostatin secretion rate found in islets from untreated diabetic rats. |
| 2349 | 6189748 | The impact of increased c-AMP levels, short-term fasting as well as experimental diabetes on glibenclamide-induced secretion of somatostatin, insulin and glucagon was studied in the isolated perfused rat pancreas. |
| 2350 | 6189748 | Dose-response curves revealed that 1 microgram/ml of glibenclamide (in the presence of 3.3 mmol/l of glucose) induced maximal stimulation of insulin and near maximal stimulation of somatostatin release, but did not significantly affect glucagon release. |
| 2351 | 6189748 | Fasting the rats for 24 h significantly suppressed the insulin and glucagon responses to glibenclamide while the concomitant somatostatin response was slightly enhanced. |
| 2352 | 6189748 | The impact of increased c-AMP levels, short-term fasting as well as experimental diabetes on glibenclamide-induced secretion of somatostatin, insulin and glucagon was studied in the isolated perfused rat pancreas. |
| 2353 | 6189748 | Dose-response curves revealed that 1 microgram/ml of glibenclamide (in the presence of 3.3 mmol/l of glucose) induced maximal stimulation of insulin and near maximal stimulation of somatostatin release, but did not significantly affect glucagon release. |
| 2354 | 6189748 | Fasting the rats for 24 h significantly suppressed the insulin and glucagon responses to glibenclamide while the concomitant somatostatin response was slightly enhanced. |
| 2355 | 6189748 | The impact of increased c-AMP levels, short-term fasting as well as experimental diabetes on glibenclamide-induced secretion of somatostatin, insulin and glucagon was studied in the isolated perfused rat pancreas. |
| 2356 | 6189748 | Dose-response curves revealed that 1 microgram/ml of glibenclamide (in the presence of 3.3 mmol/l of glucose) induced maximal stimulation of insulin and near maximal stimulation of somatostatin release, but did not significantly affect glucagon release. |
| 2357 | 6189748 | Fasting the rats for 24 h significantly suppressed the insulin and glucagon responses to glibenclamide while the concomitant somatostatin response was slightly enhanced. |
| 2358 | 6200377 | Somatostatin (10 micrograms/ml), which inhibits cAMP-stimulated protein phosphorylation, suppresses insulin release evoked by IBMX, glucagon, or forskolin (inhibition: 80, 75, or 82%, respectively). |
| 2359 | 6202577 | Is somatostatin a true local inhibitory regulator of insulin secretion? |
| 2360 | 6202577 | Compared with islets from the rats not given cysteamine, the somatostatin-depleted islets released larger amounts of insulin during 1 h of incubation by glucose or 3-isobutyl-1-methylxanthine stimulation. |
| 2361 | 6202577 | Therefore, the possibility that pancreatic somatostatin may locally regulate the inhibitory effects of insulin secretion has to be considered. |
| 2362 | 6202577 | Is somatostatin a true local inhibitory regulator of insulin secretion? |
| 2363 | 6202577 | Compared with islets from the rats not given cysteamine, the somatostatin-depleted islets released larger amounts of insulin during 1 h of incubation by glucose or 3-isobutyl-1-methylxanthine stimulation. |
| 2364 | 6202577 | Therefore, the possibility that pancreatic somatostatin may locally regulate the inhibitory effects of insulin secretion has to be considered. |
| 2365 | 6202577 | Is somatostatin a true local inhibitory regulator of insulin secretion? |
| 2366 | 6202577 | Compared with islets from the rats not given cysteamine, the somatostatin-depleted islets released larger amounts of insulin during 1 h of incubation by glucose or 3-isobutyl-1-methylxanthine stimulation. |
| 2367 | 6202577 | Therefore, the possibility that pancreatic somatostatin may locally regulate the inhibitory effects of insulin secretion has to be considered. |
| 2368 | 6204535 | Insulin treatment for 2 days did not affect the somatostatin response to glucose in normal rats, did not restore a somatostatin response to glucose 3 days after alloxan, but partially restored (P less than 0.01) a response to glucose (28% of normal) 14 days after alloxan. |
| 2369 | 6205318 | Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. |
| 2370 | 6205318 | The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. |
| 2371 | 6205318 | Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. |
| 2372 | 6205318 | Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. |
| 2373 | 6205318 | The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. |
| 2374 | 6205318 | Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. |
| 2375 | 6205318 | Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. |
| 2376 | 6205318 | The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. |
| 2377 | 6205318 | Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. |
| 2378 | 6247229 | At this stage, insulin-, glucagon-, and occasional somatostatin-positive islet cells could be demonstrated, and the 3H-thymidine incorporation index of the beta cells was significantly decreased to 16.7 +/- 2.8. |
| 2379 | 6261628 | Possible explanations for this anomaly: compensatory insulin or somatostatin secretion, production of a non functional glucagon, or low levels of circulating glucagon, are envisaged but without a formal response. |
| 2380 | 6277529 | Three hormones, Thyrotropin Releasing Hormone (TRH), Gonadotropin Releasing Hormone (GnRH or LHRH) and somatostatin have been identified, synthesized and tested for clinical applications. |
| 2381 | 6281878 | Acidethanol extraction of the tumor and immunohistochemistry provided evidence of the presence of all four islet hormones, particularly that of glucagon and pancreatic polypeptide and to a lesser extent of somatostatin and insulin. |
| 2382 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2383 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2384 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2385 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2386 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2387 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2388 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2389 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2390 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2391 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2392 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2393 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2394 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2395 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2396 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2397 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2398 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2399 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2400 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2401 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2402 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2403 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2404 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2405 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2406 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2407 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2408 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2409 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2410 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2411 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2412 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2413 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2414 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2415 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2416 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2417 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2418 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2419 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2420 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2421 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2422 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2423 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2424 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2425 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2426 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2427 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2428 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2429 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2430 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2431 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2432 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2433 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2434 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2435 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2436 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2437 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2438 | 6295859 | Insulin, glucagon, and somatostatin receptors on cultured cells and clones from rat islet cell tumor. |
| 2439 | 6295859 | Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. |
| 2440 | 6295859 | The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. |
| 2441 | 6295859 | Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. |
| 2442 | 6295859 | Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. |
| 2443 | 6295859 | Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. |
| 2444 | 6295859 | Insulin secreting versus somatostatin secreting clones. |
| 2445 | 6295859 | Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). |
| 2446 | 6311653 | Circulating levels of insulin, proinsulin-like component, glucagon, growth hormone, and pancreatic polypeptide were measured in 12 patients with functioning insulinomas, and the suppressibility of serum insulin by somatostatin and diazoxide was assessed before surgical removal of the tumors. |
| 2447 | 6311653 | Based on these findings, we propose a new classification of insulinomas in two groups: group A is characterized morphologically by abundant well-granulated typical B-cells, trabecular arrangement of tumor cells, and uniform insulin immunofluorescence; functionally, these tumors are associated with a moderate elevation of proinsulin-like component and with an almost complete suppressibility of serum insulin by somatostatin and diazoxide. |
| 2448 | 6311653 | In contrast, tumors of group B are characterized by scarce well-granulated typical B-cells, a medullary-type histologic structure, and irregular insulin immunofluorescence; functionally these tumors show elevated circulating levels of proinsulin-like component and a marked resistance of insulin secretion to somatostatin and diazoxide inhibition. |
| 2449 | 6311653 | Circulating levels of insulin, proinsulin-like component, glucagon, growth hormone, and pancreatic polypeptide were measured in 12 patients with functioning insulinomas, and the suppressibility of serum insulin by somatostatin and diazoxide was assessed before surgical removal of the tumors. |
| 2450 | 6311653 | Based on these findings, we propose a new classification of insulinomas in two groups: group A is characterized morphologically by abundant well-granulated typical B-cells, trabecular arrangement of tumor cells, and uniform insulin immunofluorescence; functionally, these tumors are associated with a moderate elevation of proinsulin-like component and with an almost complete suppressibility of serum insulin by somatostatin and diazoxide. |
| 2451 | 6311653 | In contrast, tumors of group B are characterized by scarce well-granulated typical B-cells, a medullary-type histologic structure, and irregular insulin immunofluorescence; functionally these tumors show elevated circulating levels of proinsulin-like component and a marked resistance of insulin secretion to somatostatin and diazoxide inhibition. |
| 2452 | 6311653 | Circulating levels of insulin, proinsulin-like component, glucagon, growth hormone, and pancreatic polypeptide were measured in 12 patients with functioning insulinomas, and the suppressibility of serum insulin by somatostatin and diazoxide was assessed before surgical removal of the tumors. |
| 2453 | 6311653 | Based on these findings, we propose a new classification of insulinomas in two groups: group A is characterized morphologically by abundant well-granulated typical B-cells, trabecular arrangement of tumor cells, and uniform insulin immunofluorescence; functionally, these tumors are associated with a moderate elevation of proinsulin-like component and with an almost complete suppressibility of serum insulin by somatostatin and diazoxide. |
| 2454 | 6311653 | In contrast, tumors of group B are characterized by scarce well-granulated typical B-cells, a medullary-type histologic structure, and irregular insulin immunofluorescence; functionally these tumors show elevated circulating levels of proinsulin-like component and a marked resistance of insulin secretion to somatostatin and diazoxide inhibition. |
| 2455 | 6336705 | Pancreatic content of insulin and glucagon was doubled, while that of somatostatin was constant. |
| 2456 | 6339304 | Pancreatic sections from 21 cases of rhesus disease and 20 control newborn infants of 30--40-wk gestational age were stained by the immunoperoxidase method for insulin, glucagon, somatostatin, and pancreatic polypeptide (PP). |
| 2457 | 6342807 | Twenty weeks after pancreas transplantation, the volume fractions of insulin, glucagon, somatostatin and pancreatic polypeptide cells in the graft islets did not differ from those of the normal control pancreas. |
| 2458 | 6342807 | However, the insulin cell mass was significantly increased, and comprised about 20% of the islet volume, while cells containing pancreatic polypeptide were found only sporadically. |
| 2459 | 6347769 | Circulating somatostatin concentrations in healthy and non-insulin-dependent (type II) diabetic subjects. |
| 2460 | 6347769 | It is concluded that further investigations are necessary before hypotheses linking somatostatin deficiency with the hormonal and metabolic abnormalities of non-insulin-dependent diabetes can be accepted. |
| 2461 | 6347769 | Circulating somatostatin concentrations in healthy and non-insulin-dependent (type II) diabetic subjects. |
| 2462 | 6347769 | It is concluded that further investigations are necessary before hypotheses linking somatostatin deficiency with the hormonal and metabolic abnormalities of non-insulin-dependent diabetes can be accepted. |
| 2463 | 6347773 | Reciprocal gastropancreatic modulations for the release of somatostatin-like immunoreactivity, glucagon, and insulin in the rat. |
| 2464 | 6347773 | In order to assess the interrelationships between stomach and pancreas regarding the secretions of somatostatin-like immunoreactivity (SLI), glucagon (IRG), and insulin (IRI), concentrations of the three hormones were assayed in portal plasma and portal blood flow was measured in enterectomized rats before and after the selective removal of stomach or pancreas. |
| 2465 | 6347773 | Reciprocal gastropancreatic modulations for the release of somatostatin-like immunoreactivity, glucagon, and insulin in the rat. |
| 2466 | 6347773 | In order to assess the interrelationships between stomach and pancreas regarding the secretions of somatostatin-like immunoreactivity (SLI), glucagon (IRG), and insulin (IRI), concentrations of the three hormones were assayed in portal plasma and portal blood flow was measured in enterectomized rats before and after the selective removal of stomach or pancreas. |
| 2467 | 6347784 | Insulin, glucagon, somatostatin and pancreatic polypeptide cells were stained by immunoperoxidase techniques and quantitated morphometrically in sections of pancreases obtained from eight control subjects, four Type 1 (insulin-dependent) and eight Type 2 (non-insulin-dependent) diabetic patients. |
| 2468 | 6354816 | An immunoperoxidase procedure with insulin, glucagon, somatostatin and pancreatic polypeptide antisera was used to show the persistence of pancreatic endocrine cells. |
| 2469 | 6360782 | Pancreases from normal and db/db mice between 3 and 20 weeks of age were stained immunocytochemically for glucagon, somatostatin and pancreatic polypeptide (PP), and changes in A, D and PP cell volume densities quantified by image analysis. |
| 2470 | 6365738 | The pancreases of 17 patients who had cystic fibrosis with and without diabetes mellitus were evaluated at autopsy by routine staining and immunohistochemical methods for insulin, glucagon, somatostatin, and pancreatic polypeptide. |
| 2471 | 6365738 | Young adult diabetic patients with cystic fibrosis have total loss of exocrine pancreas with fat replacement, lack of nesidioblastosis, a qualitative decrease in the number of islets, fibrosis of and amyloid deposits in islets, decreased numbers of insulin-containing cells in each islet, and atrophy of islet cells, probably resulting from progressive ischemia. |
| 2472 | 6405099 | Serum gastrin levels are responsive to many physiologic and pharmacologic factors including hyperglycemia, somatostatin, and glucagon. |
| 2473 | 6444782 | Insulin, glucagon, and somatostatin secretion from isolated perfused rat and chicken pancreas-duodenum. |
| 2474 | 6444782 | Insulin, glucagon, and somatostatin secretion were evaluated in the following isolated perfused models: rat pancreas-duodenum (both normal and streptozotocin-diabetic animals) and the chicken pancreas with and without duodenum. |
| 2475 | 6444782 | Insulin, glucagon, and somatostatin secretion from isolated perfused rat and chicken pancreas-duodenum. |
| 2476 | 6444782 | Insulin, glucagon, and somatostatin secretion were evaluated in the following isolated perfused models: rat pancreas-duodenum (both normal and streptozotocin-diabetic animals) and the chicken pancreas with and without duodenum. |
| 2477 | 6543182 | Somatostatin analogue caused a fall in serum insulin levels in all but one patient, who had diabetes mellitus and in whom serum insulin was undetectable. |
| 2478 | 6543182 | However, in one patient in whom prolactin and hGH levels were elevated during bromocriptine treatment, the infusion of somatostatin analogue decreased both hormones. |
| 2479 | 6543182 | Somatostatin analogue caused a fall in serum insulin levels in all but one patient, who had diabetes mellitus and in whom serum insulin was undetectable. |
| 2480 | 6543182 | However, in one patient in whom prolactin and hGH levels were elevated during bromocriptine treatment, the infusion of somatostatin analogue decreased both hormones. |
| 2481 | 6624911 | The levels of peptide hormones believed to produce the same physiological responses as antidiuretic hormone on the thick ascending limb (glucagon, parathyroid hormone, and calcitonin) and the cortical collecting ducts (calcitonin) were reduced by acute thyroparathyroidectomy and somatostatin administration. |
| 2482 | 6671044 | The result are attributed to the increased secretion of the gastrointestinal hormones (Bombesin and Somatostatin) in the diabetic patients. |
| 2483 | 6759221 | In islets of all sizes, the afferent arterioles entered the islet of all sizes, the afferent arterioles entered the islet at discontinuities of the mantle of non-B-(glucagon, somatostatin, and pancreatic polypeptide) cells. |
| 2484 | 6759225 | We previously showed that infusion of glucagon at four times the basal rate into conscious dogs given somatostatin and basal replacement amounts of insulin caused hyperglycemia (217 15 mg/dl) for at least 3 h and an initial increment in hepatic glucose production of 5.5 0.8 mg/kg . min. |
| 2485 | 6759225 | Six overnight-fasted conscious dogs were given somatostatin (0.8 microgram/kg . min) plus basal intraportal replacement amounts of insulin (263 microunits/kg . min) and glucagon (0.65 ng/kg . min). |
| 2486 | 6759225 | We previously showed that infusion of glucagon at four times the basal rate into conscious dogs given somatostatin and basal replacement amounts of insulin caused hyperglycemia (217 15 mg/dl) for at least 3 h and an initial increment in hepatic glucose production of 5.5 0.8 mg/kg . min. |
| 2487 | 6759225 | Six overnight-fasted conscious dogs were given somatostatin (0.8 microgram/kg . min) plus basal intraportal replacement amounts of insulin (263 microunits/kg . min) and glucagon (0.65 ng/kg . min). |
| 2488 | 6759227 | Labeling of islets with anti-insulin, anti-glucagon, anti-somatostatin, and anti-human pancreatic polypeptide antibodies showed the avidin binding subset to correspond to islet cells identified by anti-glucagon antibody. |
| 2489 | 6759227 | Conversely, avidin reacted with no insulin, somatostatin, or cells containing HPP. |
| 2490 | 6759227 | Labeling of islets with anti-insulin, anti-glucagon, anti-somatostatin, and anti-human pancreatic polypeptide antibodies showed the avidin binding subset to correspond to islet cells identified by anti-glucagon antibody. |
| 2491 | 6759227 | Conversely, avidin reacted with no insulin, somatostatin, or cells containing HPP. |
| 2492 | 6759233 | Insulin and multiplication stimulating activity (an insulin-like growth factor) stimulate islet (beta-cell replication in neonatal rat pancreatic monolayer cultures. |
| 2493 | 6759233 | The effects of insulin were not associated with any significant changes in glucagon or somatostatin levels in the culture media. |
| 2494 | 6759233 | Multiplication stimulating activity (MSA), an insulin-like growth factor, was about 100-fold more potent than insulin: 3 ng/ml MSA stimulated a half-maximal increase in thymidine labeling of beta-cell (+63%, P less than 0.005), whereas 300 ng/ml insulin was required for a similar effect. |
| 2495 | 6759233 | These results demonstrate that insulin can stimulate islet beta-cell replication directly, possibly through a receptor for MSA or another insulin-like growth factor. |
| 2496 | 6759262 | Sera from patients with insulin-dependent diabetes mellitus (IDDM) containing islet cell surface antibodies (ICSA) were studied for their capacity to lyse cultured rat islet cells. |
| 2497 | 6759262 | The uptake of ethidium bromide was used to identify lysed cells and immunofluorescent staining with antisera to insulin, glucagon, somatostatin, or pancreatic polypeptide was used to identify the different islet cell types (B-, A-, D-, and PP-cells, respectively). |
| 2498 | 6761438 | Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. |
| 2499 | 6761438 | Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). |
| 2500 | 6761438 | Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. |
| 2501 | 6761438 | Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. |
| 2502 | 6761438 | Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. |
| 2503 | 6761438 | Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. |
| 2504 | 6761438 | Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). |
| 2505 | 6761438 | Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. |
| 2506 | 6761438 | Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. |
| 2507 | 6761438 | Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. |
| 2508 | 6761438 | Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. |
| 2509 | 6761438 | Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). |
| 2510 | 6761438 | Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. |
| 2511 | 6761438 | Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. |
| 2512 | 6761438 | Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. |
| 2513 | 6761438 | Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. |
| 2514 | 6761438 | Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). |
| 2515 | 6761438 | Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. |
| 2516 | 6761438 | Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. |
| 2517 | 6761438 | Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. |
| 2518 | 6761438 | Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. |
| 2519 | 6761438 | Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). |
| 2520 | 6761438 | Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. |
| 2521 | 6761438 | Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. |
| 2522 | 6761438 | Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. |
| 2523 | 6784807 | Somatostatin was infused during the experiment to suppress endogenous insulin secretin. |
| 2524 | 6818069 | The effect of "low-dose" (6--10 U/h) insulin treatment on the rate of decline of plasma glucose concentration was determined in 15 diabetic subjects admitted in ketoacidosis (plasma glucose = 948 79 mg/dl) and in six normal volunteers rendered hyperglycemic by a combined infusion of somatostatin and glucose (plasma glucose = 653 28 mg/dl). |
| 2525 | 6986312 | Insulin, glucagon, somatostatin, and pancreatic polypeptide immunoreactivities were also seen in very early stages of the transplant development within the monolayered ducts. |
| 2526 | 6987118 | Effects of insulin and pancreatic polypeptide on gastric somatostatin release. |
| 2527 | 6987118 | Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. |
| 2528 | 6987118 | Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. |
| 2529 | 6987118 | Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. |
| 2530 | 6987118 | Effects of insulin and pancreatic polypeptide on gastric somatostatin release. |
| 2531 | 6987118 | Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. |
| 2532 | 6987118 | Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. |
| 2533 | 6987118 | Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. |
| 2534 | 6987118 | Effects of insulin and pancreatic polypeptide on gastric somatostatin release. |
| 2535 | 6987118 | Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. |
| 2536 | 6987118 | Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. |
| 2537 | 6987118 | Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. |
| 2538 | 6987118 | Effects of insulin and pancreatic polypeptide on gastric somatostatin release. |
| 2539 | 6987118 | Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. |
| 2540 | 6987118 | Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. |
| 2541 | 6987118 | Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. |
| 2542 | 6987123 | Starvation-induced changes of somatostatin, glucagon, and insulin secretion from the isolated perfused rat pancreas. |
| 2543 | 6987123 | The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. |
| 2544 | 6987123 | In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. |
| 2545 | 6987123 | The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. |
| 2546 | 6987123 | These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis. |
| 2547 | 6987123 | Starvation-induced changes of somatostatin, glucagon, and insulin secretion from the isolated perfused rat pancreas. |
| 2548 | 6987123 | The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. |
| 2549 | 6987123 | In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. |
| 2550 | 6987123 | The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. |
| 2551 | 6987123 | These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis. |
| 2552 | 6987123 | Starvation-induced changes of somatostatin, glucagon, and insulin secretion from the isolated perfused rat pancreas. |
| 2553 | 6987123 | The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. |
| 2554 | 6987123 | In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. |
| 2555 | 6987123 | The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. |
| 2556 | 6987123 | These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis. |
| 2557 | 6987123 | Starvation-induced changes of somatostatin, glucagon, and insulin secretion from the isolated perfused rat pancreas. |
| 2558 | 6987123 | The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. |
| 2559 | 6987123 | In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. |
| 2560 | 6987123 | The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. |
| 2561 | 6987123 | These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis. |
| 2562 | 6987123 | Starvation-induced changes of somatostatin, glucagon, and insulin secretion from the isolated perfused rat pancreas. |
| 2563 | 6987123 | The effect of 16- and 48-h fasting on pancreatic somatostatin, insulin, and glucagon secretion was studied, using the isolated perfused rat pancreas. |
| 2564 | 6987123 | In the presence of 4.4 mM glucose, basal somatostatin and insulin concentrations in the perfusate were significantly lower in 48-h fasted rats than in fed animals, whereas basal glucagon secretion was significantly elevated in fasted rats. |
| 2565 | 6987123 | The infusion of 19 mM arginine significantly augmented secretion of somatostatin and glucagon and attenuated insulin secretion in 48-h fasted rats. |
| 2566 | 6987123 | These results suggest that not only insulin and glucagon, but also somatostatin contribute to nutrient homeostasis. |
| 2567 | 6987534 | The hypothalamic tetradecapeptide, somatostatin (SRIF), inhibits the secretion of growth hormone (GH) and numerous other hormones, including insulin and glucagon. |
| 2568 | 7005532 | When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias. |
| 2569 | 7007435 | Cytotoxicity is independent of insulin synthesis, as evidenced by the linear correlation of cytotoxicity of sera for the insulin-producing clone RINm 5F and the somatostatin-producing clone RINm 14B. |
| 2570 | 7008781 | The anti-ketogenic effect of alanine has been studied in normal starved and diabetic rats by infusing l-alanine for 90min in the presence of somatostatin (10mug/kg body wt. per h) to suppress endogenous insulin and glucagon secretion. 2. |
| 2571 | 7035407 | In contrast, the islet cells containing somatostatin, glucagon and pancreatic polypeptide are nearly free of glycogen. |
| 2572 | 7037515 | The four-layer double immunofluorescence technique showed that the surface antibody stained insulin secreting cells, but owing to rarity of A and D cells in the fetal cultures it has not yet been possible to exclude the reactivity of islet cell surface antibodies with glucagon or somatostatin cells. |
| 2573 | 7037514 | Already a number of hormones including somatostatin, human growth hormone and human insulin [4] have been produced by these new methods. |
| 2574 | 7042431 | We conclude that any indirect effects of potassium ion on arginine-stimulated glucagon secretion are not mediated by insulin, but could be related to changes in somatostatin secretion. |
| 2575 | 7047110 | Insulin, pancreatic polypeptide, and glucagon antibodies in insulin-dependent diabetes mellitus. |
| 2576 | 7047110 | To assess the possible value of the use of high-purity pork insulin (HPPI) in the United States, the serum insulin (I), pancreatic polypeptide (PP), glucagon (G), and somatostatin (SRIF) antibody binding characteristics have been determined in 90 conventional insulin-treated diabetic subjects and related to their degree of metabolic control, as assessed by glycosylated hemoglobin (HbA1) concentration. |
| 2577 | 7047110 | All diabetic subjects had antibodies to insulin, but there was no relationship between any of the antibody binding characteristics and HbA1 level: 47% possessed PP antibodies; mean +/- SEM HbA1 in these patients was 14.5 +/- 0.3%, identical to those without PP antibodies (14.5 +/- 0.4%); 10% had G binding antibodies with HbA1 levels of 14.6 +/- 0.8%, similar to those without G antibodies. |
| 2578 | 7088751 | In addition, development of analogs of somatostatin holds promise of therapeutic benefit in both insulin-dependent and non-insulin-dependent types of the disease. |
| 2579 | 7152136 | The 2 CP chronic administration did not change the plasma somatostatin, glucagon, and insulin levels. |
| 2580 | 7152136 | In the alloxan-diabetic dogs, treated with insulin alone, blood glucose, ketone body concentrations, and plasma somatostatin and glucagon levels were elevated. |
| 2581 | 7152136 | The 2 CP chronic administration did not change the plasma somatostatin, glucagon, and insulin levels. |
| 2582 | 7152136 | In the alloxan-diabetic dogs, treated with insulin alone, blood glucose, ketone body concentrations, and plasma somatostatin and glucagon levels were elevated. |
| 2583 | 7152137 | To determine if the glucagon-suppressing action of glucagon was mediated by an increase in glucagon-stimulated insulin or somatostatin secretion, these hormones were measured in the various experiments. |
| 2584 | 7152137 | Insulin and somatostatin increased significantly when glucagon was perfused with the glucose arginine-containing solution but did not rise significantly when the glucopenic buffer was used, although suppression of endogenous glucagon was similar in each instance. |
| 2585 | 7152137 | Evidence that insulin and/or somatostatin mediate this action could not be obtained. |
| 2586 | 7152137 | To determine if the glucagon-suppressing action of glucagon was mediated by an increase in glucagon-stimulated insulin or somatostatin secretion, these hormones were measured in the various experiments. |
| 2587 | 7152137 | Insulin and somatostatin increased significantly when glucagon was perfused with the glucose arginine-containing solution but did not rise significantly when the glucopenic buffer was used, although suppression of endogenous glucagon was similar in each instance. |
| 2588 | 7152137 | Evidence that insulin and/or somatostatin mediate this action could not be obtained. |
| 2589 | 7152137 | To determine if the glucagon-suppressing action of glucagon was mediated by an increase in glucagon-stimulated insulin or somatostatin secretion, these hormones were measured in the various experiments. |
| 2590 | 7152137 | Insulin and somatostatin increased significantly when glucagon was perfused with the glucose arginine-containing solution but did not rise significantly when the glucopenic buffer was used, although suppression of endogenous glucagon was similar in each instance. |
| 2591 | 7152137 | Evidence that insulin and/or somatostatin mediate this action could not be obtained. |
| 2592 | 7476317 | Pharmacological interventions aimed at reducing growth factor alterations, among other actions in diabetic vasculopathy, include a multitude of classes of drugs, such as angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, lipid-lowering drugs, and somatostatin analogs. |
| 2593 | 7490542 | Somatostatin analogue (octreotide) treatment initiated at the onset of diabetes prevents kidney IGF-I accumulation and renal growth. |
| 2594 | 7494779 | Like any other pancreatic islet cell carcinoma, a somatostatinoma may also produce several different hormones such as adrenocorticotropic hormone, calcitonin, vasoactive intestinal polypeptide, pancreatic polypeptide, gastrin, insulin, and glucagon. |
| 2595 | 7494779 | We present a patient with somatostatinoma in which an immunocytochemical study of the specimens from pancreas and liver showed a weak positive reaction for gastrin besides a strong positive reaction for somatostatin. |
| 2596 | 7505469 | Inhibition of IGF-I and b-FGF stimulated growth of human retinal endothelial cells by the somatostatin analogue, octreotide: a potential treatment for ocular neovascularization. |
| 2597 | 7506601 | They are comprised primarily of four endocrine cell types: insulin-secreting beta-cells which represent about 70% of the cells in the islet along with smaller number of cells secreting glucagon, somatostatin and pancreatic polypeptide. |
| 2598 | 7506819 | To address the possibility that patients with CFDM might have suppressed pituitary growth hormone (GH) release as a result of increased plasma somatostatin, GH secretion in 8 CFDM patients and 8 normal male controls was studied using a standard arginine infusion stimulus. |
| 2599 | 7506819 | Concentrations of the GH-dependent peptides, insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein 3 (IGFBP-3) were also measured. |
| 2600 | 7506819 | Despite higher GH levels in the CFDM patients, their IGF-I and IGFBP-3 concentrations were low. |
| 2601 | 7525123 | Inverse correlation between insulin-like growth factor binding protein-1 and insulin in patients with acromegaly during treatment with the somatostatin analogue octreotide. |
| 2602 | 7529396 | Using sensitive ribonuclease protection assays, in situ hybridization, and the polymerase chain reaction, our results indicate the following: 1) Transcriptional levels of insulin and amylin remain lower in the fetal than in the adult pancreas, whereas glucagon and somatostatin mRNA levels are consistently greater after 14 wk gestation than postnatally. |
| 2603 | 7533732 | We observed by immunohistochemistry and confocal microscopy that beta TC-6 cells contain abundant insulin and small amounts of glucagon and somatostatin (SRIF). |
| 2604 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 2605 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 2606 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 2607 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 2608 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 2609 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 2610 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 2611 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 2612 | 7562555 | Tiapride dose-dependently attenuated the biphasic nociceptive responses induced by s.c. injection of formalin to the hindpaw of mice, and its activity on the first (ED50 = 110 mg/kg p.o.) and the second (ED50 = 32.0 mg/kg p.o.) phases paralleled that on the nociceptive response to intrathecal injection of substance P (ED50 = 190 mg/kg p.o.) and somatostatin (ED50 = 56.0 mg/kg p.o.), respectively. |
| 2613 | 7562555 | The effects of tiapride (100 mg/kg p.o.) on both phases of the formalin test in normal mice were abolished by pretreatment with p-chlorophenylalanine (800 x 2 mg/kg p.o.), a 5-hydroxytryptamine (5-HT) depletor, or pindolol (1 mg/kg i.p.), a 5-HT1 antagonist, but were scarcely affected by 3-tropanyl-indole-3-carboxylate, a 5-HT3 antagonist. |
| 2614 | 7562561 | Recently it has been established that both a gastrin-releasing peptide (GRP) receptor and a neuromedin B (NMB) receptor mediate the actions of bombesin-related peptides in mammals. |
| 2615 | 7562561 | Five different classes of peptides that function as GRP receptor antagonists have been identified; however, it is unknown whether similar strategies will yield antagonists for the closely related NMB receptor. |
| 2616 | 7562561 | In the present study we have used either native cells possessing only one bombesin (Bn) receptor subtype or cells stably transfected with one subtype to determine whether using the strategies that were used successfully for GRP receptors would allow NMB receptor antagonists to be identified. |
| 2617 | 7562561 | [DPhe12]Bn analogs; des Met14 amides, esters and alkylamides; psi 13-14 Bn pseudopeptides; and D-amino acid-substituted analogs of substance P (SP) or SP(4-11) were all synthesized and each functioned as a GRP receptor antagonist. |
| 2618 | 7562561 | All of these antagonists had low affinity for the NMB receptor. |
| 2619 | 7562561 | Application of similar strategies to NMB by formation of [DPhe8]NMB, [psi 9-10]NMB pseudopeptides, des-Met10 NMB amides, alkylamide or esters did not result in any potent NMB receptor antagonists. |
| 2620 | 7562561 | D-Amino acid SP and SP(4-11) analogs were weakly selective NMB receptor antagonists. |
| 2621 | 7562561 | No COOH-terminal fragments of NMB or GRP functioned as a GRP or NMB receptor antagonist. |
| 2622 | 7562561 | These results demonstrate that none of the known strategies used to prepare peptide GRP receptor antagonists are successful at the NMB receptor, suggesting that a different strategy will be needed for this peptide, such as the formation of somatostatin octapeptide or D-amino acid-substituted substance P analogs. |
| 2623 | 7562561 | These results suggest that even though there is a close homology between GRP and NMB and their receptors, their structure-function relations are markedly different. |
| 2624 | 7565332 | [Relation between pyloric dysmotility and serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide in patients with non-insulin dependent diabetes mellitus]. |
| 2625 | 7565332 | Serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were evaluated in 105 noninsulin dependent diabetics (25 of them had a pyloric dysfunction). |
| 2626 | 7565332 | The basal gastrin level was significantly higher in patients with the pyloric dysfunction (p < 0.001). 45 minutes later the serum levels of vasoactive intestinal polypeptide and somatostatin were significantly higher in diabetics with the pyloric dysfunction (p < 0.001). |
| 2627 | 7565332 | The serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were impaired in diabetics with the pyloric dysfunction and might be associated with its pathogenesis. |
| 2628 | 7565332 | [Relation between pyloric dysmotility and serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide in patients with non-insulin dependent diabetes mellitus]. |
| 2629 | 7565332 | Serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were evaluated in 105 noninsulin dependent diabetics (25 of them had a pyloric dysfunction). |
| 2630 | 7565332 | The basal gastrin level was significantly higher in patients with the pyloric dysfunction (p < 0.001). 45 minutes later the serum levels of vasoactive intestinal polypeptide and somatostatin were significantly higher in diabetics with the pyloric dysfunction (p < 0.001). |
| 2631 | 7565332 | The serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were impaired in diabetics with the pyloric dysfunction and might be associated with its pathogenesis. |
| 2632 | 7565332 | [Relation between pyloric dysmotility and serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide in patients with non-insulin dependent diabetes mellitus]. |
| 2633 | 7565332 | Serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were evaluated in 105 noninsulin dependent diabetics (25 of them had a pyloric dysfunction). |
| 2634 | 7565332 | The basal gastrin level was significantly higher in patients with the pyloric dysfunction (p < 0.001). 45 minutes later the serum levels of vasoactive intestinal polypeptide and somatostatin were significantly higher in diabetics with the pyloric dysfunction (p < 0.001). |
| 2635 | 7565332 | The serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were impaired in diabetics with the pyloric dysfunction and might be associated with its pathogenesis. |
| 2636 | 7565332 | [Relation between pyloric dysmotility and serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide in patients with non-insulin dependent diabetes mellitus]. |
| 2637 | 7565332 | Serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were evaluated in 105 noninsulin dependent diabetics (25 of them had a pyloric dysfunction). |
| 2638 | 7565332 | The basal gastrin level was significantly higher in patients with the pyloric dysfunction (p < 0.001). 45 minutes later the serum levels of vasoactive intestinal polypeptide and somatostatin were significantly higher in diabetics with the pyloric dysfunction (p < 0.001). |
| 2639 | 7565332 | The serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were impaired in diabetics with the pyloric dysfunction and might be associated with its pathogenesis. |
| 2640 | 7575177 | The growth promoting actions of growth hormone are indirect and mediated through generations of insulin-like growth factors. |
| 2641 | 7575177 | Growth hormone release is determined by a dynamic equilibrium between the inhibitory and stimulatory hypothalamic peptides, somatostatin and growth hormone-releasing hormone. |
| 2642 | 7630583 | We will provide evidence for the involvement of adrenergic transmitters and two neuropeptides, neuropeptide Y and somatostatin, in the neuroendocrine regulation of sexual behavior. |
| 2643 | 7647774 | We have also investigated the role of endogenous somatostatin (SS) and cholinergic manipulation on the GH responses to GH-releasing hormone (GHRH). |
| 2644 | 7647774 | Pretreatment of older rats (16 weeks) with anti-somatostatin antibodies (SS-Ab) significantly increased GH responses to GHRH in both normal and GK groups. |
| 2645 | 7647774 | We have also investigated the role of endogenous somatostatin (SS) and cholinergic manipulation on the GH responses to GH-releasing hormone (GHRH). |
| 2646 | 7647774 | Pretreatment of older rats (16 weeks) with anti-somatostatin antibodies (SS-Ab) significantly increased GH responses to GHRH in both normal and GK groups. |
| 2647 | 7664670 | To elucidate the roles of the hypothalamic peptides, GH-releasing hormone (GRH) and somatostatin (SRIH), potentially responsible for altered GH dynamics in diabetes, we studied the time courses of their changes in level associated with altered GH secretion in streptozotocin (STZ)-induced diabetic mice. |
| 2648 | 7672492 | Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. |
| 2649 | 7678435 | Nociceptive responses to intrathecally administered substance P and somatostatin in diabetic mice. |
| 2650 | 7678435 | The nociceptive behavioral responses to i.t. injection of somatostatin (SST) but nor substance P (SP) were attenuated in diabetic mice compared with that in non-diabetic mice. |
| 2651 | 7678435 | Nociceptive responses to intrathecally administered substance P and somatostatin in diabetic mice. |
| 2652 | 7678435 | The nociceptive behavioral responses to i.t. injection of somatostatin (SST) but nor substance P (SP) were attenuated in diabetic mice compared with that in non-diabetic mice. |
| 2653 | 7682680 | These results suggest that a negative control system, which is mediated by delta-opioid receptors and links substance P with somatostatin-mediated nociceptive transmission, may inhibit the formalin-induced second-phase of the nociceptive response in diabetic mice. |
| 2654 | 7683739 | Insulin-like growth factor-binding protein-1 response to insulin during suppression of endogenous insulin secretion. |
| 2655 | 7683739 | Insulin-like growth factor-binding protein-1 (IGFBP-1) is one of several related proteins that bind and modulate the actions of IGFs. |
| 2656 | 7683739 | The liver is the primary source of IGFBP-1, and insulin is a major regulator of hepatic IGFBP-1 production. |
| 2657 | 7683739 | In normal subjects, a continuous high-dose insulin infusion caused a rapid decrease in plasma IGFBP-1 concentrations, with a rate of 0.24 +/- 0.04 microgram/L.min-1 and a t1/2 of 89 +/- 4 minutes. |
| 2658 | 7683739 | Conversely, a 3-hour somatostatin (SRIF) infusion caused a 4.5-fold increase in plasma IGFBP-1 levels. |
| 2659 | 7683739 | SRIF plus low-dose insulin infusion (to inhibit break-through insulin secretion) resulted in a plateau in IGFBP-1 concentrations at 5 to 8 hours, with a t1/2 to achieve steady state of 60 to 75 minutes. |
| 2660 | 7683739 | Under similar conditions, a stepped increase in plasma glucose level from 5 to 9 mmol/L had no effect on the rate of IGFBP-1 increase in plasma, indicating that an acute increase in glucose concentration within a physiologic range has no independent inhibitory effect on IGFBP-1 production in the presence of a nonsuppressive insulin level. |
| 2661 | 7683739 | Using SRIF plus sequential graded insulin infusions, the threshold peripheral (= portal) plasma insulin concentration for IGFBP-1 suppression was between 65 and 172 pmol/L. |
| 2662 | 7683739 | Subjects with insulin-dependent diabetes mellitus (IDDM) showed a similar dose-response pattern, suggesting that insulin regulation of IGFBP-1 may be normal in IDDM. |
| 2663 | 7686682 | We also investigated the effects of mexiletine on intrathecally-administered substance P- and somatostatin-induced nociceptive responses in both non-diabetic and diabetic mice. |
| 2664 | 7698503 | The histological and immunocytochemical studies demonstrated the identity and integrity of the islets with well-preserved insulin-, glucagon-, and somatostatin-containing cells. |
| 2665 | 7729789 | Blunted GH response to growth hormone-releasing hormone (GHRH) alone or combined with arginine in non-insulin-dependent diabetes mellitus. |
| 2666 | 7729789 | In 14 patients with NIDDM, 7 normal weight (NWD) and 7 obese (OD), we investigated the somatotrope responsiveness to GHRH (1 microgram/kg) alone or combined with arginine (ARG, 0.5 g/kg), which is able to enhance the GH response to GHRH, probably by inhibiting somatostatin release from hypothalamus. |
| 2667 | 7729789 | GH but not IGF-I levels were higher (p < 0.05) in NS than in OP (1.5 +/- 0.5 vs 0.5 +/- 0.2 microgram/l). |
| 2668 | 7735371 | A randomized trial of a somatostatin analog for preserving beta cell function in children with insulin dependent diabetes mellitus. |
| 2669 | 7735371 | Although there were no differences in either insulin requirements or in hemoglobin A1 levels, there were significant increases in the glucagon-stimulated C-peptide levels of the experimental group at six and 12 months after diagnosis, compared to control patients. |
| 2670 | 7739457 | Basal and postprandial levels of gastrin, somatostatin, vasoactive intestinal polypeptide (VIP) and pancreatic polypeptide (PP) were followed up in 105 patients with non insulin dependent diabetes mellitus (20 with autonomic neuropathy only, 35 with peripheric neuropathy only, 30 with autonomic and peripheric neuropathy simultaneously and 20 without any sign of neuropathy) and in the control group of 40 individuals. |
| 2671 | 7739457 | Serum levels of gastrin, somatostatin, VIP and PP are determined by a RIA (used kits of Prof. |
| 2672 | 7739457 | Basal and postprandial levels of gastrin, somatostatin, vasoactive intestinal polypeptide (VIP) and pancreatic polypeptide (PP) were followed up in 105 patients with non insulin dependent diabetes mellitus (20 with autonomic neuropathy only, 35 with peripheric neuropathy only, 30 with autonomic and peripheric neuropathy simultaneously and 20 without any sign of neuropathy) and in the control group of 40 individuals. |
| 2673 | 7739457 | Serum levels of gastrin, somatostatin, VIP and PP are determined by a RIA (used kits of Prof. |
| 2674 | 7758881 | To determine if, and the mechanism by which, lack of postprandial suppression of glucagon contributes to hyperglycaemia, nine subjects with insulin-dependent diabetes mellitus (IDDM) ingested 50 g of glucose containing both [2-3H] glucose and [6-3H] glucose on two occasions. [6-14C] glucose, insulin and low-dose somatostatin were infused intravenously at the same rates on both occasions. |
| 2675 | 7762657 | Six SS-8 analogues that distinguish SS subtypes showed that 125I-SS-14 bound to somatostatin receptor subtype 3 (SSTR3). |
| 2676 | 7771503 | In this article, the authors report on a 46-year-old woman with a glucagonoma cosecreting pancreatic polypeptide, somatostatin, and serotonin diagnosed 8 months before the onset of diabetic ketoacidosis. |
| 2677 | 7771503 | She was treated with hydration, insulin, and octreotide, with improvement in her clinical course and a decrease in the glucagon, pancreatic polypeptide, and chromogranin A plasma levels. |
| 2678 | 7775624 | Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. |
| 2679 | 7775624 | It has also been suggested that, in addition to its well known suppressive effects, somatostatin per se may increase insulin sensitivity. |
| 2680 | 7775624 | Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). |
| 2681 | 7775624 | Intraarterial somatostatin perfusion did not alter basal forearm glucose uptake (0.14 +/- 0.07 vs. 0.17 +/- 0.12 mmol/L), the amount of glucose administered during the clamp (M-value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg.min), or the levels of insulin, C-peptide, glucagon, or GH. |
| 2682 | 7775624 | Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. |
| 2683 | 7775624 | Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. |
| 2684 | 7775624 | It has also been suggested that, in addition to its well known suppressive effects, somatostatin per se may increase insulin sensitivity. |
| 2685 | 7775624 | Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). |
| 2686 | 7775624 | Intraarterial somatostatin perfusion did not alter basal forearm glucose uptake (0.14 +/- 0.07 vs. 0.17 +/- 0.12 mmol/L), the amount of glucose administered during the clamp (M-value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg.min), or the levels of insulin, C-peptide, glucagon, or GH. |
| 2687 | 7775624 | Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. |
| 2688 | 7775624 | Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. |
| 2689 | 7775624 | It has also been suggested that, in addition to its well known suppressive effects, somatostatin per se may increase insulin sensitivity. |
| 2690 | 7775624 | Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). |
| 2691 | 7775624 | Intraarterial somatostatin perfusion did not alter basal forearm glucose uptake (0.14 +/- 0.07 vs. 0.17 +/- 0.12 mmol/L), the amount of glucose administered during the clamp (M-value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg.min), or the levels of insulin, C-peptide, glucagon, or GH. |
| 2692 | 7775624 | Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. |
| 2693 | 7775624 | Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. |
| 2694 | 7775624 | It has also been suggested that, in addition to its well known suppressive effects, somatostatin per se may increase insulin sensitivity. |
| 2695 | 7775624 | Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). |
| 2696 | 7775624 | Intraarterial somatostatin perfusion did not alter basal forearm glucose uptake (0.14 +/- 0.07 vs. 0.17 +/- 0.12 mmol/L), the amount of glucose administered during the clamp (M-value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg.min), or the levels of insulin, C-peptide, glucagon, or GH. |
| 2697 | 7775624 | Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. |
| 2698 | 7775624 | Somatostatin enhances insulin-stimulated glucose uptake in the perfused human forearm. |
| 2699 | 7775624 | It has also been suggested that, in addition to its well known suppressive effects, somatostatin per se may increase insulin sensitivity. |
| 2700 | 7775624 | Compared with the systemic control infusion, local forearm perfusion with somatostatin caused a 55% increase in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs. 0.47 +/- 0.19 mmol/L, P < 0.05). |
| 2701 | 7775624 | Intraarterial somatostatin perfusion did not alter basal forearm glucose uptake (0.14 +/- 0.07 vs. 0.17 +/- 0.12 mmol/L), the amount of glucose administered during the clamp (M-value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg.min), or the levels of insulin, C-peptide, glucagon, or GH. |
| 2702 | 7775624 | Our data suggest that somatostatin increases insulin-stimulated muscle utilization of glucose through local mechanisms. |
| 2703 | 7789632 | In all protocols, selective insulin deficiency was created during the experimental period by infusing somatostatin peripherally (0.8 micrograms.kg-1.min-1) with basal replacement of glucagon intraportally (0.65 ng.kg-1.min-1). |
| 2704 | 7791356 | Plasma insulin and IGF-1 levels were significantly decreased in the streptozotocin-treated animals compared to those of control (insulin: 23 microU/ml vs 31 microU/ml, P < 0.001; IGF-1: 254 ng/ml vs 324 ng/ml, P < 0.001). |
| 2705 | 7791356 | Competitive binding studies revealed specific cell surface receptors for insulin (Kd = 15.5 nM), IGF-1 (Kd = 30.0 nM), and somatostatin (Kd = 2.5 nM) on the MIA PaCa-2 cells. |
| 2706 | 7791356 | In an in vitro cell proliferation assay, cell division was promoted by insulin (P < 0.01, max + 11%) and IGF-1 (P < 0.01, max + 10%). |
| 2707 | 7796922 | Both galanin and somatostatin inhibit insulin release from pancreatic beta-cells by opening KATP through the activation of G-protein. |
| 2708 | 7796922 | Glucagon-like peptide-1[7-36], which stimulates insulin secretion by indirectly blocking KATP in beta-cells, shows antidiabetic effects in patients with non-insulin-dependent diabetes mellitus. |
| 2709 | 7798026 | The number of GH-releasing factor (GRF)-labelled axons and the amount of axonal tyrosine hydroxylase (TH)-immunoreactivity increased in STZ-D. |
| 2710 | 7798026 | There were no significant differences in any of the other densitometrical measurements performed on GRF-, somatostatin-, thyrotropin-releasing hormone- and TH-labelled ME axon cross-sections as well as those on tuberoinfundibular-dopaminergic neurones of the AN in STZ-D compared with control rats. |
| 2711 | 7809020 | In the present work the effects of ADP beta S on insulin somatostatin, and glucagon secretions were investigated in dogs. |
| 2712 | 7809020 | ADP beta S (0.1 mg kg-1) induced an immediate increase in insulin and somatostatin-like immunoreactivity (SLI) but not in glucagon pancreaticoduodenal outputs. |
| 2713 | 7809020 | In the present work the effects of ADP beta S on insulin somatostatin, and glucagon secretions were investigated in dogs. |
| 2714 | 7809020 | ADP beta S (0.1 mg kg-1) induced an immediate increase in insulin and somatostatin-like immunoreactivity (SLI) but not in glucagon pancreaticoduodenal outputs. |
| 2715 | 7813819 | Previously, we have demonstrated that somatostatin mediates all of its inhibitory effects on glucose-induced insulin secretion from the HIT-T15 cell through pertussis toxin-sensitive G-proteins and that the membrane fraction of this clonal line of pancreatic beta-cells contains six such proteins: G(i) alpha 1, G(i) alpha 2, G(i) alpha 3, and three forms of G(o) alpha. |
| 2716 | 7813819 | To determine the specificity of somatostatin receptor-G-protein coupling in HIT-T15 cells, we examined the ability of antisera specific for the COOH-terminus of G alpha subtypes to inhibit somatostatin-induced augmentation of membrane GTPase activity. |
| 2717 | 7813819 | Previously, we have demonstrated that somatostatin mediates all of its inhibitory effects on glucose-induced insulin secretion from the HIT-T15 cell through pertussis toxin-sensitive G-proteins and that the membrane fraction of this clonal line of pancreatic beta-cells contains six such proteins: G(i) alpha 1, G(i) alpha 2, G(i) alpha 3, and three forms of G(o) alpha. |
| 2718 | 7813819 | To determine the specificity of somatostatin receptor-G-protein coupling in HIT-T15 cells, we examined the ability of antisera specific for the COOH-terminus of G alpha subtypes to inhibit somatostatin-induced augmentation of membrane GTPase activity. |
| 2719 | 7854164 | To determine the physiological significance of basal insulin in the maintenance of glucose metabolism in NIDDM, we studied nine subjects with NIDDM in the basal and insulin-deficient state produced by 3 hours of somatostatin (SRIF) infusion (0.08 pmol/kg/min). |
| 2720 | 7859939 | Glucagon (approximately 3 ng.kg-1.min-1), somatostatin (0.1 microgram.kg-1.min-1), and insulin (0.9 pmol.kg-1.min-1) were infused for 3 h. |
| 2721 | 7888695 | ICA-positive sera reacted to insulin-, glucagon-, and somatostatin-positive cells of fetal pancreata of all gestational ages. |
| 2722 | 7895951 | To examine the effect of acute hyperglycaemia on nerve conduction eight non-diabetic men (20-49 years of age) with no signs of peripheral neuropathy were studied before and after 3 h of hyperglycaemic clamping (plasma glucose approximately 15 mmol/l), while insulin secretion was suppressed by somatostatin [Study 1]. |
| 2723 | 7901752 | Discovery of a novel class of neuromedin B receptor antagonists, substituted somatostatin analogues. |
| 2724 | 7901752 | Recent studies show two subtypes of receptors; a gastrin-releasing peptide (GRP) receptor subtype and a neuromedin B (NMB) receptor subtype exist. |
| 2725 | 7901752 | In contrast to the GRP receptor, no antagonists exist for the NMB receptor. |
| 2726 | 7901752 | In the present study we report that certain somatostatin (SS) octapeptide analogues function as selective NMB receptor antagonists. |
| 2727 | 7901752 | The most potent analogue, D-Nal-Cys-Tyr-D-Trp-Lys-Val-Cys-Nal-NH2, inhibited binding of 125I-[D-Tyr degree]NMB to NMB receptor-transfected 3T3 cells and C6 cells. |
| 2728 | 7901752 | The stereochemistry at positions 1, 2, 7, and 8, the hydrophobicity and ring size of the substitution in positions 1, 3, and 4, and the basicity of the group in position 5 were all important in determining NMB receptor affinity. |
| 2729 | 7901752 | No SS octapeptide analogue increased [3H]inositol phosphates in NMB receptor-transfected cells; however, each analogue inhibited NMB-stimulated increases. |
| 2730 | 7901752 | The results demonstrate for the first time a class of antagonists with > 100-fold selectivity for NMB versus GRP receptors. |
| 2731 | 7901752 | Because the structural requirements for determining NMB, SS, and mu-opioid receptor activity differ, it is likely that highly selective, specific, high affinity NMB receptor antagonists can now be developed that will be useful in defining the role of NMB in various physiological processes. |
| 2732 | 7901752 | Discovery of a novel class of neuromedin B receptor antagonists, substituted somatostatin analogues. |
| 2733 | 7901752 | Recent studies show two subtypes of receptors; a gastrin-releasing peptide (GRP) receptor subtype and a neuromedin B (NMB) receptor subtype exist. |
| 2734 | 7901752 | In contrast to the GRP receptor, no antagonists exist for the NMB receptor. |
| 2735 | 7901752 | In the present study we report that certain somatostatin (SS) octapeptide analogues function as selective NMB receptor antagonists. |
| 2736 | 7901752 | The most potent analogue, D-Nal-Cys-Tyr-D-Trp-Lys-Val-Cys-Nal-NH2, inhibited binding of 125I-[D-Tyr degree]NMB to NMB receptor-transfected 3T3 cells and C6 cells. |
| 2737 | 7901752 | The stereochemistry at positions 1, 2, 7, and 8, the hydrophobicity and ring size of the substitution in positions 1, 3, and 4, and the basicity of the group in position 5 were all important in determining NMB receptor affinity. |
| 2738 | 7901752 | No SS octapeptide analogue increased [3H]inositol phosphates in NMB receptor-transfected cells; however, each analogue inhibited NMB-stimulated increases. |
| 2739 | 7901752 | The results demonstrate for the first time a class of antagonists with > 100-fold selectivity for NMB versus GRP receptors. |
| 2740 | 7901752 | Because the structural requirements for determining NMB, SS, and mu-opioid receptor activity differ, it is likely that highly selective, specific, high affinity NMB receptor antagonists can now be developed that will be useful in defining the role of NMB in various physiological processes. |
| 2741 | 7902197 | Increase in somatostatin to glucagon ratio in islets of alloxan-diabetic dogs: effect of insulin-induced euglycemia. |
| 2742 | 7902197 | We have previously shown that acute insulin-induced normalization of glycemia in alloxan-diabetic (A-D) dogs results in marked inhibition of total pancreatic glucagon content, but normalization of somatostatin content. |
| 2743 | 7902197 | Increase in somatostatin to glucagon ratio in islets of alloxan-diabetic dogs: effect of insulin-induced euglycemia. |
| 2744 | 7902197 | We have previously shown that acute insulin-induced normalization of glycemia in alloxan-diabetic (A-D) dogs results in marked inhibition of total pancreatic glucagon content, but normalization of somatostatin content. |
| 2745 | 7903584 | Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. |
| 2746 | 7903584 | Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2747 | 7903584 | CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. |
| 2748 | 7903584 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process. |
| 2749 | 7903584 | Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. |
| 2750 | 7903584 | Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2751 | 7903584 | CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. |
| 2752 | 7903584 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process. |
| 2753 | 7903584 | Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. |
| 2754 | 7903584 | Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2755 | 7903584 | CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. |
| 2756 | 7903584 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process. |
| 2757 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 2758 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2759 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 2760 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 2761 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 2762 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2763 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 2764 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 2765 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 2766 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2767 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 2768 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 2769 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 2770 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 2771 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 2772 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 2773 | 7907998 | We observed in the HIT cell, a clonal insulin-secreting cell line, that epinephrine and somatostatin lower insulin mRNA levels and intracellular insulin content in addition to the well-recognized effect of these hormones to inhibit insulin secretion. |
| 2774 | 7907998 | Somatostatin significantly inhibited expression of the human insulin-CAT reporter gene (65 +/- 4% of control) and, to a lesser extent, expression of a control reporter gene, pRSVCAT (78 +/- 4% of control). |
| 2775 | 7907998 | Thus, somatostatin may inhibit insulin gene transcription by insulin gene-specific effects as well as more general effects on gene expression. |
| 2776 | 7907998 | Both epinephrine and somatostatin inhibited expression of the human insulin-CAT reporter gene in a concentration-dependent manner that paralleled inhibition of insulin secretion. |
| 2777 | 7907998 | These studies indicate that epinephrine and somatostatin lower HIT cell insulin mRNA levels in part by inhibiting insulin gene transcription. |
| 2778 | 7907998 | We observed in the HIT cell, a clonal insulin-secreting cell line, that epinephrine and somatostatin lower insulin mRNA levels and intracellular insulin content in addition to the well-recognized effect of these hormones to inhibit insulin secretion. |
| 2779 | 7907998 | Somatostatin significantly inhibited expression of the human insulin-CAT reporter gene (65 +/- 4% of control) and, to a lesser extent, expression of a control reporter gene, pRSVCAT (78 +/- 4% of control). |
| 2780 | 7907998 | Thus, somatostatin may inhibit insulin gene transcription by insulin gene-specific effects as well as more general effects on gene expression. |
| 2781 | 7907998 | Both epinephrine and somatostatin inhibited expression of the human insulin-CAT reporter gene in a concentration-dependent manner that paralleled inhibition of insulin secretion. |
| 2782 | 7907998 | These studies indicate that epinephrine and somatostatin lower HIT cell insulin mRNA levels in part by inhibiting insulin gene transcription. |
| 2783 | 7907998 | We observed in the HIT cell, a clonal insulin-secreting cell line, that epinephrine and somatostatin lower insulin mRNA levels and intracellular insulin content in addition to the well-recognized effect of these hormones to inhibit insulin secretion. |
| 2784 | 7907998 | Somatostatin significantly inhibited expression of the human insulin-CAT reporter gene (65 +/- 4% of control) and, to a lesser extent, expression of a control reporter gene, pRSVCAT (78 +/- 4% of control). |
| 2785 | 7907998 | Thus, somatostatin may inhibit insulin gene transcription by insulin gene-specific effects as well as more general effects on gene expression. |
| 2786 | 7907998 | Both epinephrine and somatostatin inhibited expression of the human insulin-CAT reporter gene in a concentration-dependent manner that paralleled inhibition of insulin secretion. |
| 2787 | 7907998 | These studies indicate that epinephrine and somatostatin lower HIT cell insulin mRNA levels in part by inhibiting insulin gene transcription. |
| 2788 | 7907998 | We observed in the HIT cell, a clonal insulin-secreting cell line, that epinephrine and somatostatin lower insulin mRNA levels and intracellular insulin content in addition to the well-recognized effect of these hormones to inhibit insulin secretion. |
| 2789 | 7907998 | Somatostatin significantly inhibited expression of the human insulin-CAT reporter gene (65 +/- 4% of control) and, to a lesser extent, expression of a control reporter gene, pRSVCAT (78 +/- 4% of control). |
| 2790 | 7907998 | Thus, somatostatin may inhibit insulin gene transcription by insulin gene-specific effects as well as more general effects on gene expression. |
| 2791 | 7907998 | Both epinephrine and somatostatin inhibited expression of the human insulin-CAT reporter gene in a concentration-dependent manner that paralleled inhibition of insulin secretion. |
| 2792 | 7907998 | These studies indicate that epinephrine and somatostatin lower HIT cell insulin mRNA levels in part by inhibiting insulin gene transcription. |
| 2793 | 7907998 | We observed in the HIT cell, a clonal insulin-secreting cell line, that epinephrine and somatostatin lower insulin mRNA levels and intracellular insulin content in addition to the well-recognized effect of these hormones to inhibit insulin secretion. |
| 2794 | 7907998 | Somatostatin significantly inhibited expression of the human insulin-CAT reporter gene (65 +/- 4% of control) and, to a lesser extent, expression of a control reporter gene, pRSVCAT (78 +/- 4% of control). |
| 2795 | 7907998 | Thus, somatostatin may inhibit insulin gene transcription by insulin gene-specific effects as well as more general effects on gene expression. |
| 2796 | 7907998 | Both epinephrine and somatostatin inhibited expression of the human insulin-CAT reporter gene in a concentration-dependent manner that paralleled inhibition of insulin secretion. |
| 2797 | 7907998 | These studies indicate that epinephrine and somatostatin lower HIT cell insulin mRNA levels in part by inhibiting insulin gene transcription. |
| 2798 | 7912577 | Effects of mutation of the CREB binding site of the somatostatin promoter on cyclic AMP responsiveness in CV-1 cells. |
| 2799 | 7912577 | The transcription factors CREB (cAMP response element binding protein) and ATF (activating transcription factor) recognize DNA containing the consensus sequence TGACGTCA. |
| 2800 | 7912577 | We compared the neuropeptide somatostatin promoter, which binds CREB and is activated by cAMP, to the adenovirus E2A promoter, which binds ATF but is not activated by cAMP, to determine which specific nucleotides within a CREB/ATF recognition sequence confer cAMP responsiveness. |
| 2801 | 7912577 | Several mutant somatostatin promoters were generated containing part of all of the E2A ATF binding site. |
| 2802 | 7912577 | Some of the hybrid CREB/ATF binding sites competed for factor binding to a wild-type somatostatin promoter probe. |
| 2803 | 7912577 | Furthermore, this wild-type CREB binding site could confer cAMP activation on the CAT plasmid only if it was adjacent to a wild-type somatostatin TATA box and cap site. |
| 2804 | 7912577 | Effects of mutation of the CREB binding site of the somatostatin promoter on cyclic AMP responsiveness in CV-1 cells. |
| 2805 | 7912577 | The transcription factors CREB (cAMP response element binding protein) and ATF (activating transcription factor) recognize DNA containing the consensus sequence TGACGTCA. |
| 2806 | 7912577 | We compared the neuropeptide somatostatin promoter, which binds CREB and is activated by cAMP, to the adenovirus E2A promoter, which binds ATF but is not activated by cAMP, to determine which specific nucleotides within a CREB/ATF recognition sequence confer cAMP responsiveness. |
| 2807 | 7912577 | Several mutant somatostatin promoters were generated containing part of all of the E2A ATF binding site. |
| 2808 | 7912577 | Some of the hybrid CREB/ATF binding sites competed for factor binding to a wild-type somatostatin promoter probe. |
| 2809 | 7912577 | Furthermore, this wild-type CREB binding site could confer cAMP activation on the CAT plasmid only if it was adjacent to a wild-type somatostatin TATA box and cap site. |
| 2810 | 7912577 | Effects of mutation of the CREB binding site of the somatostatin promoter on cyclic AMP responsiveness in CV-1 cells. |
| 2811 | 7912577 | The transcription factors CREB (cAMP response element binding protein) and ATF (activating transcription factor) recognize DNA containing the consensus sequence TGACGTCA. |
| 2812 | 7912577 | We compared the neuropeptide somatostatin promoter, which binds CREB and is activated by cAMP, to the adenovirus E2A promoter, which binds ATF but is not activated by cAMP, to determine which specific nucleotides within a CREB/ATF recognition sequence confer cAMP responsiveness. |
| 2813 | 7912577 | Several mutant somatostatin promoters were generated containing part of all of the E2A ATF binding site. |
| 2814 | 7912577 | Some of the hybrid CREB/ATF binding sites competed for factor binding to a wild-type somatostatin promoter probe. |
| 2815 | 7912577 | Furthermore, this wild-type CREB binding site could confer cAMP activation on the CAT plasmid only if it was adjacent to a wild-type somatostatin TATA box and cap site. |
| 2816 | 7912577 | Effects of mutation of the CREB binding site of the somatostatin promoter on cyclic AMP responsiveness in CV-1 cells. |
| 2817 | 7912577 | The transcription factors CREB (cAMP response element binding protein) and ATF (activating transcription factor) recognize DNA containing the consensus sequence TGACGTCA. |
| 2818 | 7912577 | We compared the neuropeptide somatostatin promoter, which binds CREB and is activated by cAMP, to the adenovirus E2A promoter, which binds ATF but is not activated by cAMP, to determine which specific nucleotides within a CREB/ATF recognition sequence confer cAMP responsiveness. |
| 2819 | 7912577 | Several mutant somatostatin promoters were generated containing part of all of the E2A ATF binding site. |
| 2820 | 7912577 | Some of the hybrid CREB/ATF binding sites competed for factor binding to a wild-type somatostatin promoter probe. |
| 2821 | 7912577 | Furthermore, this wild-type CREB binding site could confer cAMP activation on the CAT plasmid only if it was adjacent to a wild-type somatostatin TATA box and cap site. |
| 2822 | 7912577 | Effects of mutation of the CREB binding site of the somatostatin promoter on cyclic AMP responsiveness in CV-1 cells. |
| 2823 | 7912577 | The transcription factors CREB (cAMP response element binding protein) and ATF (activating transcription factor) recognize DNA containing the consensus sequence TGACGTCA. |
| 2824 | 7912577 | We compared the neuropeptide somatostatin promoter, which binds CREB and is activated by cAMP, to the adenovirus E2A promoter, which binds ATF but is not activated by cAMP, to determine which specific nucleotides within a CREB/ATF recognition sequence confer cAMP responsiveness. |
| 2825 | 7912577 | Several mutant somatostatin promoters were generated containing part of all of the E2A ATF binding site. |
| 2826 | 7912577 | Some of the hybrid CREB/ATF binding sites competed for factor binding to a wild-type somatostatin promoter probe. |
| 2827 | 7912577 | Furthermore, this wild-type CREB binding site could confer cAMP activation on the CAT plasmid only if it was adjacent to a wild-type somatostatin TATA box and cap site. |
| 2828 | 7912625 | When the insulin response to glucose was suppressed with somatostatin and diazoxide, metformin improved glucose disposal to a similar extent to that in rats with a normal insulin response. |
| 2829 | 7913205 | Endogenous insulin release was suppressed by infusion of somatostatin (250 micrograms/h). |
| 2830 | 7914371 | Localization of inositol trisphosphate receptor subtype 3 to insulin and somatostatin secretory granules and regulation of expression in islets and insulinoma cells. |
| 2831 | 7914371 | We have confirmed the expression of IP3R-3 in pancreatic islets by immunohistocytochemistry and localized this protein to the secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells by immunogold electron microscopy. |
| 2832 | 7914371 | The localization of IP3R-3 to secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells suggests that granule Ca2+ stores actively participate in the secretory process and that their release is regulated by inositol 1,4,5-trisphosphate. |
| 2833 | 7914371 | The regulation of IP3R-3 levels by glucose, diabetes, and refeeding may allow the beta cell to adjust the insulin secretory response to changing physiological conditions. |
| 2834 | 7914371 | Localization of inositol trisphosphate receptor subtype 3 to insulin and somatostatin secretory granules and regulation of expression in islets and insulinoma cells. |
| 2835 | 7914371 | We have confirmed the expression of IP3R-3 in pancreatic islets by immunohistocytochemistry and localized this protein to the secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells by immunogold electron microscopy. |
| 2836 | 7914371 | The localization of IP3R-3 to secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells suggests that granule Ca2+ stores actively participate in the secretory process and that their release is regulated by inositol 1,4,5-trisphosphate. |
| 2837 | 7914371 | The regulation of IP3R-3 levels by glucose, diabetes, and refeeding may allow the beta cell to adjust the insulin secretory response to changing physiological conditions. |
| 2838 | 7914371 | Localization of inositol trisphosphate receptor subtype 3 to insulin and somatostatin secretory granules and regulation of expression in islets and insulinoma cells. |
| 2839 | 7914371 | We have confirmed the expression of IP3R-3 in pancreatic islets by immunohistocytochemistry and localized this protein to the secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells by immunogold electron microscopy. |
| 2840 | 7914371 | The localization of IP3R-3 to secretory granules of insulin-secreting beta cells and somatostatin-secreting delta cells suggests that granule Ca2+ stores actively participate in the secretory process and that their release is regulated by inositol 1,4,5-trisphosphate. |
| 2841 | 7914371 | The regulation of IP3R-3 levels by glucose, diabetes, and refeeding may allow the beta cell to adjust the insulin secretory response to changing physiological conditions. |
| 2842 | 7915225 | We compared immunoreactivity of the monoclonal antibody 14A20 with anti-insulin, -glucagon or -somatostatin antibodies. |
| 2843 | 7915646 | Following a control period somatostatin was infused into 42h-fasted, conscious dogs and insulin (3X-basal) and glucagon (basal) were replaced intraportally. |
| 2844 | 7937696 | Double immunostaining enabled localization of PYY to a major subpopulation of the glucagon cells and to subpopulations of the pancreatic polypeptide (PP) cells and the somatostatin cells. |
| 2845 | 7937696 | In contrast, no PYY immunoreactivity occurred in the insulin cells. |
| 2846 | 7937696 | In alloxan-treated hyperglycemic mice, PYY immunoreactive cells were increased in number and distributed throughout the islets, in parallel with the glucagon, PP, and somatostatin cells. |
| 2847 | 7937696 | Double immunostaining enabled localization of PYY to a major subpopulation of the glucagon cells and to subpopulations of the pancreatic polypeptide (PP) cells and the somatostatin cells. |
| 2848 | 7937696 | In contrast, no PYY immunoreactivity occurred in the insulin cells. |
| 2849 | 7937696 | In alloxan-treated hyperglycemic mice, PYY immunoreactive cells were increased in number and distributed throughout the islets, in parallel with the glucagon, PP, and somatostatin cells. |
| 2850 | 7951531 | The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved. |
| 2851 | 7951531 | The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. |
| 2852 | 7988345 | To clarify whether the effect of sulfonylurea on glucagon secretion is directly on the pancreatic A cell, we examined changes produced by gliclazide in glucagon (IRG), insulin (IRI) and somatostatin (IRS) release from the isolated perfused rat pancreas. |
| 2853 | 7988345 | Neither cysteamine treatment alone (somatostatin-depleted) nor combined with streptozotocin-treatment (combined depletion of somatostatin and insulin) changed gliclazide-induced glucagon suppression. |
| 2854 | 7988345 | To clarify whether the effect of sulfonylurea on glucagon secretion is directly on the pancreatic A cell, we examined changes produced by gliclazide in glucagon (IRG), insulin (IRI) and somatostatin (IRS) release from the isolated perfused rat pancreas. |
| 2855 | 7988345 | Neither cysteamine treatment alone (somatostatin-depleted) nor combined with streptozotocin-treatment (combined depletion of somatostatin and insulin) changed gliclazide-induced glucagon suppression. |
| 2856 | 7995625 | Resistance to insulin-mediated glucose disposal was estimated by determining the steady-state plasma insulin and glucose concentrations during the last 30 minutes of a continuous infusion of somatostatin (5 micrograms/min), exogenous insulin (25 mU/m2 per minute), and glucose (240 mg/m2 per minute). |
| 2857 | 8005563 | As pirenzepine (PZ), a cholinergic muscarinic antagonist, is able to inhibit GH hypersecretion in insulin-dependent diabetes mellitus (IDDM), we investigated whether PZ is also able to inhibit spontaneous and stimulated GH-release in non-insulin-dependent diabetes mellitus (NIDDM). |
| 2858 | 8005563 | Glucose, insulin, glucagon and somatostatin responses to arginine infusion were not changed by pirenzepine treatment. |
| 2859 | 8013747 | During low-dose insulin infusions (14 pmol.kg-1.min-1) with concomitant somatostatin administration, neither hepatic glucose output nor total body glucose uptake differed between the untreated SH and WKY rats. |
| 2860 | 8022753 | Interleukin-1, tumor necrosis factor, and interleukin-6 inhibit insulin release and may be cytotoxic to isolated pancreatic islets. |
| 2861 | 8022753 | The present study was designed to investigate the effect of the above cytokines on insulin, glucagon, somatostatin, and thyrotropin-releasing hormone secretion by isolated human islets. |
| 2862 | 8022753 | All three cytokines studied, although not modifying insulin and somatostatin release to glucose 5 mmol/L, inhibited the response of both hormones to glucose 20 mmol/L. |
| 2863 | 8022753 | Interleukin-1, tumor necrosis factor, and interleukin-6 inhibit insulin release and may be cytotoxic to isolated pancreatic islets. |
| 2864 | 8022753 | The present study was designed to investigate the effect of the above cytokines on insulin, glucagon, somatostatin, and thyrotropin-releasing hormone secretion by isolated human islets. |
| 2865 | 8022753 | All three cytokines studied, although not modifying insulin and somatostatin release to glucose 5 mmol/L, inhibited the response of both hormones to glucose 20 mmol/L. |
| 2866 | 8024263 | Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. |
| 2867 | 8024263 | Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. |
| 2868 | 8039595 | Glucose-mediated glucose uptake (GMGU) was assessed on another day with hyperglycemic clamp studies, during which insulin and somatostatin were infused to hold insulin-mediated glucose uptake constant between the two clamp studies. |
| 2869 | 8058664 | The development of diabetes mellitus was characterized by beta-cell destruction and insulin concentrations reduction in these cells and the blood, by increase of glucagon and somatostatin levels in the alpha- and delta-cells, respectively, as well as by the growth of these substances concentrations in the peripheral blood. |
| 2870 | 8082872 | Insulin sensitivity test using a somatostatin analogue, octreotide (Sandostatin). |
| 2871 | 8085478 | Insulin, glucagon, somatostatin, and PP cells were found by immunotopochemical and electron-optical techniques in the islets of Langerhans of the sand rat, proving that the islets in this species also contain the four basic cell types known to be found in the islets in mammals in general. |
| 2872 | 8093878 | Somatostatin inhibits insulin-gene expression through a posttranscriptional mechanism in a hamster islet cell line. |
| 2873 | 8094610 | To look for a possible functional correlate to this finding basal and arginine stimulated plasma somatostatin and serum C peptide concentrations in eight insulin treated patients with cystic fibrosis and eight normal male controls were measured. |
| 2874 | 8094610 | Selective preservation of somatostatin secretion in patients with cystic fibrosis may further complicate pancreatic endocrine insufficiencies through paracrine inhibition of insulin and glucagon secretion. |
| 2875 | 8094610 | To look for a possible functional correlate to this finding basal and arginine stimulated plasma somatostatin and serum C peptide concentrations in eight insulin treated patients with cystic fibrosis and eight normal male controls were measured. |
| 2876 | 8094610 | Selective preservation of somatostatin secretion in patients with cystic fibrosis may further complicate pancreatic endocrine insufficiencies through paracrine inhibition of insulin and glucagon secretion. |
| 2877 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2878 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2879 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2880 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2881 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2882 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2883 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2884 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2885 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2886 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2887 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2888 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2889 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2890 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2891 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2892 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2893 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2894 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2895 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2896 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2897 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2898 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2899 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2900 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2901 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2902 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2903 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2904 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2905 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2906 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2907 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2908 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2909 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2910 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2911 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2912 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2913 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2914 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2915 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2916 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2917 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2918 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2919 | 8102504 | Both somatostatin and insulin responses to glucose are impaired in the perfused pancreas of the spontaneously noninsulin-dependent diabetic GK (Goto-Kakizaki) rats. |
| 2920 | 8102504 | We have studied the responses of insulin and somatostatin to glucose and arginine in the perfused pancreas of GK rats, which spontaneously develop mild noninsulin-dependent diabetes without concomitant obesity. |
| 2921 | 8102504 | During perfusion with a high (16.7 mmol l-1) glucose concentration, normal responses of insulin and somatostatin were found in pancreata from non-diabetic control rats. |
| 2922 | 8102504 | When the glucose concentration of the perfusion medium was switched from 16.7 to 3.3 mmol l-1 glucose, a transient increase- 'off-response' -in both insulin and somatostatin secretion was noted in GK but not in control pancreata. |
| 2923 | 8102504 | During the subsequent stimulation with arginine (20 mmol l-1), insulin and somatostatin responses were similar in pancreata from non-diabetic and GK rats. |
| 2924 | 8102504 | The pancreatic content of insulin did not differ between non-diabetic and GK rats, whereas the content of somatostatin was increased by 56% (P < 0.025) in GK glands. |
| 2925 | 8102504 | In conclusion, abnormalities assigned to pancreatic hormone secretion in the GK rat comprise not only markedly impaired insulin but also somatostatin response to glucose. |
| 2926 | 8104197 | This was associated with the development of beta cell outgrowths from undifferentiated epithelial cell clusters and an increase in the expression of the insulin, glucagon, and somatostatin genes. |
| 2927 | 8105515 | Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. |
| 2928 | 8105515 | At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. |
| 2929 | 8105515 | Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. |
| 2930 | 8105515 | We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD. |
| 2931 | 8105515 | Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. |
| 2932 | 8105515 | At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. |
| 2933 | 8105515 | Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. |
| 2934 | 8105515 | We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD. |
| 2935 | 8105515 | Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. |
| 2936 | 8105515 | At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. |
| 2937 | 8105515 | Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. |
| 2938 | 8105515 | We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD. |
| 2939 | 8105515 | Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. |
| 2940 | 8105515 | At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. |
| 2941 | 8105515 | Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. |
| 2942 | 8105515 | We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD. |
| 2943 | 8108347 | Reduction of insulin level was parallelled by a compensatory activation of glucagon- and somatostatin-producing systems. |
| 2944 | 8141841 | We investigated the relationship between serum apolipoprotein(a) (apo(a)) and growth hormone (GH) levels in 15 patients with acromegaly before and during treatment with octreotide, a long-acting somatostatin analogue, 288-600 micrograms/day s.c., for 6 months. |
| 2945 | 8141841 | There were significant reductions in serum GH (F = 7.30; P < 0.01), insulin growth factor 1 (IGF1) (F = 31.4, P < 0.001) and insulin (F = 4.57; P < 0.05) concentrations. |
| 2946 | 8200182 | In conclusion, a short-time insulin suppression, as obtained by the somatostatin analogue octreotide, enhances the natriuretic response to intravenous saline load in lean type II diabetic hypertensives. |
| 2947 | 8285838 | Shrunken islets were composed of insulin cells, glucagon cells, somatostatin cells, and pancreatic polypeptide cells. |
| 2948 | 8320184 | The proportion of insulin-, glucagon-, and somatostatin-containing cells in the cultures was characteristic of whole islets. |
| 2949 | 8320184 | BrdU incorporation was noted in insulin-, glucagon-, and somatostatin-containing cells and also in non-endocrine cells. |
| 2950 | 8320184 | The proportion of insulin-, glucagon-, and somatostatin-containing cells in the cultures was characteristic of whole islets. |
| 2951 | 8320184 | BrdU incorporation was noted in insulin-, glucagon-, and somatostatin-containing cells and also in non-endocrine cells. |
| 2952 | 8340056 | To examine whether the ability of hyperglycemia per se to enhance glucose uptake (by means of mass-action effect) is impaired in cirrhosis, we measured (insulin-independent) whole-body glucose disposal during hyperglycemia (hyperglycemic clamp studies, +125 mg/dl, in combination with an infusion of somatostatin (500 micrograms/hr), insulin (0.1 mU/kg min) and glucagon (0.5 ng/kg min) to "clamp" hormone levels at baseline), whole-body glucose oxidation (indirect calorimetry) and glucose turnover (prime-continuous infusion of [6,6-2H2-]glucose in a clinically homogeneous group of cirrhotic patients with glucose intolerance (n = 7) or frank diabetes mellitus (n = 7) and in control individuals (n = 7). |
| 2953 | 8349044 | In these subjects, we determined the plasma glucose and insulin responses over a 3-h period to a 75-g oral glucose challenge, and the steady-state plasma glucose concentration during a continuous infusion of somatostatin, glucose, and insulin (a quantitative measure of insulin resistance). |
| 2954 | 8360677 | Scatchard analysis of binding data indicated a single class of high-affinity binding sites with a KD of 35 +/- 11 pM and a Bmax of 168 +/- 60 fmol/mg of protein. 125I-ET-1 binding to retinal particulate preparations was not inhibited by 1 microM concentrations of somatostatin, atrial natriuretic factor, brain natriuretic peptide, thyroid-stimulating hormone, growth hormone, or insulin. |
| 2955 | 8378743 | Insulin clearance and glucose metabolism was assessed with a 240 min euglycaemic insulin clamp in combination with infusion of somatostatin (400 micrograms h-1) to completely suppress endogenous insulin secretion. |
| 2956 | 8397219 | To examine the relationship between the plasma glucose concentration (PG) and the pathways of hepatic glucose production (HGP), five groups of conscious rats were studied after a 6-h fast: (a) control rats (PG = 8.0 +/- 0.2 mM); (b) control rats (PG = 7.9 +/- 0.2 mM) with somatostatin and insulin replaced at the basal level; (c) control rats (PG = 18.1 +/- 0.2 mM) with somatostatin, insulin replaced at the basal level, and glucose infused to acutely raise plasma glucose by 10 mM; (d) control rats (PG = 18.0 +/- 0.2 mM) with somatostatin and glucose infusions to acutely reproduce the metabolic conditions of diabetic rats, i.e., hyperglycemia and moderate hypoinsulinemia; (e) diabetic rats (PG = 18.4 +/- 2.3 mM). |
| 2957 | 8397219 | These data indicate that: (a) hyperglycemia causes a marked inhibition of HGP mainly through the suppression of glycogenolysis and the increase in glucokinase flux, with no apparent changes in the fluxes through gluconeogenesis and glucose-6-phosphatase; under similar hyperglycemic hypoinsulinemic conditions: (b) HGP is markedly increased in diabetic rats; however, (c) the contribution of glycogenolysis and gluconeogenesis to HGP is similar to control animals. |
| 2958 | 8448012 | Neuropeptides were degraded by membranes with specific activities in the order of [Leu5]enkephalin > [Met5]enkephalin > gastrin-releasing peptide-10 (GRP-10) > [D-Ala2][Leu5]enkephalin > somatostatin-14. |
| 2959 | 8448012 | Phosphoramidon and DL-thiorphan similarly inhibited the degradation of GRP-10 (mean of 35% inhibition), somatostatin-14 (57%) and the aminopeptidase-resistant analogue, [D-Ala2][Leu5]enkephalin (75%). |
| 2960 | 8448012 | Phosphoramidon increased the potency of the contractile effects of neuropeptides on muscle cells by > 280-fold for somatostatin-14, 17-fold for GRP-10, 18-fold for [Met5]enkephalin and 14-fold for [Leu5]enkephalin. |
| 2961 | 8448012 | The results show that an NEP-like enzyme on the surface of gastric muscle cells degrades and inactivates enkephalins, GRP-10 and somatostatin-14 and acts in a manner analogous to that of acetylcholinesterase in the neuromuscular junction of skeletal muscle. |
| 2962 | 8448012 | Neuropeptides were degraded by membranes with specific activities in the order of [Leu5]enkephalin > [Met5]enkephalin > gastrin-releasing peptide-10 (GRP-10) > [D-Ala2][Leu5]enkephalin > somatostatin-14. |
| 2963 | 8448012 | Phosphoramidon and DL-thiorphan similarly inhibited the degradation of GRP-10 (mean of 35% inhibition), somatostatin-14 (57%) and the aminopeptidase-resistant analogue, [D-Ala2][Leu5]enkephalin (75%). |
| 2964 | 8448012 | Phosphoramidon increased the potency of the contractile effects of neuropeptides on muscle cells by > 280-fold for somatostatin-14, 17-fold for GRP-10, 18-fold for [Met5]enkephalin and 14-fold for [Leu5]enkephalin. |
| 2965 | 8448012 | The results show that an NEP-like enzyme on the surface of gastric muscle cells degrades and inactivates enkephalins, GRP-10 and somatostatin-14 and acts in a manner analogous to that of acetylcholinesterase in the neuromuscular junction of skeletal muscle. |
| 2966 | 8448012 | Neuropeptides were degraded by membranes with specific activities in the order of [Leu5]enkephalin > [Met5]enkephalin > gastrin-releasing peptide-10 (GRP-10) > [D-Ala2][Leu5]enkephalin > somatostatin-14. |
| 2967 | 8448012 | Phosphoramidon and DL-thiorphan similarly inhibited the degradation of GRP-10 (mean of 35% inhibition), somatostatin-14 (57%) and the aminopeptidase-resistant analogue, [D-Ala2][Leu5]enkephalin (75%). |
| 2968 | 8448012 | Phosphoramidon increased the potency of the contractile effects of neuropeptides on muscle cells by > 280-fold for somatostatin-14, 17-fold for GRP-10, 18-fold for [Met5]enkephalin and 14-fold for [Leu5]enkephalin. |
| 2969 | 8448012 | The results show that an NEP-like enzyme on the surface of gastric muscle cells degrades and inactivates enkephalins, GRP-10 and somatostatin-14 and acts in a manner analogous to that of acetylcholinesterase in the neuromuscular junction of skeletal muscle. |
| 2970 | 8448012 | Neuropeptides were degraded by membranes with specific activities in the order of [Leu5]enkephalin > [Met5]enkephalin > gastrin-releasing peptide-10 (GRP-10) > [D-Ala2][Leu5]enkephalin > somatostatin-14. |
| 2971 | 8448012 | Phosphoramidon and DL-thiorphan similarly inhibited the degradation of GRP-10 (mean of 35% inhibition), somatostatin-14 (57%) and the aminopeptidase-resistant analogue, [D-Ala2][Leu5]enkephalin (75%). |
| 2972 | 8448012 | Phosphoramidon increased the potency of the contractile effects of neuropeptides on muscle cells by > 280-fold for somatostatin-14, 17-fold for GRP-10, 18-fold for [Met5]enkephalin and 14-fold for [Leu5]enkephalin. |
| 2973 | 8448012 | The results show that an NEP-like enzyme on the surface of gastric muscle cells degrades and inactivates enkephalins, GRP-10 and somatostatin-14 and acts in a manner analogous to that of acetylcholinesterase in the neuromuscular junction of skeletal muscle. |
| 2974 | 8495594 | Pancreatic polypeptide secretion was absent in chronic pancreatitis without endogenous insulin production. |
| 2975 | 8495594 | Increased plasma concentration of somatostatin was found in patients with insulin-dependent diabetes secondary to chronic pancreatitis. |
| 2976 | 8495594 | The source of somatostatin in the patients is unknown, but somatostatin may contribute to a reduction in overall blood glucose level in patients without endogenous insulin secretion due to inhibition of glucagon secretion. |
| 2977 | 8495594 | Pancreatic polypeptide secretion was absent in chronic pancreatitis without endogenous insulin production. |
| 2978 | 8495594 | Increased plasma concentration of somatostatin was found in patients with insulin-dependent diabetes secondary to chronic pancreatitis. |
| 2979 | 8495594 | The source of somatostatin in the patients is unknown, but somatostatin may contribute to a reduction in overall blood glucose level in patients without endogenous insulin secretion due to inhibition of glucagon secretion. |
| 2980 | 8501854 | It was previously demonstrated that initial kidney hypertrophy has been seen in diabetic animals and somatostatin infusion suppresses GFR and serum insulin like growth factor (IGF-1) in diabetic patients. |
| 2981 | 8513977 | Basal insulin was maintained with somatostatin and insulin replacement. |
| 2982 | 8514980 | Growth hormone and insulin-like growth factor-1 in blood and urine as response markers during treatment of acromegaly with octreotide: a double-blind placebo-controlled study. |
| 2983 | 8514980 | Growth hormone (GH), insulin-like growth factor-1 (IGF-1) and prolactin (PRL) in blood and urine were observed in 20 patients with acromegaly in a double-blind placebo-controlled 14-day clinical trial with the somatostatin analog octreotide. |
| 2984 | 8532657 | The immunoperoxidase technique for the identification of insulin, glucagon, somatostatin, and pancreatic polypeptide, as well as the point-counting method, was used on serial sections of pancreas tissue. |
| 2985 | 8549855 | During both stages, somatostatin (250 micrograms/h) was infused to suppress endogenous insulin secretion. |
| 2986 | 8549858 | To define the relative roles of catecholamine versus glucagon/insulin responses in stimulating Ra, normal subjects in the postabsorptive state exercised at 87 +/- 2% VO2max during an islet cell clamp (IC): intravenous octreotide (somatostatin analog), 30 ng.kg-1.min-1; glucagon, 0.8 ng.kg-1.min-1; growth hormone, 10 ng.kg-1.min-1; and insulin adjusted to achieve euglycemia, then constant 56 +/- 7 min before exercise. |
| 2987 | 8549866 | Furthermore, IDDM was delayed with somatostatin (0.2 microgram, twice daily, n = 11), an agent that suppresses endogenous insulin production. |
| 2988 | 8549866 | In an assessment of when therapies can be initiated and still maintain clinical efficiency, only prophylactic somatostatin therapy delayed IDDM (n = 10, P = 0.02) when initiated at 14 days post-transfer, whereas the short-acting insulin regimen did not retard the onset of IDDM (n = 8, P = 0.25) compared with diluent-treated controls. |
| 2989 | 8549866 | The 24-h urinary C-peptide levels were significantly reduced with short-acting (-56%, P = 0.01) and long-acting (-67%, P = 0.02) insulin products and somatostatin (-59%, P = 0.02) compared with diluent-treated controls. |
| 2990 | 8549866 | Furthermore, IDDM was delayed with somatostatin (0.2 microgram, twice daily, n = 11), an agent that suppresses endogenous insulin production. |
| 2991 | 8549866 | In an assessment of when therapies can be initiated and still maintain clinical efficiency, only prophylactic somatostatin therapy delayed IDDM (n = 10, P = 0.02) when initiated at 14 days post-transfer, whereas the short-acting insulin regimen did not retard the onset of IDDM (n = 8, P = 0.25) compared with diluent-treated controls. |
| 2992 | 8549866 | The 24-h urinary C-peptide levels were significantly reduced with short-acting (-56%, P = 0.01) and long-acting (-67%, P = 0.02) insulin products and somatostatin (-59%, P = 0.02) compared with diluent-treated controls. |
| 2993 | 8549866 | Furthermore, IDDM was delayed with somatostatin (0.2 microgram, twice daily, n = 11), an agent that suppresses endogenous insulin production. |
| 2994 | 8549866 | In an assessment of when therapies can be initiated and still maintain clinical efficiency, only prophylactic somatostatin therapy delayed IDDM (n = 10, P = 0.02) when initiated at 14 days post-transfer, whereas the short-acting insulin regimen did not retard the onset of IDDM (n = 8, P = 0.25) compared with diluent-treated controls. |
| 2995 | 8549866 | The 24-h urinary C-peptide levels were significantly reduced with short-acting (-56%, P = 0.01) and long-acting (-67%, P = 0.02) insulin products and somatostatin (-59%, P = 0.02) compared with diluent-treated controls. |
| 2996 | 8575727 | All patients were treated with cyclosporine, azathioprine and prednisolone, and the following measurements were performed prior to hospital discharge (mean +/- SEM) 36 +/- 3 days after successful transplantation: 1) fasting plasma lipid and lipoprotein concentrations; 2) plasma glucose and insulin concentrations in response to a 75 g oral glucose challenge; and 3) steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a continuous infusion of somatostatin, insulin, and glucose. |
| 2997 | 8578004 | Amylin immunoreactivity in the rat trachea and characterization of the interaction of amylin and somatostatin on airway mucus secretion. |
| 2998 | 8578004 | It is the major component of the islet amyloid typically found in non-insulin-dependent diabetes mellitus. |
| 2999 | 8578004 | Amylin may influence airway mucus secretion by paracrine and endocrine mechanisms, and our data suggest that amylin and somatostatin belong to the increasing number of peptides that are known to influence airway function. |
| 3000 | 8578004 | Amylin immunoreactivity in the rat trachea and characterization of the interaction of amylin and somatostatin on airway mucus secretion. |
| 3001 | 8578004 | It is the major component of the islet amyloid typically found in non-insulin-dependent diabetes mellitus. |
| 3002 | 8578004 | Amylin may influence airway mucus secretion by paracrine and endocrine mechanisms, and our data suggest that amylin and somatostatin belong to the increasing number of peptides that are known to influence airway function. |
| 3003 | 8586028 | Secretion of growth hormone (GH) is excessive in acromegaly, but also in a number of other pathological states such as anorexia nervosa, insulin-dependent diabetes mellitus (IDDM), liver cirrhosis, depression, renal failure and GH-insensitivity syndrome. |
| 3004 | 8586028 | In the cohort of brain neurotransmitters, catecholamines and acetylcholine reportedly play a major role in the control of neurosecretory GH-releasing hormone (GHRH) and somatostatin (SS)-producing neurons, and hence GH secretion. |
| 3005 | 8596492 | Effects of the somatostatin analog, octreotide, on glucose metabolism and insulin sensitivity in insulin-dependent diabetes mellitus. |
| 3006 | 8596492 | To examine the effect of the somatostatin analog, octreotide, on insulin-mediated glucose uptake, seven insulin-dependent diabetic (IDDM) subjects were studied with and without 4 days of continuous subcutaneous octreotide administration (1 mg/kg/d). |
| 3007 | 8596492 | Growth hormone (GH) (0.39 +/- 0.10 v 0.78 +/- 0.23 mg/L, P < .05), insulin-like growth factor-1 (IGF-1) (127 +/- 17 v 157 +/- 21 mg/L, P < .05), and nonesterified fatty acids (NEFA) (239 +/- 25 v 405 +/- 44 mmol/L, P < .01) were lower following octreotide administration. |
| 3008 | 8596492 | In conclusion, a low-dose octrotide infusion for 4 days to IDDM subjects leads to significantly increased insulin sensitivity. |
| 3009 | 8596492 | Effects of the somatostatin analog, octreotide, on glucose metabolism and insulin sensitivity in insulin-dependent diabetes mellitus. |
| 3010 | 8596492 | To examine the effect of the somatostatin analog, octreotide, on insulin-mediated glucose uptake, seven insulin-dependent diabetic (IDDM) subjects were studied with and without 4 days of continuous subcutaneous octreotide administration (1 mg/kg/d). |
| 3011 | 8596492 | Growth hormone (GH) (0.39 +/- 0.10 v 0.78 +/- 0.23 mg/L, P < .05), insulin-like growth factor-1 (IGF-1) (127 +/- 17 v 157 +/- 21 mg/L, P < .05), and nonesterified fatty acids (NEFA) (239 +/- 25 v 405 +/- 44 mmol/L, P < .01) were lower following octreotide administration. |
| 3012 | 8596492 | In conclusion, a low-dose octrotide infusion for 4 days to IDDM subjects leads to significantly increased insulin sensitivity. |
| 3013 | 8603768 | Therefore, we studied the effects of physiological hyperglucagonemia on Phe rate of appearance (Ra), hydroxylation, and oxidation in seven normal volunteers during infusions of somatostatin with replacement doses of insulin and growth hormone. |
| 3014 | 8621002 | We infused somatostatin (SS) intravenously (500 or 1,000 microgram/h) in 13 healthy subjects to suppress insulin and glucagon secretion from the endocrine pancreas, together with infusion of either GLP-I (50 pmol / kg / h) or saline intravenously. |
| 3015 | 8636416 | On each occasion, insulin secretion was inhibited with somatostatin and glucose was infused in a pattern and amount that mimicked the systemic delivery rate normally observed after ingestion of 50 g of glucose. |
| 3016 | 8638694 | Euglycemic and hyperglycemic clamp experiments were performed with somatostatin infusions so that insulin could be replaced to basal levels or to physiological hyperinsulinemia. |
| 3017 | 8638694 | Percutaneous biopsies of the vastus lateralis muscle were taken to determine the pyruvate dehydrogenase complex or glycogen synthase activities. |
| 3018 | 8698866 | Endogenous insulin and glucagon were suppressed with somatostatin (1 microgram/min/kg), and insulin was infused at a rate of either 0.125 or 0.5 mU/min/kg. |
| 3019 | 8698866 | Thus, resistance to insulin control of hepatic glucose production in obesity and/or non-insulin-dependent diabetes mellitus may reflect resistance of the adipocyte to insulin suppression of lipolysis. |
| 3020 | 8699131 | GRF mRNA was significantly (P < 0.001) decreased in the hypothalamus of STZ-diabetic rats (0.2 +/- 0.07 mean relative densitometric units, n = 8) compared with controls (1.0 +/- 0.19, n = 8) with no change in somatostatin mRNA expression. |
| 3021 | 8699131 | Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1.1 +/- 0.17, n = 5) with no effect on testicular GRF mRNA expression. |
| 3022 | 8699131 | While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. |
| 3023 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 3024 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 3025 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 3026 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 3027 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 3028 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 3029 | 8740200 | The attenuated inhibitory action of octreotide, a somatostatin analogue on GHRH-induced growth hormone response in type I diabetes mellitus. |
| 3030 | 8750572 | The long-term effect of low protein diet on the somatostatin hypothalamic neuronal system and the pituitary growth hormone cells in growing ewe. |
| 3031 | 8754739 | Compared to levels in NC rats, diabetes resulted in decreased insulin, but elevated glucagon and somatostatin concentrations in the pancreatic tissue. |
| 3032 | 8768572 | This is, first of all, an inverse dependence between insulin content on one hand and between glucagon and somatostatin on the other. |
| 3033 | 8768572 | Besides, positive effect of adaptation to hypoxic hypoxia on the course of the experimental diabetes was demonstrated, which may be expressed in several ways: by insulin biosynthesis stimulation and new B-cells appearance, by normalization of glucagon secretion by A-cells and their reaction to hyperglycemia, depending on insulin and somatostatin content in D-cells and by inhibition of destructive process in B-cells. |
| 3034 | 8768572 | This is, first of all, an inverse dependence between insulin content on one hand and between glucagon and somatostatin on the other. |
| 3035 | 8768572 | Besides, positive effect of adaptation to hypoxic hypoxia on the course of the experimental diabetes was demonstrated, which may be expressed in several ways: by insulin biosynthesis stimulation and new B-cells appearance, by normalization of glucagon secretion by A-cells and their reaction to hyperglycemia, depending on insulin and somatostatin content in D-cells and by inhibition of destructive process in B-cells. |
| 3036 | 8769394 | Somatostatin, growth hormone, insulin-like growth factor-1, and diabetes: friends or foes? |
| 3037 | 8769394 | Major findings with regard to the somatostatin-growth hormone (GH)-insulin-like growth factor (IGF-1) axis and diabetes are summarized. |
| 3038 | 8769394 | GH hypersecretion and reduced circulating IGF-1 levels are prevalent in insulin-dependent diabetes. |
| 3039 | 8769394 | Somatostatin improves metabolism in insulin-dependent diabetics. |
| 3040 | 8769394 | Diabetic hypersomatotrophinemia may be due to hepatic resistance to GH and increased hepatic production of IGF-1-binding protein-1 (IGFBP-1), leading to reduced levels of circulating IGF-1 and further stimulation of GH production. |
| 3041 | 8769394 | Somatostatin, growth hormone, insulin-like growth factor-1, and diabetes: friends or foes? |
| 3042 | 8769394 | Major findings with regard to the somatostatin-growth hormone (GH)-insulin-like growth factor (IGF-1) axis and diabetes are summarized. |
| 3043 | 8769394 | GH hypersecretion and reduced circulating IGF-1 levels are prevalent in insulin-dependent diabetes. |
| 3044 | 8769394 | Somatostatin improves metabolism in insulin-dependent diabetics. |
| 3045 | 8769394 | Diabetic hypersomatotrophinemia may be due to hepatic resistance to GH and increased hepatic production of IGF-1-binding protein-1 (IGFBP-1), leading to reduced levels of circulating IGF-1 and further stimulation of GH production. |
| 3046 | 8769394 | Somatostatin, growth hormone, insulin-like growth factor-1, and diabetes: friends or foes? |
| 3047 | 8769394 | Major findings with regard to the somatostatin-growth hormone (GH)-insulin-like growth factor (IGF-1) axis and diabetes are summarized. |
| 3048 | 8769394 | GH hypersecretion and reduced circulating IGF-1 levels are prevalent in insulin-dependent diabetes. |
| 3049 | 8769394 | Somatostatin improves metabolism in insulin-dependent diabetics. |
| 3050 | 8769394 | Diabetic hypersomatotrophinemia may be due to hepatic resistance to GH and increased hepatic production of IGF-1-binding protein-1 (IGFBP-1), leading to reduced levels of circulating IGF-1 and further stimulation of GH production. |
| 3051 | 8772592 | Resistance to insulin-mediated glucose disposal was quantified by measurement of the steady state plasma glucose (SSPG) and insulin (SSPI) concentrations during the last 30 min of an 180-min infusion of somatostatin (5 micrograms/min), insulin (25 mU/min-m2), and glucose (240 mg/min-m2). |
| 3052 | 8772715 | Effect of enterostatin on insulin, glucagon, and somatostatin secretion in the perfused rat pancreas. |
| 3053 | 8772715 | In the present study, we have investigated the effect of exogenous enterostatin on insulin, glucagon, and somatostatin secretion by the isolated perfused rat pancreas. |
| 3054 | 8772715 | In summary, in the perfused rat pancreas, enterostatin, at putatively physiological concentrations, inhibits insulin secretion without affecting glucagon or somatostatin output, thus pointing to a direct effect of enterostatin on the beta-cell and not through an alpha-cell or delta-cell paracrine effect. |
| 3055 | 8772715 | Effect of enterostatin on insulin, glucagon, and somatostatin secretion in the perfused rat pancreas. |
| 3056 | 8772715 | In the present study, we have investigated the effect of exogenous enterostatin on insulin, glucagon, and somatostatin secretion by the isolated perfused rat pancreas. |
| 3057 | 8772715 | In summary, in the perfused rat pancreas, enterostatin, at putatively physiological concentrations, inhibits insulin secretion without affecting glucagon or somatostatin output, thus pointing to a direct effect of enterostatin on the beta-cell and not through an alpha-cell or delta-cell paracrine effect. |
| 3058 | 8772715 | Effect of enterostatin on insulin, glucagon, and somatostatin secretion in the perfused rat pancreas. |
| 3059 | 8772715 | In the present study, we have investigated the effect of exogenous enterostatin on insulin, glucagon, and somatostatin secretion by the isolated perfused rat pancreas. |
| 3060 | 8772715 | In summary, in the perfused rat pancreas, enterostatin, at putatively physiological concentrations, inhibits insulin secretion without affecting glucagon or somatostatin output, thus pointing to a direct effect of enterostatin on the beta-cell and not through an alpha-cell or delta-cell paracrine effect. |
| 3061 | 8781291 | Lack of a relationship between urinary albumin excretion rate and insulin resistance in patients with non-insulin-dependent diabetes mellitus. |
| 3062 | 8781291 | The study was performed to determine the relationship between urinary albumin excretion (UAE) and resistance to insulin-mediated glucose disposal in patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 3063 | 8781291 | Twenty-five non-obese male patients were enrolled; UAE rates were determined on two 24-hour urine collections, and resistance to insulin-mediated glucose disposal was quantified by measurement of steady-state plasma glucose (SSPG) and steady-state plasma insulin concentrations during the last 30 minutes of a 180-minute infusion of somatostatin, insulin, and glucose. |
| 3064 | 8781760 | Islet amyloid polypeptide (amylin) and insulin are differentially expressed in chronic diabetes induced by streptozotocin in rats. |
| 3065 | 8781760 | Islet amyloid polypeptide (IAPP) is overexpressed relative to insulin under several experimental conditions relevant to diabetes mellitus, including the immediate phase (7 days) following induction of streptozotocin diabetes. |
| 3066 | 8781760 | Immunocytochemistry revealed that IAPP predominantly occurred in insulin cells and to a lesser extent in somatostatin cells at all treatments examined. |
| 3067 | 8781760 | An over-expression of IAPP relative to insulin may therefore be involved in diabetes pathogenesis, contributing to its metabolic perturbations, possibly through the capacity of IAPP to restrain insulin release and action and to form islet amyloid. |
| 3068 | 8783333 | Finally, there was a 35-55% increase (p < 0.05) in the levels of insulin, glucagon, and somatostatin mRNAs in cells cultured for 6 weeks on matrigel. |
| 3069 | 8799695 | We hypothesize that a reduction in the hypothalamic somatostatin inhibitory tone combined with increased pituitary GH production may be responsible for the pattern of the GH responses to hexarelin and GHRH observed in our type I diabetic patients. |
| 3070 | 8808981 | Samples were subjected to slot-blot analysis by using homologous probes for insulin, glucagon, somatostatin, glucose transporter-2 (glut-2), glucokinase, elastase-I, and beta-actin. |
| 3071 | 8808981 | This paralleled decreases in glut-2 (p = .001) mRNA levels, but it was in contrast with glucokinase mRNA levels which increased markedly (p = .0003). |
| 3072 | 8808981 | Somatostatin mRNA levels were unchanged, glucagon mRNA levels decreased modesty (p = .01), and mRNA levels for elastase-I and beta-actin increased with age (p = .0001 for either one). |
| 3073 | 8808981 | Samples were subjected to slot-blot analysis by using homologous probes for insulin, glucagon, somatostatin, glucose transporter-2 (glut-2), glucokinase, elastase-I, and beta-actin. |
| 3074 | 8808981 | This paralleled decreases in glut-2 (p = .001) mRNA levels, but it was in contrast with glucokinase mRNA levels which increased markedly (p = .0003). |
| 3075 | 8808981 | Somatostatin mRNA levels were unchanged, glucagon mRNA levels decreased modesty (p = .01), and mRNA levels for elastase-I and beta-actin increased with age (p = .0001 for either one). |
| 3076 | 8817239 | This 8-bp repeat is inserted into a sequence that is highly homologous to a sequence motif, called PISCES (pancreatic islet cell-specific enhancer sequences), found within cell-specific enhancer elements of the rat insulin I (Ins-E1, from -332 to -285), rat glucagon (Glu-G3) and rat somatostatin (SMS-UE) genes. |
| 3077 | 8824478 | Furthermore, immunohistochemistry for insulin, glucagon, and somatostatin showed positively staining, while amylase was negative in the Cudt group, compared with the positive stain for cells in the control group. |
| 3078 | 8826967 | To maintain equal plasma insulin and glucagon concentrations throughout the studies, somatostatin and insulin (basal replacement) were infused for 4 h. [3-(3H)]-glucose and [U-(14C)]-lactate were infused to measure HGP, gluconeogenesis, and glucose cycling (GC) during 2 h of euglycemia (glucose approximately 8 mmol/l) followed by 2 h of hyperglycemia (glucose approximately 18 mmol/l). |
| 3079 | 8843172 | And in study C, five patients received a somatostatin infusion with basal replacing doses of insulin and glucagon. |
| 3080 | 8845050 | Glutamic acid decarboxylase (GAD) has been shown to exist as two isoforms with molecular weights of 65 kD (GAD65) and 67 kD (GAD67) in the central nervous system as well as in several non-neuronal tissues, including the pancreatic islets. |
| 3081 | 8845050 | Recently, this enzyme has been proposed as a key beta-cell autoantigen in insulin-dependent diabetes mellitus (IDDM). |
| 3082 | 8845050 | In the adult pig, GAD65 was localized exclusively in most of the beta cells, whereas GAD67, in addition to being present in a majority of the beta cells, was also seen in a proportion of glucagon and somatostatin labelled cells. |
| 3083 | 8845050 | The predominant expression of both the isoforms in porcine beta cells suggests that islet cells from this species may act as a suitable cellular model for study of GAD autoreactivity during the early stages of IDDM. |
| 3084 | 8866566 | A pancreatic clamp (somatostatin plus basal insulin and basal glucagon infusions) was used to control the endocrine pancreas. |
| 3085 | 8884164 | Alcohol (ethanol), over-zealous glycaemic control, hypoglycaemic unawareness, detective counterregulation especially in insulin-dependent diabetes mellitus (IDDM), and renal and liver impairment are all important predisposing factors. |
| 3086 | 8884164 | Although antihyperglycaemic agents such as metformin and alpha-glucosidase inhibitors do not cause hypoglycaemia alone, they may enhance the hypoglycaemic effects of potent hypoglycaemic agents such as insulin and sulphonylureas. |
| 3087 | 8884164 | On the other hand, the potential hypoglycaemic effects of ACE inhibitors, alpha-blockers, lipid-lowering agents and recombinant human insulin-like growth factor demonstrated in experimental settings, are of potential therapeutic interest. |
| 3088 | 8884164 | In refractory hypoglycaemia due to hyperinsulinaemia such as during sulphonylurea overdosage or quinine treatment, the long-acting somatostatin, octreotide, may suppress insulin release and restore euglycaemia. |
| 3089 | 8896654 | The average heart rate (as calculated by a mean of 30,720 +/- 208 beats per subject over a monitoring time of 6.9 +/- 0.6 h) was significantly related (r = 0.61; P < .001) to insulin resistance as expressed by the steady-state plasma glucose (SSPG) response to a continuous infusion of glucose, insulin and somatostatin and to the plasma insulin response to a 75 g of oral glucose challenge (r = 0.51; P < .001). |
| 3090 | 8897861 | Decreased glucose-induced cAMP and insulin release in islets of diabetic rats: reversal by IBMX, glucagon, GIP. |
| 3091 | 8897861 | Somatostatin, prostaglandin E2, UK-14304, or galanin inhibited cAMP accumulation and insulin release to the same extent in both types of islets. |
| 3092 | 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. |
| 3093 | 8899822 | Somatostatin (SOM), calcitenin gene-related peptide (CGRP), and substance P (SP) are neuropeptides that modulate pain responses transmitted by primary sensory afferents, the cell bodies of which are located in the dorsal root ganglion (DRG). |
| 3094 | 8899822 | These data suggest that CGRP and SOM synthesis in primary sensory neurons is reduced in STZ-induced diabetic rats. |
| 3095 | 8914425 | Plama insulin-like growth factor-1 levels decrease in spite of their strong relation with diabetic retinopathy. 2) Blood thyroid hormones show the similarity with low T3 syndrome. 3) Hyporeninemic hypoaldosteronism occurs especially with patients who have hypertension or moderate diabetic complications. 4) Plasma pancreatic glucagon levels are elevated. |
| 3096 | 8914425 | Glucose administration shows impaired inhibition or paradoxical hypersecretion. 5) Other plasma levels of pancreatic hormones such as gastrin, secretin, motilin and somatostatin are usually elevated. |
| 3097 | 8922364 | The cells respond to various well-known stimulators of insulin secretion, including leucine and arginine; to modulators such as carbachol, glucagon-like peptide I, and pituitary adenylyl cyclase activating polypeptide; and to the inhibitors norepinephrine, somatostatin, and galanin. |
| 3098 | 8922369 | We assessed the response to insulin-induced hypoglycemia in the absence of counterregulatory hormones in overnight-fasted conscious adrenalectomized dogs that were given somatostatin and intraportal insulin (30 pmol x kg(-1) x min(-1)) for 360 min. |
| 3099 | 8931985 | Initial diabetic renal hypertrophy is preceded by a transient increase in kidney insulin-like growth factor I(IGF-I). |
| 3100 | 8931985 | In the present study streptozotocin-diabetic rats were treated with a new somatostatin analogue (lanreotide), insulin or placebo for 7 days and compared to non-diabetic control rats. |
| 3101 | 8931985 | In conclusion, IGF-I accumulated transiently and was more pronounced in the real cortex compared to the renal medulla and, further, lanreotide prevented diabetic renal and glomerular growth bringing new evidence that intervention with somatostatin analogues may have a role in the prevention of experimental diabetic kidney disease. |
| 3102 | 8931985 | Initial diabetic renal hypertrophy is preceded by a transient increase in kidney insulin-like growth factor I(IGF-I). |
| 3103 | 8931985 | In the present study streptozotocin-diabetic rats were treated with a new somatostatin analogue (lanreotide), insulin or placebo for 7 days and compared to non-diabetic control rats. |
| 3104 | 8931985 | In conclusion, IGF-I accumulated transiently and was more pronounced in the real cortex compared to the renal medulla and, further, lanreotide prevented diabetic renal and glomerular growth bringing new evidence that intervention with somatostatin analogues may have a role in the prevention of experimental diabetic kidney disease. |
| 3105 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 3106 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 3107 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 3108 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 3109 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 3110 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 3111 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 3112 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 3113 | 8950610 | In IHC, insulin (Ins)-secreting cells accounted for the majority of the islet cells, while glucagon(Glu)-somatostatin (Som)- and polypeptide(PP)-immunoreactive cells, in decreasing number, were found in the mantle around the core of Ins-cells. |
| 3114 | 8961137 | Polymer-based controlled-release technology has enabled us to demonstrate: that the controlled release of insulin from polymer matrices can indeed be used to control diabetes mellitus but does so at the expense of hyperinsulinemia and hypoglycemia; and that somatostatin can be delivered in similar fashion, so as to provide glucose homeostasis in a more physiologic range, at lower insulin levels and at somatostatin doses below those used in intermittent infusion studies; and, that microgram quantities of a drug can be delivered successfully in vivo with intact biological function and in a manner that can be monitored continuously. |
| 3115 | 8961137 | In the present study the simultaneous polymer-matrix-controlled release of insulin with somatostatin extended glycemic control in diabetic rats. |
| 3116 | 8961137 | When somatostatin was delivered at 0.75-1.1 micrograms/kg/day together with insulin, plasma glucose control persisted for 12 days until insulin release decreased below 3.6 units/kg/day. |
| 3117 | 8961137 | It is our hope that further experiments regarding the potential role of both controlled-release devices and somatostatin will be performed to provide continuing therapeutic alternatives to the insulin-dependent diabetic. |
| 3118 | 8961137 | Polymer-based controlled-release technology has enabled us to demonstrate: that the controlled release of insulin from polymer matrices can indeed be used to control diabetes mellitus but does so at the expense of hyperinsulinemia and hypoglycemia; and that somatostatin can be delivered in similar fashion, so as to provide glucose homeostasis in a more physiologic range, at lower insulin levels and at somatostatin doses below those used in intermittent infusion studies; and, that microgram quantities of a drug can be delivered successfully in vivo with intact biological function and in a manner that can be monitored continuously. |
| 3119 | 8961137 | In the present study the simultaneous polymer-matrix-controlled release of insulin with somatostatin extended glycemic control in diabetic rats. |
| 3120 | 8961137 | When somatostatin was delivered at 0.75-1.1 micrograms/kg/day together with insulin, plasma glucose control persisted for 12 days until insulin release decreased below 3.6 units/kg/day. |
| 3121 | 8961137 | It is our hope that further experiments regarding the potential role of both controlled-release devices and somatostatin will be performed to provide continuing therapeutic alternatives to the insulin-dependent diabetic. |
| 3122 | 8961137 | Polymer-based controlled-release technology has enabled us to demonstrate: that the controlled release of insulin from polymer matrices can indeed be used to control diabetes mellitus but does so at the expense of hyperinsulinemia and hypoglycemia; and that somatostatin can be delivered in similar fashion, so as to provide glucose homeostasis in a more physiologic range, at lower insulin levels and at somatostatin doses below those used in intermittent infusion studies; and, that microgram quantities of a drug can be delivered successfully in vivo with intact biological function and in a manner that can be monitored continuously. |
| 3123 | 8961137 | In the present study the simultaneous polymer-matrix-controlled release of insulin with somatostatin extended glycemic control in diabetic rats. |
| 3124 | 8961137 | When somatostatin was delivered at 0.75-1.1 micrograms/kg/day together with insulin, plasma glucose control persisted for 12 days until insulin release decreased below 3.6 units/kg/day. |
| 3125 | 8961137 | It is our hope that further experiments regarding the potential role of both controlled-release devices and somatostatin will be performed to provide continuing therapeutic alternatives to the insulin-dependent diabetic. |
| 3126 | 8961137 | Polymer-based controlled-release technology has enabled us to demonstrate: that the controlled release of insulin from polymer matrices can indeed be used to control diabetes mellitus but does so at the expense of hyperinsulinemia and hypoglycemia; and that somatostatin can be delivered in similar fashion, so as to provide glucose homeostasis in a more physiologic range, at lower insulin levels and at somatostatin doses below those used in intermittent infusion studies; and, that microgram quantities of a drug can be delivered successfully in vivo with intact biological function and in a manner that can be monitored continuously. |
| 3127 | 8961137 | In the present study the simultaneous polymer-matrix-controlled release of insulin with somatostatin extended glycemic control in diabetic rats. |
| 3128 | 8961137 | When somatostatin was delivered at 0.75-1.1 micrograms/kg/day together with insulin, plasma glucose control persisted for 12 days until insulin release decreased below 3.6 units/kg/day. |
| 3129 | 8961137 | It is our hope that further experiments regarding the potential role of both controlled-release devices and somatostatin will be performed to provide continuing therapeutic alternatives to the insulin-dependent diabetic. |
| 3130 | 9000693 | A pancreatic clamp (somatostatin, basal portal insulin, and glucagon infusions) was used to control the endocrine pancreas. |
| 3131 | 9000693 | One group (INS + FAT; n = 6) received an infusion of 20% intralipid + heparin (0.5 U x kg(-1) x min(-1)) to clamp the nonesterified fatty acid (NEFA) levels during hyperinsulinemia; the other group (INS; n = 7) received only saline during the experimental period. |
| 3132 | 9000693 | In the INS + FAT group, a similar increase in peripheral insulin was achieved (36 +/- 6 to 114 +/- 6 pmol/l, last 30 min); again, portal insulin was unaltered (96 +/- 12 pmol/l). |
| 3133 | 9000693 | In the INS group, NEFA levels dropped from 700 +/- 90 (basal) to 230 +/- 65 micromol/l (last 30 min; P > 0.05), but in the INS + FAT group changed minimally (723 +/- 115 [basal] to 782 +/- 125 micromol/l [last 30 min]). |
| 3134 | 9000693 | In the INS group, net hepatic glucose output dropped by 6.7 micromol x kg(-1) x min(-1) (P < 0.05), whereas in the INS + FAT group it dropped by 3.9 micromol x kg(-1) x min(-1) (P < 0.05). |
| 3135 | 9000693 | In the INS group, net hepatic gluconeogenic substrate uptake (alanine, glutamine, glutamate, glycerol, glycine, lactate, threonine, and serine) fell slightly (10.4 +/- 1.3 [basal] to 7.2 +/- 1.3 micromol x kg(-1) x min(-1) [last 30 min]), whereas in the INS + FAT group it did not change (7.3 +/- 1.5 [basal] to 7.4 +/- 0.6 micromol x kg(-1) x min(-1) [last 30 min]), and in the control group it increased slightly (9.6 +/- 1.3 [basal] to 10.3 +/- 1.4 micromol x kg(-1) x min(-1) [last 30 min). |
| 3136 | 9022089 | Chronic exposure of HIT-T15 cells to supraphysiologic glucose concentration diminishes insulin gene expression and decreased binding of two critical insulin gene transcription factors, STF-1 and RIPE-3b1 activator. |
| 3137 | 9022089 | They regained binding of STF-1 and RIPE-3b1 activator and had a partial but minimal return of insulin mRNA expression. |
| 3138 | 9022089 | In a second study, inclusion of somatostatin in the media-containing 11.1 mM glucose inhibited insulin secretion; however, despite this protection against beta cell exhaustion, dramatic decreases in insulin gene expression, STF-1 and RIPE-3b1 binding, and insulin gene promoter activity still occurred. |
| 3139 | 9030824 | Animals were treated with somatostatin to suppress insulin secretion, and nondiabetic swine received intravenous (IV) glucose to match the hyperglycemia in the diabetic animals. |
| 3140 | 9066086 | Furthermore, within these vacuolated areas, some cells were positive to varying degrees for insulin, glucagon, somatostatin, and pancreatic polypeptide. |
| 3141 | 9075740 | After SZ-mediated elimination of existing IN+/PDX-1+ cells, a population of somatostatin (SOM)+/PDX-1+ cells, a cell type thought to represent an embryonic islet precursor cell, appeared in islets. |
| 3142 | 9075740 | The appearance of SOM+/PDX-1+ cells was followed in time by the differentiation to SOM+/IN+/PDX-1+ cells. |
| 3143 | 9075740 | SOM+/PDX-1+ cells also appeared in islets of nonobese diabetic mice, a strain of mice in which beta cell destruction is immune-mediated. |
| 3144 | 9092341 | We have examined the relationship between visceral fat measured by MRI on a transverse cut through L3, insulin sensitivity assessed by the somatostatin-insulin-glucose test, and arterial blood pressure in 18 obese (11 women and 7 men), non insulin-dependent diabetic patients with android body fat distribution. |
| 3145 | 9101063 | Endogenous insulin and glucagon were suppressed by somatostatin infusion and replaced singly or in combination to match the hormonal concentrations observed during similar exercise in saline-treated control subjects. |
| 3146 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 3147 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 3148 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 3149 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 3150 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 3151 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 3152 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 3153 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 3154 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 3155 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 3156 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 3157 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 3158 | 9133545 | Glucagon-like peptide I (GLP-I), an intestine-derived incretin hormone, is a potent stimulator of insulin and somatostatin secretion. |
| 3159 | 9133545 | The localization of the GLP-I receptor on insulin and somatostatin-producing cells in the islets is well established. |
| 3160 | 9133545 | In dispersed rat islet cells analyzed by double immunofluorescent staining, 90% of the insulin, 76% of the somatostatin, and 20% of the glucagon positive cells colocalized with the GLP-I receptor immunoreactivity. |
| 3161 | 9133545 | Glucagon-like peptide I (GLP-I), an intestine-derived incretin hormone, is a potent stimulator of insulin and somatostatin secretion. |
| 3162 | 9133545 | The localization of the GLP-I receptor on insulin and somatostatin-producing cells in the islets is well established. |
| 3163 | 9133545 | In dispersed rat islet cells analyzed by double immunofluorescent staining, 90% of the insulin, 76% of the somatostatin, and 20% of the glucagon positive cells colocalized with the GLP-I receptor immunoreactivity. |
| 3164 | 9133545 | Glucagon-like peptide I (GLP-I), an intestine-derived incretin hormone, is a potent stimulator of insulin and somatostatin secretion. |
| 3165 | 9133545 | The localization of the GLP-I receptor on insulin and somatostatin-producing cells in the islets is well established. |
| 3166 | 9133545 | In dispersed rat islet cells analyzed by double immunofluorescent staining, 90% of the insulin, 76% of the somatostatin, and 20% of the glucagon positive cells colocalized with the GLP-I receptor immunoreactivity. |
| 3167 | 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. |
| 3168 | 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. |
| 3169 | 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. |
| 3170 | 9137900 | Interest has focused on basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF beta) and more recently vascular endothelial cell growth factor (VEGF). |
| 3171 | 9137900 | Histologic studies have demonstrated the presence of growth factor proteins and receptors and/or their mRNA, mainly VEGF, PDGF, and bFGF, in preretinal membranes of patients with proliferative diabetic retinopathy. |
| 3172 | 9137900 | Elevated intravitreal levels of IGF-1 and VEGF correlating with neovascular activity have been found in some patients. |
| 3173 | 9137900 | Inhibition of IGF-1 by somatostatin analogs has produced unsatisfactory results. |
| 3174 | 9137906 | Islet peptide hormones (insulin, glucagon, and somatostatin), as well as DDC, were detected immunohistochemically using the double-immunofluorescence technique and specific antibodies. |
| 3175 | 9144203 | Reverse transcription-coupled PCR analysis showed that somatostatin and pancreatic polypeptide mRNAs were present, although at reduced levels, accounting for the presence also of delta and pancreatic polypeptide cells, respectively. |
| 3176 | 9166412 | This was associated with an increase in mRNA levels of insulin, glucagon, and somatostatin, as well as an increase in the insulin protein content and secretion in response to secretagogues. |
| 3177 | 9166412 | The activity of PI3K was inversely correlated with the hepatocyte growth factor/scatter factor-induced downregulation or nicotinamideinduced upregulation of islet-specific gene expression, giving support to the role of PI3K, as a negative regulator of endocrine differentiation. |
| 3178 | 9178028 | Repeated administration of growth hormone-releasing hormone with or without previous administration of pyridostigmine in insulin-dependent diabetes mellitus. |
| 3179 | 9178028 | Since the GH-releasing effect of PD is likely to be mediated by the inhibition of hypothalamic somatostatin release, our results suggest that there is also an impaired somatostatin tone in hyperglycemic type 1 diabetic patients with normal GH response to GHRH. |
| 3180 | 9186309 | In insulin-dependent diabetes mellitus (IDDM), inappropriate growth hormone (GH) responses to several stimuli, including GH-releasing hormone (GHRH), have been described. |
| 3181 | 9186309 | The aim of this study was to evaluate whether there is a differential effect of IDDM on GHRP-6- and GHRH-induced GH secretion. |
| 3182 | 9186309 | In summary, the effectiveness of GHRP-6 in IDDM could reinforce the evidence that this peptide probably does not release GH through a decrease in hypothalamic somatostatin secretion. |
| 3183 | 9186309 | Moreover, our data suggest that both GHRH and GHRP-6 releasing mechanisms are unaltered in IDDM. |
| 3184 | 9200642 | With the infusion of somatostatin (0.8 microg x kg(-1) x min(-1)), glucagon (0.65 ng x kg(-1) x min(-1)), and insulin (27 pmol x kg(-1) x min(-1)), arterial glucose levels could be maintained at 8 mmol/l by adjusting the intravenous glucose infusion (G(inf)) according to the following three periods: 1) peripheral glucose infusion period (PE), G(inf) alone; 2) portal glucose infusion period (PO), G(inf) plus constant glucose infusion into the portal vein (GIR(PV), 55.6 micromol x kg(-1) x min(-1)); 3) portal and brain glucose infusion period (PO+CNS), G(inf) and GIR(PV) plus additional glucose infusion into the unilateral carotid and vertebral arteries to abolish the positive glucose gradient between HPS and CNS. |
| 3185 | 9211494 | Fasting levels of islet amyloid polypeptide (IAPP), glucagon, and somatostatin were elevated in NIRD and IRD patients. |
| 3186 | 9225823 | Substance P (SP), vasoactive intestinal polypeptide (VIP), and somatostatin content in rectal mucosa were determined by radioimmunoassay (RIA) in 38 diabetic patients (12 with normal bowel function, 13 with diabetic diarrhea, and 13 with constipation) and in 10 nondiabetic controls with normal bowel function. |
| 3187 | 9231665 | We have studied the acute effects of selective hyperglucagonemia (raised from -200 to -350 pg/ml for 3 h) on fibrinogen fractional secretion rate (FSR) in eight normal subjects during infusion of somatostatin and replacement doses of insulin, glucagon, and growth hormone. |
| 3188 | 9240760 | Insulin sensitivity was determined using glucose-clamp method or glucose, insulin, and somatostatin infusion method. |
| 3189 | 9271225 | However, the cell line appears to have dedifferentiated with regard to the ability to secrete somatostatin, maintaining the highly differentiated function of both insulin biosynthesis and exocytosis. |
| 3190 | 9287042 | To study the regulation of growth and differentiated function of insulin-secreting cells, the rat insulinoma cell line INS-1 was cultured in a defined serum-free medium containing prolactin, IGF-I, and triiodothyronine, which was originally reported to maintain insulin secretion of islet cells. |
| 3191 | 9287042 | Interestingly, conditioned serum-free medium from rat islets maintained the insulin secretory function of INS-1 cells, although glucagon, somatostatin, and some other factors failed to restore the function. |
| 3192 | 9287044 | Kir6.2, a member of the inward rectifier K+ channel family, is a component of the ATP-sensitive K+ (K[ATP]) channel considered to play a key role in glucose-induced insulin secretion. |
| 3193 | 9287044 | In situ hybridization and immunofluorescence staining of serial sections with the anti-insulin, the anti-glucagon, and the anti-somatostatin antibodies showed Kir6.2 mRNA to be present in alpha-, beta-, and delta-cells. |
| 3194 | 9287044 | Kir6.2 was further shown to be located together with insulin, glucagon, or somatostatin. |
| 3195 | 9287044 | These results suggest that Kir6.2, as a component of K(ATP) channels, is an important molecule in the regulation of all the release of insulin, glucagon, and somatostatin. |
| 3196 | 9289688 | Under physiological conditions, the pancreas scarcely influences the function of the cardiovascular system, although the hormones produced in the healthy pancreas (insulin, glucagon and somatostatin) affect the myocardial contractility in pharmacological doses. |
| 3197 | 9294779 | Octreotide, a synthetic analogue of somatostatin, may improve metabolic control and reduce GH and glucagon levels in insulin-dependent diabetic patients. |
| 3198 | 9347241 | Therefore the size and the structure of the endocrine pancreas, as well as the contribution of the insulin-, glucagon-, somatostatin- and PP-cells, were investigated morphometrically in the adult youngsters of mildly and of severely diabetic mothers, since both display a disturbed glucose tolerance but with divergent characteristics. |
| 3199 | 9361690 | To investigate the influence of cholinergic pathways on somatostatin (SS) tone in type I diabetes mellitus, we studied the effect of the muscarinic receptor antagonist pirenzepine ([PZP] 100 mg orally) on spontaneous nocturnal growth hormone (GH) and thyrotropin (TSH) secretion and on their response to GH-releasing hormone (GHRH) in the morning in a group of nine insulin-dependent diabetic patients with poor diabetic control. |
| 3200 | 9361690 | The inhibitory effect of PZP on GHRH-induced GH secretion may help to predict nocturnal GH behavior following administration of the drug. |
| 3201 | 9364340 | Growth hormone (GH) secretion is controlled via somatostatin and growth hormone releasing hormone (GHRH). |
| 3202 | 9398728 | Isoproterenol and somatostatin decrease plasma leptin in humans: a novel mechanism regulating leptin secretion. |
| 3203 | 9398728 | In cultured adipocytes, leptin is increased by insulin and decreased by cAMP. |
| 3204 | 9398728 | In animal models, insulin and agents that increase intracellular cAMP have been shown to similarly affect plasma leptin in vivo. |
| 3205 | 9398728 | Five groups of normal weight subjects were studied; 1) subjects infused with isoproterenol at a rate of 24 ng/kg/min (ISO24); 2) subjects infused with isoproterenol at a rate of 8 ng/kg/min (ISO8); 3) subjects infused with somatostatin/insulin/GH followed by coinfusion with 8 ng/kg/min isoproterenol (ISO8 + SRIH); 4) subjects infused with somatostatin/insulin/GH alone (SRIH); and 5) control subjects infused with saline (NS). |
| 3206 | 9398728 | Therefore both isoproterenol and somatostatin reduce plasma leptin in humans. |
| 3207 | 9398728 | Isoproterenol and somatostatin decrease plasma leptin in humans: a novel mechanism regulating leptin secretion. |
| 3208 | 9398728 | In cultured adipocytes, leptin is increased by insulin and decreased by cAMP. |
| 3209 | 9398728 | In animal models, insulin and agents that increase intracellular cAMP have been shown to similarly affect plasma leptin in vivo. |
| 3210 | 9398728 | Five groups of normal weight subjects were studied; 1) subjects infused with isoproterenol at a rate of 24 ng/kg/min (ISO24); 2) subjects infused with isoproterenol at a rate of 8 ng/kg/min (ISO8); 3) subjects infused with somatostatin/insulin/GH followed by coinfusion with 8 ng/kg/min isoproterenol (ISO8 + SRIH); 4) subjects infused with somatostatin/insulin/GH alone (SRIH); and 5) control subjects infused with saline (NS). |
| 3211 | 9398728 | Therefore both isoproterenol and somatostatin reduce plasma leptin in humans. |
| 3212 | 9398728 | Isoproterenol and somatostatin decrease plasma leptin in humans: a novel mechanism regulating leptin secretion. |
| 3213 | 9398728 | In cultured adipocytes, leptin is increased by insulin and decreased by cAMP. |
| 3214 | 9398728 | In animal models, insulin and agents that increase intracellular cAMP have been shown to similarly affect plasma leptin in vivo. |
| 3215 | 9398728 | Five groups of normal weight subjects were studied; 1) subjects infused with isoproterenol at a rate of 24 ng/kg/min (ISO24); 2) subjects infused with isoproterenol at a rate of 8 ng/kg/min (ISO8); 3) subjects infused with somatostatin/insulin/GH followed by coinfusion with 8 ng/kg/min isoproterenol (ISO8 + SRIH); 4) subjects infused with somatostatin/insulin/GH alone (SRIH); and 5) control subjects infused with saline (NS). |
| 3216 | 9398728 | Therefore both isoproterenol and somatostatin reduce plasma leptin in humans. |
| 3217 | 9421296 | When the insulin-releasing effect of BTS 67 582 (100 mg kg(-1)) was inhibited by infusion of somatostatin, there was no effect on glycaemia. 6. |
| 3218 | 9439624 | We have reported earlier that somatostatin (SST) induced DNA fragmentation and apoptosis is signaled in a receptor subtype selective manner uniquely via human somatostatin receptor subtype 3 (hSSTR3). |
| 3219 | 9439624 | In the present study we investigated the pH dependence and cation sensitivity of endonuclease induced in hSSTR3 expressing CHO-K1 cells by the SST agonist octreotide (OCT) and its effect on intracellular pH. |
| 3220 | 9439624 | We have reported earlier that somatostatin (SST) induced DNA fragmentation and apoptosis is signaled in a receptor subtype selective manner uniquely via human somatostatin receptor subtype 3 (hSSTR3). |
| 3221 | 9439624 | In the present study we investigated the pH dependence and cation sensitivity of endonuclease induced in hSSTR3 expressing CHO-K1 cells by the SST agonist octreotide (OCT) and its effect on intracellular pH. |
| 3222 | 9451476 | Islet cells containing immunoreactive insulin and islet amyloid polypeptide were plentiful, while those staining positive for glucagon and somatostatin were scarce in these grafts. |
| 3223 | 9453015 | Treatment with angiotensin converting enzyme (ACE) inhibitors has proven effective in delaying progression of human and experimental diabetic renal changes, and so has somatostatin analog treatment in experimental diabetes. |
| 3224 | 9453241 | The transcriptional control of the gene in beta-cells involves at least two islet-specific DNA-binding proteins, GTIIa and PDX-1, which also transactivates the insulin, somatostatin and glucokinase genes. |
| 3225 | 9453241 | In this report, we assessed the DNA-binding activities of GTIIa and PDX-1 to their respective cis-elements of the GLUT2 promoter using nuclear extracts prepared from pancreatic islets of 12 week old db/db diabetic mice. |
| 3226 | 9453241 | We show that the decreased GLUT2 mRNA expression correlates with a decrease of the GTIIa DNA-binding activity, whereas the PDX-1 binding activity is increased. |
| 3227 | 9453241 | The adjunction of dexamethasone to isolated pancreatic islets, a treatment previously shown to decrease PDX-1 expression in the insulin-secreting HIT-T15 cells, has no effect on the GTIIa and PDX-1 DNA-binding activities. |
| 3228 | 9474868 | For the determination of the proliferative activity of the different cell types immunohistochemistry for insulin, glucagon and somatostatin was combined with a 5-Bromo-2'-desoxyuridine immunohistochemistry. |
| 3229 | 9479010 | GLP-1 modulates insulin, glucagon and somatostatin secretion by binding to guanine nucleotide binding protein-coupled receptors resulting in the activation of adenylate cyclase and generation of cyclic adenosine monophosphate (cAMP). |
| 3230 | 9479010 | In the B-cell, cAMP, via activation of protein kinase A, interacts with a plethora of signal transduction processes including ion channel activity, intracellular Ca2+ handling and exocytosis of the insulin-containing granules. |
| 3231 | 9479010 | The stimulatory action of GLP-1 on insulin secretion, contrary to that of the currently used hypoglycaemic sulphonylureas, is glucose dependent and requires the presence of normal or elevated concentrations of the sugar. |
| 3232 | 9519720 | Plasma leptin concentrations do not appear to decrease insulin-mediated glucose disposal or glucose-stimulated insulin secretion in women with normal glucose tolerance. |
| 3233 | 9519720 | The aim of this study was to test the hypothesis that plasma leptin concentrations contributed to the pathophysiology of NIDDM by decreasing both insulin-mediated glucose disposal and glucose-stimulated insulin secretion. |
| 3234 | 9519720 | Differences in insulin-mediated glucose disposal were determined by comparing the steady-state plasma glucose (SSPG) concentrations attained at the end of a 180-min constant infusion of somatostatin, glucose, and insulin, while comparisons of glucose-stimulated insulin secretion were based on the incremental increase in insulin concentration 30 min after an oral glucose challenge (deltaIns) as compared with the fasting value. |
| 3235 | 9519720 | The results showed that the higher the fasting plasma leptin concentration, the greater the degree of insulin resistance (r = 0.47, P < 0.01). |
| 3236 | 9519720 | However, since the total integrated plasma insulin response was highly correlated with both SSPG (r = 0.80, P < 0.001) and leptin (r = 0.55, P < 0.01), multiple regression analysis was repeated, adding total insulin response to the model. |
| 3237 | 9519720 | When this was done, the significant relationship between leptin and SSPG disappeared, whereas both BMI (P < 0.03) and insulin response (P < 0.001) were correlated with SSPG. |
| 3238 | 9519720 | A significant relationship between leptin and deltaIns was seen, but it was a positive one (r = 0.31, P < 0.02), not a negative one as would be expected if circulating levels of leptin inhibited glucose-stimulated insulin secretion. |
| 3239 | 9519720 | The results of these studies do not support the view that circulating leptin has a primary effect on either insulin action or secretion in normal female volunteers. |
| 3240 | 9519720 | It seems more likely that chronic hyperinsulinemia in insulin-resistant individuals acts to increase adipose tissue leptin synthesis and secretion, leading to higher ambient leptin concentrations. |
| 3241 | 9524732 | Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2. |
| 3242 | 9524732 | Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. |
| 3243 | 9524732 | At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3. |
| 3244 | 9524732 | Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. |
| 3245 | 9524732 | Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2. |
| 3246 | 9524732 | Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. |
| 3247 | 9524732 | At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3. |
| 3248 | 9524732 | Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. |
| 3249 | 9537589 | Induction of wild-type p53, Bax, and acidic endonuclease during somatostatin-signaled apoptosis in MCF-7 human breast cancer cells. |
| 3250 | 9537589 | Here, we report that OCT elicits cytotoxic response in these cells, leading to apoptosis, which is associated with a rapid, time-dependent induction of wild-type p53 and an increase in Bax. |
| 3251 | 9537589 | There was no G1 cell-cycle arrest in these cells during OCT treatment as suggested by the decrease in G1/S ratio and the lack of induction of pRb and p21. |
| 3252 | 9537589 | Our data provide a rationale for utilizing SST analogs to treat SSTR-positive breast cancer cells expressing wild-type p53. |
| 3253 | 9537589 | Induction of wild-type p53, Bax, and acidic endonuclease during somatostatin-signaled apoptosis in MCF-7 human breast cancer cells. |
| 3254 | 9537589 | Here, we report that OCT elicits cytotoxic response in these cells, leading to apoptosis, which is associated with a rapid, time-dependent induction of wild-type p53 and an increase in Bax. |
| 3255 | 9537589 | There was no G1 cell-cycle arrest in these cells during OCT treatment as suggested by the decrease in G1/S ratio and the lack of induction of pRb and p21. |
| 3256 | 9537589 | Our data provide a rationale for utilizing SST analogs to treat SSTR-positive breast cancer cells expressing wild-type p53. |
| 3257 | 9568682 | A pancreatic clamp (somatostatin plus basal portal insulin and glucagon) was used to control the endocrine pancreas. |
| 3258 | 9588447 | In a final series of experiments, glucose-stimulated insulin release was profoundly inhibited by somatostatin, clonidine, and prostaglandin E2, but not by galanin. |
| 3259 | 9590418 | The number of gastrin- and somatostatin-immunoreactive cells was significantly decreased in both prediabetic and diabetic mice. |
| 3260 | 9604861 | During the latter period, somatostatin (489 pmol x kg(-1) x min(-1)) was given, along with intraportal insulin (7.2 pmol x kg(-1) x min(-1)) and glucagon (0.5 ng x kg(-1) x min(-1)). |
| 3261 | 9604870 | Octreotide prevents the early increase in renal insulin-like growth factor binding protein 1 in streptozotocin diabetic rats. |
| 3262 | 9604870 | The early renal growth in streptozotocin (STZ)-induced diabetic rats is preceded by a transient rise in renal tissue insulin-like growth factor (IGF)-I concentration. |
| 3263 | 9604870 | Administration of the long-acting somatostatin analog octreotide to STZ diabetic rats inhibits the early increase in kidney IGF-I and the increase in kidney size without affecting metabolic control. |
| 3264 | 9604870 | Renal IGF-I mRNA was significantly decreased to the same extent in both diabetic groups 2 and 7 days after the induction of diabetes, while renal IGF-I receptor (IGF-IR) mRNA was unchanged in rats from either group. |
| 3265 | 9604870 | Two days after induction of diabetes, renal insulin-like growth factor binding protein (IGFBP)-1 mRNA and 30-kDa IGFBPs (containing IGFBP-1) increased by 186 and 192%, respectively, in untreated diabetic animals compared with controls. |
| 3266 | 9604870 | We conclude that the well-known inhibitory effect of octreotide on the early increase in renal IGF-I concentration and renal size in diabetes may be mediated through a direct effect on renal IGFBP-1 levels. |
| 3267 | 9628246 | Thyrotropin-releasing hormone and somatostatin inhibit each others release in vitro in the rat retina. |
| 3268 | 9628246 | The effect of thyrotropin-releasing hormone (TRH), somatostatin (SS) or octreotide, an analogue of SS, on release of TRH or SS from the rat retina was studied in vitro. |
| 3269 | 9628246 | The SS release from the retina was inhibited by TRH, and the inhibitory effect of TRH on SS release from the rat retina was blocked by the addition of anti-TRH receptor antiserum immunoglobulin fraction. |
| 3270 | 9628246 | Thyrotropin-releasing hormone and somatostatin inhibit each others release in vitro in the rat retina. |
| 3271 | 9628246 | The effect of thyrotropin-releasing hormone (TRH), somatostatin (SS) or octreotide, an analogue of SS, on release of TRH or SS from the rat retina was studied in vitro. |
| 3272 | 9628246 | The SS release from the retina was inhibited by TRH, and the inhibitory effect of TRH on SS release from the rat retina was blocked by the addition of anti-TRH receptor antiserum immunoglobulin fraction. |
| 3273 | 9657067 | Stimulation of insulin and somatostatin release by two meglitinide analogs. |
| 3274 | 9657067 | The present study aimed to further insight into the effect of these agents on the secretion of insulin, glucagon, and somatostatin by the isolated perfused pancreas. |
| 3275 | 9657067 | Both repaglinide (0.01 microM) and A-4166 (1.0 microM) stimulated insulin and somatostatin release, but failed to affect glucagon output, from pancreases exposed to 5.6 mM D-glucose. |
| 3276 | 9657067 | Although repaglinide was tested at a concentration a hundred times lower than that of A-4166, the drug-induced increase in both insulin and somatostatin secretion persisted for a longer time after exposure to repaglinide, than to A-4166. |
| 3277 | 9657067 | First, they document that these drugs, although enhancing both insulin and somatostatin release, do not provoke an undesirable stimulation of glucagon secretion. |
| 3278 | 9657067 | Stimulation of insulin and somatostatin release by two meglitinide analogs. |
| 3279 | 9657067 | The present study aimed to further insight into the effect of these agents on the secretion of insulin, glucagon, and somatostatin by the isolated perfused pancreas. |
| 3280 | 9657067 | Both repaglinide (0.01 microM) and A-4166 (1.0 microM) stimulated insulin and somatostatin release, but failed to affect glucagon output, from pancreases exposed to 5.6 mM D-glucose. |
| 3281 | 9657067 | Although repaglinide was tested at a concentration a hundred times lower than that of A-4166, the drug-induced increase in both insulin and somatostatin secretion persisted for a longer time after exposure to repaglinide, than to A-4166. |
| 3282 | 9657067 | First, they document that these drugs, although enhancing both insulin and somatostatin release, do not provoke an undesirable stimulation of glucagon secretion. |
| 3283 | 9657067 | Stimulation of insulin and somatostatin release by two meglitinide analogs. |
| 3284 | 9657067 | The present study aimed to further insight into the effect of these agents on the secretion of insulin, glucagon, and somatostatin by the isolated perfused pancreas. |
| 3285 | 9657067 | Both repaglinide (0.01 microM) and A-4166 (1.0 microM) stimulated insulin and somatostatin release, but failed to affect glucagon output, from pancreases exposed to 5.6 mM D-glucose. |
| 3286 | 9657067 | Although repaglinide was tested at a concentration a hundred times lower than that of A-4166, the drug-induced increase in both insulin and somatostatin secretion persisted for a longer time after exposure to repaglinide, than to A-4166. |
| 3287 | 9657067 | First, they document that these drugs, although enhancing both insulin and somatostatin release, do not provoke an undesirable stimulation of glucagon secretion. |
| 3288 | 9657067 | Stimulation of insulin and somatostatin release by two meglitinide analogs. |
| 3289 | 9657067 | The present study aimed to further insight into the effect of these agents on the secretion of insulin, glucagon, and somatostatin by the isolated perfused pancreas. |
| 3290 | 9657067 | Both repaglinide (0.01 microM) and A-4166 (1.0 microM) stimulated insulin and somatostatin release, but failed to affect glucagon output, from pancreases exposed to 5.6 mM D-glucose. |
| 3291 | 9657067 | Although repaglinide was tested at a concentration a hundred times lower than that of A-4166, the drug-induced increase in both insulin and somatostatin secretion persisted for a longer time after exposure to repaglinide, than to A-4166. |
| 3292 | 9657067 | First, they document that these drugs, although enhancing both insulin and somatostatin release, do not provoke an undesirable stimulation of glucagon secretion. |
| 3293 | 9657067 | Stimulation of insulin and somatostatin release by two meglitinide analogs. |
| 3294 | 9657067 | The present study aimed to further insight into the effect of these agents on the secretion of insulin, glucagon, and somatostatin by the isolated perfused pancreas. |
| 3295 | 9657067 | Both repaglinide (0.01 microM) and A-4166 (1.0 microM) stimulated insulin and somatostatin release, but failed to affect glucagon output, from pancreases exposed to 5.6 mM D-glucose. |
| 3296 | 9657067 | Although repaglinide was tested at a concentration a hundred times lower than that of A-4166, the drug-induced increase in both insulin and somatostatin secretion persisted for a longer time after exposure to repaglinide, than to A-4166. |
| 3297 | 9657067 | First, they document that these drugs, although enhancing both insulin and somatostatin release, do not provoke an undesirable stimulation of glucagon secretion. |
| 3298 | 9662042 | In a quantitative analysis of nine organs consecutively recruited from adult donors, 15 percent of all beta cells were found in units with a diameter less than < 20 microm and without associated glucagon-, somatostatin-, or pancreatic polypeptide cells. |
| 3299 | 9662042 | The use of ductal cell markers such as cytokeratin 19, carbonic anhydrase-II and carbohydrate antigen 19.9 identified a close topographical association between ductal cells and budding beta cells; it also indicated that pancreatic lobules are composed of nearly one third ductal cells. |
| 3300 | 9663652 | Hypothalamic somatostatin release in response to incubation with 1 mM D-glucose was inhibited by the ionotropic glutamate receptor antagonists MK801, D-AP5 and DNQX but not by the metabotropic antagonists L-AP3 or MCPG. |
| 3301 | 9667523 | We describe the changes in B cells and calcitonin gene-related peptide (CGRP)-like immunoreactivity in the pancreatic islets of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of human non-insulin-dependent diabetes mellitus (NIDDM). |
| 3302 | 9667523 | In the OLETF rat pancreatic islets, CGRP immunoreactivity was seen in the nerve fibers with multiple varicosities and in endocrine cells that were identical to somatostatin-containing cells, but some somatostatin-immunoreactive cells lacked CGRP immunoreactivity. |
| 3303 | 9667523 | These results suggest that CGRP is a B-cell growth factor and probably an inhibitory factor for insulin secretion. |
| 3304 | 9720606 | We also performed experiments to characterise in more detail the mechanism of T. crispa-evoked insulin release by challenging it with insulin secretory antagonists viz. adrenaline, somatostatin, verapamil and nifedipine. |
| 3305 | 9741461 | Some cells stained positively for insulin; others stained positively for glucagon, somatostatin or chromagranin A. |
| 3306 | 9751489 | Glucagon-like peptide-1 (GLP-1) released from the intestine is a potent stimulator of glucose-dependent insulin secretion. |
| 3307 | 9751489 | GLP-1 secretion was stimulated in a dose-dependent fashion by activation of protein kinase A or C with forskolin or phorbol 12,13-dibutyrate, respectively (by 2.3 +/- 0.5-fold at 100 microM and 4.3 +/- 0.6-fold at 0.3 microM, respectively; P < 0.01-0.001). |
| 3308 | 9751489 | Of the regulatory peptides tested, only glucose-dependent insulinotropic peptide stimulated the release of GLP-1 (by 2.3 +/- 0.2-fold at 0.1 microM; P < 0.001); glucagon was without effect, and paradoxically, the inhibitory neuropeptide somatostatin-14 increased secretion slightly (by 1.6 +/- 0.3-fold at 0.01 microM; P < 0.05). |
| 3309 | 9792544 | Five protocols were used: insulin treatment, insulin deprivation, insulin deprivation with suppression of endogenous glucagon with somatostatin (SRIH) and growth hormone replacement, insulin deprivation with endogenous glucagon suppression with SRIH (no growth hormone replacement), and insulin deprivation with SRIH and a high level of glucagon replacement (no growth hormone replacement). |
| 3310 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3311 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3312 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3313 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3314 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3315 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3316 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3317 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3318 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3319 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3320 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3321 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3322 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3323 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3324 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3325 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3326 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3327 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3328 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3329 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3330 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3331 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3332 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3333 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3334 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3335 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3336 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3337 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3338 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3339 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3340 | 9813163 | Effects of imidazoline derivative RX871024 on insulin, glucagon, and somatostatin secretion from isolated perfused rat pancreas. |
| 3341 | 9813163 | The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. |
| 3342 | 9813163 | Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. |
| 3343 | 9813163 | RX871024, at 10 microM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. |
| 3344 | 9813163 | RX871024 (1 microM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. |
| 3345 | 9813163 | In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. |
| 3346 | 9843741 | After the 40-min basal period, somatostatin was given peripherally along with insulin (1.8 pmol. kg-1. min-1) and glucagon (0.65 ng. kg-1. min-1) intraportally. |
| 3347 | 9892224 | Western blot showed that islet tissue expressed HO-2, and confocal microscopy revealed that HO-2 resided in insulin, glucagon, somatostatin, and pancreatic polypeptide cells. |
| 3348 | 9892225 | The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4. |
| 3349 | 9892225 | SSTR1 was strongly colocalized with insulin in all beta-cells. |
| 3350 | 9892225 | SSTR2 was found in 46% of beta-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed. |
| 3351 | 9892225 | SSTR2 was strongly colocalized with glucagon in 89% of alpha-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of alpha-cells, respectively. |
| 3352 | 9892225 | SSTR3 was detected in occasional alpha-cells, and SSTR4 was absent. |
| 3353 | 9892225 | SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal delta-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few delta-cells, and SSTR4 was absent. |
| 3354 | 9892225 | These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets. |
| 3355 | 9892225 | Beta-cells, alpha-cells, and delta-cells each express multiple SSTR isoforms, beta-cells being rich in SSTR1 and SSTR5, alpha-cells in SSTR2, and delta-cells in SSTR5. |
| 3356 | 9892225 | Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is beta-cell selective, and SSTR2 is alpha-cell selective. |
| 3357 | 9892225 | SSTR5 is well expressed in beta-cells and delta-cells and moderately well expressed in alpha-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2. |
| 3358 | 9892225 | Subtype-selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds. |
| 3359 | 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. |
| 3360 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 3361 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 3362 | 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. |
| 3363 | 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. |
| 3364 | 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. |
| 3365 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 3366 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 3367 | 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. |
| 3368 | 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. |
| 3369 | 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. |
| 3370 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 3371 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 3372 | 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. |
| 3373 | 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. |
| 3374 | 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. |
| 3375 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 3376 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 3377 | 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. |
| 3378 | 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. |
| 3379 | 10026192 | Characterization of a mutant pancreatic eIF-2alpha kinase, PEK, and co-localization with somatostatin in islet delta cells. |
| 3380 | 10026192 | Phosphorylation of eukaryotic translation initiation factor-2alpha (eIF-2alpha) is one of the key steps where protein synthesis is regulated in response to changes in environmental conditions. |
| 3381 | 10026192 | The phosphorylation is carried out in part by three distinct eIF-2alpha kinases including mammalian double-stranded RNA-dependent eIF-2alpha kinase (PKR) and heme-regulated inhibitor kinase (HRI), and yeast GCN2. |
| 3382 | 10026192 | We report the identification and characterization of a related kinase, PEK, which shares common features with other eIF-2alpha kinases including phosphorylation of eIF-2alpha in vitro. |
| 3383 | 10026192 | We show that human PEK is regulated by different mechanisms than PKR or HRI. |
| 3384 | 10026192 | In contrast to PKR or HRI, which are dependent on autophosphorylation for their kinase activity, a point mutation that replaced the conserved Lys-614 with an alanine completely abolished the eIF-2alpha kinase activity, whereas the mutant PEK was still autophosphorylated when expressed in Sf-9 cells. |
| 3385 | 10026192 | Consistent with the high levels of mRNA in pancreas, the PEK protein was only detected in human pancreatic islets, and the kinase co-localized with somatostatin, a pancreatic delta cell-specific hormone. |
| 3386 | 10026192 | Characterization of a mutant pancreatic eIF-2alpha kinase, PEK, and co-localization with somatostatin in islet delta cells. |
| 3387 | 10026192 | Phosphorylation of eukaryotic translation initiation factor-2alpha (eIF-2alpha) is one of the key steps where protein synthesis is regulated in response to changes in environmental conditions. |
| 3388 | 10026192 | The phosphorylation is carried out in part by three distinct eIF-2alpha kinases including mammalian double-stranded RNA-dependent eIF-2alpha kinase (PKR) and heme-regulated inhibitor kinase (HRI), and yeast GCN2. |
| 3389 | 10026192 | We report the identification and characterization of a related kinase, PEK, which shares common features with other eIF-2alpha kinases including phosphorylation of eIF-2alpha in vitro. |
| 3390 | 10026192 | We show that human PEK is regulated by different mechanisms than PKR or HRI. |
| 3391 | 10026192 | In contrast to PKR or HRI, which are dependent on autophosphorylation for their kinase activity, a point mutation that replaced the conserved Lys-614 with an alanine completely abolished the eIF-2alpha kinase activity, whereas the mutant PEK was still autophosphorylated when expressed in Sf-9 cells. |
| 3392 | 10026192 | Consistent with the high levels of mRNA in pancreas, the PEK protein was only detected in human pancreatic islets, and the kinase co-localized with somatostatin, a pancreatic delta cell-specific hormone. |
| 3393 | 10102687 | In the presence of soluble laminin-1, however, the number of beta-cells increased linearly by 60-fold without an increase in the total cell number; glucagon-positive cell number was unchanged, and somatostatin and pancreatic polypeptide-positive cells were not detected. |
| 3394 | 10206182 | We studied the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P in response to electrical field stimulation from isolated tracheas of rats following 4 weeks of streptozotocin (50 mg/kg i.v.) |
| 3395 | 10206182 | Field stimulation (40 V, 0.1 ms, 10 Hz for 120 s) increased the release of somatostatin, CGRP and substance P from the baseline 0.18+/-0.029, 0.17+/-0.027, and 1.77+/-0.086 to 0.51+/-0.022, 0.69+/-0.115, and 5.96+/-0.377 in control preparations and 0.31+/-0.081, 0.41+/-0.142, and 3.14+/-0.443 fmol/mg wet tissue weight in preparations from diabetic rats as measured by radioimmunoassay (control vs. diabetic P<0.01 for each). |
| 3396 | 10206182 | We studied the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P in response to electrical field stimulation from isolated tracheas of rats following 4 weeks of streptozotocin (50 mg/kg i.v.) |
| 3397 | 10206182 | Field stimulation (40 V, 0.1 ms, 10 Hz for 120 s) increased the release of somatostatin, CGRP and substance P from the baseline 0.18+/-0.029, 0.17+/-0.027, and 1.77+/-0.086 to 0.51+/-0.022, 0.69+/-0.115, and 5.96+/-0.377 in control preparations and 0.31+/-0.081, 0.41+/-0.142, and 3.14+/-0.443 fmol/mg wet tissue weight in preparations from diabetic rats as measured by radioimmunoassay (control vs. diabetic P<0.01 for each). |
| 3398 | 10207508 | It has occasionally been suggested that GH directly suppresses circulating IGFBP-1 levels, although it is generally believed that such an effect is secondary to a GH-induced increase in insulin levels. |
| 3399 | 10207508 | GH bolus caused a small but significant decrease in plasma IGFBP-1 concentrations without changes in insulin [IGFBP-1 (microgram/l): 2.6 +/- 0.3 (GH) vs 3.2 +/- 0.4 (placebo), P < 0.05]. |
| 3400 | 10207508 | Conversely, a 28-h somatostatin infusion with and without GH administration during fasting in normal subjects yielded higher IGFBP-1 levels in the non-GH substituted study [50.5 +/- 5.3 (GH-suppression) vs 22.6 +/- 5.6 (GH-substitution), P < 0.01], comparable with an increased concentration of IGFBP-1 during fasting in GH-deficient patients without usual GH substitution [23.4 +/- 7.6 (GH pause) vs 14.1 +/- 4.9 (GH substitution), P < 0.01]. |
| 3401 | 10207508 | Finally, a significant rebound increase in IGFBP-1 level in response to insulin induced hypoglycemia was only observed among GH-deficient patients, but not in control subjects, the latter of whom responded to hypoglycemia with a significant increase in serum GH levels [23.2 +/- 7.2 (GHDA) vs 2.5 +/- 0.3 (controls), P < 0.01]. |
| 3402 | 10207508 | In conclusion, a suppressive effect of GH on IGFBP-1 appears to be unmasked in the presence of low or suppressed insulin levels, making GH a potential regulator of IGF-1 bioactivity in a hitherto unrecognized way. |
| 3403 | 10225369 | Subcutaneous injection of 7-benzylidenenaltrexone (0.1, 0.3 and 1 mg/kg), an antagonist of delta1-opioid receptors, had no significant effect on either somatostatin-, bradykinin- or prostaglandin F2alpha-induced nociceptive responses in non-diabetic mice. 7-Benzylidenenaltrexone (0.1 and 0.3 mg/kg, s.c.) also had no significant effect on somatostatin- or prostaglandin F2alpha-induced nociceptive responses in diabetic mice. |
| 3404 | 10225369 | These results suggest that a spinal delta1-opioid receptor-mediated endogenous antinociceptive system may inhibit the bradykinin-mediated nociceptive responses in the second phase of the formalin-induced nociceptive response in diabetic mice. |
| 3405 | 10226151 | Understanding the calcium signals underlying glucagon and somatostatin secretion may be of importance in the treatment of non-insulin-dependent diabetes mellitus since both glucagon and somatostatin appear to regulate insulin release in a paracrine fashion. |
| 3406 | 10226172 | This study investigates the effects of the islet hormones, insulin (Ins), glucagon (Glu) and somatostatin (Som) with cholecystokinin octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration [Ca2+]i and their pattern of distribution in the isolated pancreas of normal and diabetic rats. |
| 3407 | 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. |
| 3408 | 10329988 | Somatostatin was given peripherally with insulin (4-fold basal) and glucagon (basal) intraportally. |
| 3409 | 10362614 | Somatostatin was infused, and insulin and glucagon were replaced intraportally at fourfold basal and basal rates, respectively. |
| 3410 | 10368987 | Fifteen weeks after transplantation into the subcutaneous region, insulin, glucagon, somatostatin and pancreatic polypeptide-immunoreactive cells were observed in many parts of the graft. |
| 3411 | 10404795 | A prandial glucose infusion (containing 35 g glucose) was started at 1000 h, and the variable insulin infusion was replaced by a constant infusion of insulin (0.25 mU/ kg x min), somatostatin (60 ng/kg x min), glucagon (0.65 ng/kg x min), and GH (3 ng/kg x min) to maintain hormone concentrations at constant basal levels. |
| 3412 | 10431790 | Samples (n = 3 per age group) from the dorsal and ventral pancreas of 5-, 12- and 24-week-old hybrid pigs were fixed in formal saline, processed in paraffin wax and stained with an avidin/biotin immunohistochemical kit for insulin, glucagon, somatostatin and pancreatic polypeptide. |
| 3413 | 10458104 | Histopathological and immunohistochemical analysis of the endocrine and exocrine pancreas in twelve cattle with insulin-dependent diabetes mellitus (IDDM). |
| 3414 | 10458104 | Histological and immunohistochemical studies were carried out on the pancreas of twelve cattle of insulin-dependent diabetes mellitus (IDDM). |
| 3415 | 10458104 | Immunohistochemical examination revealed that the atrophied islet cells did not react to anti-insulin antibody, but occasionally reacted to anti-glucagon or somatostatin antibodies. |
| 3416 | 10458104 | Islet fibrosis was due to the proliferation of collagen fibers reactive to both anti-collagen type I and type III antibodies. |
| 3417 | 10495291 | Adult pancreatic islets comprise four cell types, alpha, beta, delta and PP, expressing glucagon, insulin, somatostatin and pancreatic-polypeptide, respectively, arising from cell lineages whose relationships during endocrine pancreas differentiation are still uncertain [Edlund, 1998. |
| 3418 | 10495291 | Results showed that in the zebrafish pancreatic primordium (a) insulin is the first hormone gene to be expressed, and (b) somatostatin colocalizes with insulin while glucagon-expressing cells, since their appearance, are distinct from insulin- or insulin/somatostatin-expressing cells. |
| 3419 | 10495291 | Notably, both somatostatin and glucagon, but not insulin, are first expressed in extrapancreatic regions. |
| 3420 | 10495291 | Adult pancreatic islets comprise four cell types, alpha, beta, delta and PP, expressing glucagon, insulin, somatostatin and pancreatic-polypeptide, respectively, arising from cell lineages whose relationships during endocrine pancreas differentiation are still uncertain [Edlund, 1998. |
| 3421 | 10495291 | Results showed that in the zebrafish pancreatic primordium (a) insulin is the first hormone gene to be expressed, and (b) somatostatin colocalizes with insulin while glucagon-expressing cells, since their appearance, are distinct from insulin- or insulin/somatostatin-expressing cells. |
| 3422 | 10495291 | Notably, both somatostatin and glucagon, but not insulin, are first expressed in extrapancreatic regions. |
| 3423 | 10495291 | Adult pancreatic islets comprise four cell types, alpha, beta, delta and PP, expressing glucagon, insulin, somatostatin and pancreatic-polypeptide, respectively, arising from cell lineages whose relationships during endocrine pancreas differentiation are still uncertain [Edlund, 1998. |
| 3424 | 10495291 | Results showed that in the zebrafish pancreatic primordium (a) insulin is the first hormone gene to be expressed, and (b) somatostatin colocalizes with insulin while glucagon-expressing cells, since their appearance, are distinct from insulin- or insulin/somatostatin-expressing cells. |
| 3425 | 10495291 | Notably, both somatostatin and glucagon, but not insulin, are first expressed in extrapancreatic regions. |
| 3426 | 10506661 | Osteopontin is an autoantigen of the somatostatin cells in human islets: identification by screening random peptide libraries with sera of patients with insulin-dependent diabetes mellitus. |
| 3427 | 10506661 | The CH1p mimotope was detected in somatostatin cells of human islets and experimentally raised anti-osteopontin antibodies or human sera positive for the phagotope, detected a similar subpopulation of islet cells. |
| 3428 | 10506661 | Osteopontin is an autoantigen of the somatostatin cells in human islets: identification by screening random peptide libraries with sera of patients with insulin-dependent diabetes mellitus. |
| 3429 | 10506661 | The CH1p mimotope was detected in somatostatin cells of human islets and experimentally raised anti-osteopontin antibodies or human sera positive for the phagotope, detected a similar subpopulation of islet cells. |
| 3430 | 10509878 | The neuroendocrine peptides investigated were peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), neurotensin, and galanin. |
| 3431 | 10509878 | In the antrum, VIP, NPY, and galanin concentrations were all significantly lower in prediabetic and diabetic NOD mice than in controls. |
| 3432 | 10509878 | In the colon, the concentrations of PYY, somatostatin, VIP, NPY, and galanin were lower in prediabetic and diabetic NOD mice than in controls. |
| 3433 | 10509878 | The neuroendocrine peptides investigated were peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), neurotensin, and galanin. |
| 3434 | 10509878 | In the antrum, VIP, NPY, and galanin concentrations were all significantly lower in prediabetic and diabetic NOD mice than in controls. |
| 3435 | 10509878 | In the colon, the concentrations of PYY, somatostatin, VIP, NPY, and galanin were lower in prediabetic and diabetic NOD mice than in controls. |
| 3436 | 10573553 | After a sampling period with no experimental intervention (basal period), conscious dogs deprived of food for 42 h received somatostatin, intraportal infusions of insulin (3-fold basal) and glucagon (basal), and a peripheral infusion of glucose to increase the hepatic glucose load 1.5-fold basal for 240 min. |
| 3437 | 10604126 | The aim of this paper is to review five recent studies performed at the National Institutes of Health in patients with Zollinger-Ellison syndrome to define the role of somatostatin receptor scintigraphy. |
| 3438 | 10604126 | In conclusion, Somatostatin receptor scintigraphy is now the imaging method of choice in patients with Zollinger-Ellison syndrome for preoperative primary tumour localization, detection of bone or liver metastases, and to distinguish small liver metastases from small hepatic haemangiomas. |
| 3439 | 10604126 | The aim of this paper is to review five recent studies performed at the National Institutes of Health in patients with Zollinger-Ellison syndrome to define the role of somatostatin receptor scintigraphy. |
| 3440 | 10604126 | In conclusion, Somatostatin receptor scintigraphy is now the imaging method of choice in patients with Zollinger-Ellison syndrome for preoperative primary tumour localization, detection of bone or liver metastases, and to distinguish small liver metastases from small hepatic haemangiomas. |
| 3441 | 10657496 | Distribution of calcitonin-gene-related peptide, neuropeptide-Y, vasoactive intestinal polypeptide, cholecystokinin-8, substance P and islet peptides in the pancreas of normal and diabetic rats. |
| 3442 | 10657496 | This study investigates whether there is a change in the pattern of distribution of neuropeptides including calcitonin-gene-related peptide (CGRP), neuropeptide-Y (NPY), vasoactive intestinal polypeptide (VIP), cholecystokinin-octapeptide (CCK-8), substance P (SP), and islet peptides including insulin (INS), glucagon (GLU), somatostatin (SOM) and pancreatic polypeptide (PP) in the pancreas of streptozotocin (STZ)-diabetic rats. |
| 3443 | 10657496 | After the onset of diabetes, the pattern of distribution of INS, GLU, SOM and PP cells was deranged. |
| 3444 | 10657496 | In conclusion, CGRP, NPY, VIP, CCK-8 and SP are well distributed in both normal and diabetic pancreas. |
| 3445 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3446 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3447 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3448 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3449 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3450 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3451 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3452 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3453 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3454 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3455 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3456 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3457 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3458 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3459 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3460 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3461 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3462 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3463 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3464 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3465 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3466 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3467 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3468 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3469 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3470 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3471 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3472 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3473 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3474 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3475 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 3476 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 3477 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 3478 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 3479 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 3480 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 3481 | 10701496 | In neonatal pancreas, 18% of the insulin-positive cells co-stained for CK7, thus being protodifferentiated. |
| 3482 | 10701496 | NPCCs also contained protodifferentiated cells; insulin/PP and insulin/somatostatin co-stained cells were more common than insulin/glucagon cells. |
| 3483 | 10701496 | The starting NPCCs consisted of 17% insulin-staining cells, but the grafts of mice with reversed diabetes consisted of 94% beta cells, with some co-stained for CK7, indicating that the grafts still contained immature cells. |
| 3484 | 10710496 | Individualized doses of insulin were infused to maintain euglycemia during pancreatic clamps by use of somatostatin (250 microg/h), glucagon (1.0 ng. kg(-1). min(-1)), and growth hormone (GH) (3.0 ng. kg(-1). min(-1)) infusions without need for exogenous glucose. |
| 3485 | 10720081 | In the present study, 10 patients (3 men and 7 women, aged 48-63 yr) with an adrenal mass discovered serendipitously underwent, on separate occasions, a GHRH injection alone or combined with an infusion of the functional somatostatin antagonist, arginine. |
| 3486 | 10720081 | In summary, the present data suggest that in patients with incidental adrenal adenomas the GH response to GHRH is blunted due to increased somatostatinergic tone, as it can be restored to normal by pretreatment with the functional somatostatin antagonist arginine. |
| 3487 | 10720081 | In the present study, 10 patients (3 men and 7 women, aged 48-63 yr) with an adrenal mass discovered serendipitously underwent, on separate occasions, a GHRH injection alone or combined with an infusion of the functional somatostatin antagonist, arginine. |
| 3488 | 10720081 | In summary, the present data suggest that in patients with incidental adrenal adenomas the GH response to GHRH is blunted due to increased somatostatinergic tone, as it can be restored to normal by pretreatment with the functional somatostatin antagonist arginine. |
| 3489 | 10766455 | Transforming growth factor alpha (TGF-alpha) increased basal, but not glucose-stimulated, insulin release and insulin content in islets cultured in low glucose. |
| 3490 | 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. |
| 3491 | 10766455 | The addition of gastrin to TGF-alpha did not affect the results obtained with the latter peptide. |
| 3492 | 10766455 | Gastrin-releasing peptide failed to influence basal or glucose-responsive insulin secretory rates, and insulin content, at either glucose concentration during culture. |
| 3493 | 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. |
| 3494 | 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. |
| 3495 | 10766455 | To the contrary, GLP-1, but not GIP, increased the content of insulin in islets cultured in low glucose. |
| 3496 | 10766455 | We suggest that GH and TGF-alpha stimulate, while somatostatin, through paracrine interaction, may inhibit, these processes. |
| 3497 | 10766455 | Transforming growth factor alpha (TGF-alpha) increased basal, but not glucose-stimulated, insulin release and insulin content in islets cultured in low glucose. |
| 3498 | 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. |
| 3499 | 10766455 | The addition of gastrin to TGF-alpha did not affect the results obtained with the latter peptide. |
| 3500 | 10766455 | Gastrin-releasing peptide failed to influence basal or glucose-responsive insulin secretory rates, and insulin content, at either glucose concentration during culture. |
| 3501 | 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. |
| 3502 | 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. |
| 3503 | 10766455 | To the contrary, GLP-1, but not GIP, increased the content of insulin in islets cultured in low glucose. |
| 3504 | 10766455 | We suggest that GH and TGF-alpha stimulate, while somatostatin, through paracrine interaction, may inhibit, these processes. |
| 3505 | 10826999 | Insulin clamp studies (3 mU. kg(-1). min(-1) with somatostatin) were performed to assess hepatic insulin sensitivity. |
| 3506 | 10863992 | The precise interplay of a heterogeneous group of cell populations (beta, alpha, delta and PP cells) results in the fine-tuned release of counterbalanced hormones (insulin, glucagon, somatostatin and pancreatic polypeptide respectively). |
| 3507 | 10868939 | Epithelial cells in these pancreatic anlage were detected by cytokeratin staining, and differentiated endocrine cells were detected by insulin, glucagon, somatostatin, and pancreatic polypeptide staining. |
| 3508 | 10868939 | Newly differentiated endocrine cells coexpress insulin, glucagon, and somatostatin; endocrine differentiation starts within the central ducts of the epithelial mass, at a distance from the dense peripancreatic surrounding mesenchyme. |
| 3509 | 10868939 | Epithelial cells in these pancreatic anlage were detected by cytokeratin staining, and differentiated endocrine cells were detected by insulin, glucagon, somatostatin, and pancreatic polypeptide staining. |
| 3510 | 10868939 | Newly differentiated endocrine cells coexpress insulin, glucagon, and somatostatin; endocrine differentiation starts within the central ducts of the epithelial mass, at a distance from the dense peripancreatic surrounding mesenchyme. |
| 3511 | 10868962 | The extracellular calcium-sensing receptor on human beta-cells negatively modulates insulin secretion. |
| 3512 | 10868962 | Immunocytochemistry using an antibody against the extracellular region of CaR showed extensive immunoreactivity in insulin- and glucagon-containing cells but not in somatostatin-containing cells. |
| 3513 | 10868962 | The transduction mechanism that mediates this inhibitory effect is unknown, but our results suggest that it is unlikely to be through the adenylate cyclase-cyclic AMP pathway or through the phospholipase C-IP3 pathway. |
| 3514 | 10871195 | Assessment of C-peptide kinetics can be performed without infusion of somatostatin, because the endogenous insulin concentration remains constant. |
| 3515 | 10871195 | Assessment of C-peptide kinetics with and without infusion of somatostatin results in nearly identical secretion rates for insulin during an oral glucose tolerance test. |
| 3516 | 10871195 | Assessment of C-peptide kinetics can be performed without infusion of somatostatin, because the endogenous insulin concentration remains constant. |
| 3517 | 10871195 | Assessment of C-peptide kinetics with and without infusion of somatostatin results in nearly identical secretion rates for insulin during an oral glucose tolerance test. |
| 3518 | 10871199 | Effect of glucagon-like peptide 1(7-36) amide on glucose effectiveness and insulin action in people with type 2 diabetes. |
| 3519 | 10871199 | Although it is well established that glucagon-like peptide 1(7-36) amide (GLP-1) is a potent stimulator of insulin secretion, its effects on insulin action and glucose effectiveness are less clear. |
| 3520 | 10871199 | To determine whether GLP-1 increases insulin action and glucose effectiveness, subjects with type 2 diabetes were studied on two occasions. |
| 3521 | 10871199 | On the morning of study, either GLP-1 (1.2 pmol x kg(-1) x min(-1)) or saline were infused along with somatostatin and replacement amounts of glucagon. |
| 3522 | 10871199 | The increase in glucose concentration was virtually identical on the GLP-1 and saline study days during both the basal (1.21 +/- 0.15 vs. 1.32 +/- 0.19 mol/l per 6 h) and prandial (0.56 +/- 0.14 vs. 0.56 +/- 0.10 mol/l per 6 h) insulin infusions. |
| 3523 | 10871199 | During both the basal and prandial insulin infusions, glucose disappearance promptly increased after initiation of the glucose infusion to rates that did not differ on the GLP-1 and saline study days. |
| 3524 | 10871199 | Suppression of endogenous glucose production also was comparable on the GLP-1 and saline study days during both the basal (-2.7 +/- 0.3 vs. -3.1 +/- 0.2 micromol/kg) and prandial (-3.1 +/- 0.4 vs. -3.0 +/- 0.6 pmol/kg) insulin infusions. |
| 3525 | 10871199 | We conclude that when insulin and glucagon concentrations are matched, GLP-1 has negligible effects on either insulin action or glucose effectiveness in people with type 2 diabetes. |
| 3526 | 10871199 | These data strongly support the concept that GLP-1 improves glycemic control in people with type 2 diabetes by increasing insulin secretion, by inhibiting glucagon secretion, and by delaying gastric emptying rather than by altering extrapancreatic glucose metabolism. |
| 3527 | 10905476 | To exclude interaction of FFAs with insulin secretion, the study was repeated at fasting plasma insulin (approximately 35 pmol/l) and glucagon (approximately 90 ng/ml) concentrations using somatostatin-insulin-glucagon clamps. |
| 3528 | 10909980 | With the aim of investigating glucose-mediated glucose disposal (glucose effectiveness [GE]) in 15 (3 female and 12 male subjects) insulin-resistant normoglycemic relatives of patients with type 2 diabetes (DM2), and 15 age-, sex-, and BMI-matched control subjects without a family history of DM2, we performed 2 studies: 1) a 5-h euglycemic near-normoinsulinemic pancreatic clamp with somatostatin (360 microg/h), insulin (0.25 mU x kg(-1) x min(-1)), glucagon (0.5 ng x kg(-1) x min(-1)), growth hormone (6 ng x kg(-1) x min(-1)), and tritiated glucose infusion and indirect calorimetry; and 2) on a separate day, an identical 5-h clamp but at hyperglycemia (approximately 12 mmol/l) over the last 2 h. |
| 3529 | 10950818 | We report that in patients with type 2 diabetes, 1) as in nondiabetic humans, insulin is secreted in discrete insulin secretory bursts; 2) the frequency of pulsatile insulin secretion is normal; 3) the insulin pulse mass is diminished, leading to decreased insulin secretion, but this defect can be overcome acutely by beta-cell rest with somatostatin; 4) the reported loss of orderliness of insulin secretion, attenuated first-phase insulin secretion, and elevated proinsulin-to-insulin molar ratio also respond favorably to overnight inhibition by somatostatin. |
| 3530 | 10967107 | During pancreatic development, the paired homeodomain transcription factor PAX4 is required for the differentiation of the insulin-producing beta cells and somatostatin-producing delta cells. |
| 3531 | 10967107 | Serial deletions through this region reveal the presence of positive elements that bind several pancreatic transcription factors as follows: the POU homeodomain factor HNF1alpha, the orphan nuclear receptor HNF4alpha, the homeodomain factor PDX1, and a heterodimer composed of two basic helix-loop-helix factors. |
| 3532 | 11016446 | Somatostatin co-infusion with glucose in Po-mice prevented hypoglycemia without modifying the plasma insulin profile. |
| 3533 | 11016447 | Plasma insulin profiles during the infusion period were similar in control and RIPGLUT1 x GLUT2-/- Po- and Fe-mice. |
| 3534 | 11016447 | Finally, co-infusion of somatostatin with glucose prevented development of hypoglycemia in control Po-mice, but it did not affect the glycemia or insulinemia of RIPGLUT1 x GLUT2-/- Po-mice. |
| 3535 | 11016447 | Together, our data demonstrate that GLUT2 is required for the function of the hepatoportal glucose sensor and that somatostatin could inhibit the glucose signal by interfering with GLUT2-expressing sensing units. |
| 3536 | 11016447 | Plasma insulin profiles during the infusion period were similar in control and RIPGLUT1 x GLUT2-/- Po- and Fe-mice. |
| 3537 | 11016447 | Finally, co-infusion of somatostatin with glucose prevented development of hypoglycemia in control Po-mice, but it did not affect the glycemia or insulinemia of RIPGLUT1 x GLUT2-/- Po-mice. |
| 3538 | 11016447 | Together, our data demonstrate that GLUT2 is required for the function of the hepatoportal glucose sensor and that somatostatin could inhibit the glucose signal by interfering with GLUT2-expressing sensing units. |
| 3539 | 11024017 | Direct double-labeling immunofluorescence histochemistry combined with confocal laser microscopy revealed the presence of Munc-18 immunoreactivity in insulin-, glucagon-, pancreatic polypeptide-, and somatostatin-containing cells. |
| 3540 | 11036875 | Their insulin resistance (GIR) substantially recovered concomitant with an increase in slope "a" after pretreatment with somatostatin analogue in two cases studied, suggesting possible suppression of hepatic glucose production through lowering of plasma glucagon concentrations. |
| 3541 | 11095432 | On both occasions, somatostatin was infused at a rate of 4.3 nmol/kg x min, and insulin was infused in a diabetic insulin profile. |
| 3542 | 11135321 | In order to further investigate islet function and secretion during early development of pancreatic cancer, we measured the concentrations of insulin, glucagon, somatostatin, and islet amyloid polypeptide (IAPP) in plasma, pancreatic tissue, and secretin-stimulated pancreatic juice at 12 and 27 weeks after the ductal-cell-specific carcinogen, BOP had been used to induce tumors in Syrian golden hamsters. |
| 3543 | 11137179 | Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. |
| 3544 | 11137181 | Aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue that inhibits growth hormone, insulin and glucagon secretion and improves glycaemic control in insulin dependent diabetic patients was able to exert similar effects in insulin treated type 2 diabetic patients with chronic renal failure who have high plasma glucagon levels. |
| 3545 | 11147801 | The two somatostatin experiments were identical in terms of hormone replacement (except for GH), meaning that somatostatin, insulin, glucagon and GH were administered for 28 h; during the last 4 h, substrate metabolism was investigated. |
| 3546 | 11159839 | This receptor was initially cloned in rat and human and designated SLC-1 because of its homology to the somatostatin receptor. |
| 3547 | 11202572 | With time after transplantation, increasing amounts of insulin immunoperoxidase staining was seen together with chromogranin and somatostatin staining. |
| 3548 | 11230804 | Inhibition of human pancreatic islet insulin release by receptor-selective somatostatin analogs directed to somatostatin receptor subtype 5. |
| 3549 | 11230804 | Somatostatin (SS)-14 and SS28 are produced by pancreatic D cells and gut mucosa and inhibit pancreatic islet insulin and glucagon release. |
| 3550 | 11230804 | Glucose-stimulated insulin secretion in human islets incubated for 1 hr at 20 mM glucose, and in islets cultured for 24 hr at a near-physiological (6.1 mM) glucose concentration, was inhibited (<50% of the control) by SSTR5-specific analogs and by SS14 and SS28. |
| 3551 | 11230804 | SS14, SS28, and different SSTR5 preferential analogs also inhibited islet amyloid polypeptide release during the 24-hr culture. |
| 3552 | 11230804 | On the other hand, a group of SSTR2-selective analogs failed to inhibit insulin release. |
| 3553 | 11230804 | Analysis by reverse transcription-polymerase chain reaction indicated that human islets express similar amounts of SSTR2 and SSTR5 mRNAs, while human pancreatic ductal cells express much lower levels of these mRNAs. |
| 3554 | 11230804 | In conclusion, our data suggest that SSTR5 is an important mediator of the insulin inhibitory action of SS in cultured human islets. |
| 3555 | 11234631 | Plasma concentrations of insulin, insulin-like growth factor-I, thyroxine and 3,5,3'-triiodothyronine were lower than normal, whereas those of glucagon were higher than normal. |
| 3556 | 11234631 | Immunohistochemical examination of the pancreas showed that very few insulin-, glucagon-, somatostatin- and pancreatic polypeptide, insulin-like growth factor-I and adrenomedullin-producing islet cells were present. |
| 3557 | 11246871 | Nestin-positive cells within pancreatic islets express neither the hormones insulin, glucagon, somatostatin, or pancreatic polypeptide nor the markers of vascular endothelium or neurons, such as collagen IV and galanin. |
| 3558 | 11246871 | Nestin-positive cells in the islets and in pancreatic ducts are distinct from ductal epithelium because they do not express the ductal marker cytokeratin 19 (CK19). |
| 3559 | 11246871 | Upon confluence, they are able to differentiate into cells that express liver and exocrine pancreas markers, such as alpha-fetoprotein and pancreatic amylase, and display a ductal/endocrine phenotype with expression of CK19, neural-specific cell adhesion molecule, insulin, glucagon, and the pancreas/duodenum specific homeodomain transcription factor, IDX-1. |
| 3560 | 11249067 | With high glucose, insulin release was markedly potentiated by forskolin, glucagon, glucagon-like peptide-1, and arginine and inhibited by somatostatin, the Ca2+ channel blocker nitrendipine, and the ATP-sensitive K+ channel opener diazoxide. |
| 3561 | 11265260 | Elevations of insulin, C-peptide, and leptin concentrations were found in both siblings. |
| 3562 | 11265260 | Insulin resistance was also demonstrated in both siblings using the modified insulin suppression test with constant infusion of somatostatin and exogenous insulin. |
| 3563 | 11269891 | A comparison of insulin suppression tests performed with somatostatin and octreotide with particular reference to tolerability. |
| 3564 | 11269891 | To evaluate the tolerability of insulin suppression test (IST) using octreotide instead of somatostatin, we compared the steady-state plasma glucose (SSPG) values and the safety during and after the test in 17 normal volunteers. |
| 3565 | 11269891 | The SSPG and the steady-state plasma insulin (SSPI) values reached during IST were similar, irrespective of the use of somatostatin or octreotide. |
| 3566 | 11269891 | A comparison of insulin suppression tests performed with somatostatin and octreotide with particular reference to tolerability. |
| 3567 | 11269891 | To evaluate the tolerability of insulin suppression test (IST) using octreotide instead of somatostatin, we compared the steady-state plasma glucose (SSPG) values and the safety during and after the test in 17 normal volunteers. |
| 3568 | 11269891 | The SSPG and the steady-state plasma insulin (SSPI) values reached during IST were similar, irrespective of the use of somatostatin or octreotide. |
| 3569 | 11269891 | A comparison of insulin suppression tests performed with somatostatin and octreotide with particular reference to tolerability. |
| 3570 | 11269891 | To evaluate the tolerability of insulin suppression test (IST) using octreotide instead of somatostatin, we compared the steady-state plasma glucose (SSPG) values and the safety during and after the test in 17 normal volunteers. |
| 3571 | 11269891 | The SSPG and the steady-state plasma insulin (SSPI) values reached during IST were similar, irrespective of the use of somatostatin or octreotide. |
| 3572 | 11272179 | Intrauterine growth retardation and postnatal acute diabetes result from insulin deficiency in double homozygous null mutants for Ins1 and Ins2 (Duvillié B, et al., Proc. |
| 3573 | 11272179 | Immunocytochemical analysis of the islets showed normal distribution of the endocrine cells producing insulin, glucagon, somatostatin, or pancreatic polypeptide. |
| 3574 | 11272179 | Analysis of the expression of the functional insulin gene in Ins1-/- or Ins2-/- mice revealed a dramatic increase of Ins1 transcripts in Ins2-/- mutants. |
| 3575 | 11291426 | Contribution of growth hormone-releasing hormone and somatostatin to decreased growth hormone secretion in elderly men. |
| 3576 | 11334439 | This study examines, at the ultrastructural level, whether the fetal porcine endocrine pancreas (insulin, glucagon, somatostatin, and pancreatic polypeptide [PP]- and islet amyloid polypeptide [IAPP]-containing cells) develops normally after transplantation under the kidney capsule in athymic mice. |
| 3577 | 11350061 | In all mouse thymuses, preproinsulin 1 and GAD 65 were undetectable, preproinsulin 2 and proglucagon showed low expression, whereas that of GAD 67 and somatostatin were high. |
| 3578 | 11350782 | During somatostatin, replacement growth hormone, and glucagon infusions, insulin was infused to achieve moderate (approximately 75 pmol/l) and high (approximately 150 pmol/l) physiological insulin levels. |
| 3579 | 11375325 | Six healthy overnight-fasted subjects were infused for 4 h with somatostatin (0.1 micromol. kg(-1). min(-1)) and insulin (240 pmol. m(-2). min(-1)). |
| 3580 | 11375336 | Endogenous hormone secretion was inhibited with somatostatin, and insulin was infused to maintain plasma concentrations at approximately 300 pmol/l (i.e., twofold higher than our previous experiments). |
| 3581 | 11440276 | Inhibition of growth hormone secretion and the subsequent suppression of insulin-like growth factor 1 (IGF-1) production by somatostatin has been suggested as the mechanism of action, however, in vitro studies suggest that somatostatin analogues suppress endothelial cell growth through a direct, somatostatin receptor-mediated inhibition of pro-survival signaling pathways. |
| 3582 | 11440279 | Retinal photocoagulation does not influence intraocular levels of IGF-I, IGF-II and IGF-BP3 in proliferative diabetic retinopathy-evidence for combined treatment of PDR with somatostatin analogues and retinal photocoagulation? |
| 3583 | 11440279 | Reduced levels of VEGF/VPF might result in an improved function of the blood-retina barrier and cause a decrease of blood derived intraocular growth factors such as IGF-I. |
| 3584 | 11440279 | This study investigates whether retinal photocoagulation is able to normalize the concentrations of IGF-I, IGF-II and IGF-BP3 in the vitreous humor of patients undergoing vitrectomy. |
| 3585 | 11440279 | IGF-I, IGF-II, IGF-BP3 and albumin were determined by immunological methods and were confirmed to be increased in patients with PDR compared to controls. |
| 3586 | 11440279 | Retinal photocoagulation influenced neither the intraocular concentration of the permeability marker albumin (PDR+: 253.2 +/- 46 mg/dl; PDR-: 256.4 +/- 66.5 mg/dl) nor the levels of IGFs (PDR+: IGF-I: 1.2 +/- 0.1 ng/ml; p = 0.38; IGF-II: 34.8 +/- 2.2 ng/ml; p = 0.1; IGF-BP3: 75.7 +/- 9.7 ng/ml; p = 0.27; PDR-: IGF-I: 1.1 +/- 0.2ng/ml; IGF-II: 29.3 +/- 5.2 ng/ml; IGF-BP3: 61.5 +/- 18.3 ng/ml). |
| 3587 | 11440279 | The lack of influence on intraocular concentrations of the serum-derived growth factors, IGF-I, IGF-II and IGF-BP3, might in part explain the failure of previous photocoagulation in the investigated patients. |
| 3588 | 11440896 | An additional infusion of somatostatin into hyperglycemic fetuses blocked fetal hyperinsulinemia and completely prevented these increases, specifying insulin as the causative factor. |
| 3589 | 11472078 | Determination of free insulin-like growth factor-I in human serum: comparison of ultrafiltration and direct immunoradiometric assay. |
| 3590 | 11472078 | Two fundamentally different methods are currently used for the determination of free insulin-like growth factor-I (IGF-I): ultrafiltration by centrifugation (UF) and direct immunoradiometric assay (IRMA). |
| 3591 | 11472078 | Addition of IGF-binding protein-1 (IGFBP-1) to normal sera (n = 6) dose-dependently decreased ultrafiltered free IGF-I only (P< 0.0007). |
| 3592 | 11472078 | IRMA and UF yielded similar results in healthy subjects treated with IGF-I (n = 5) or growth hormone (n = 7) and in acromegalic patients (n = 6) before and after somatostatin analogue treatment. |
| 3593 | 11472078 | However, marked differences were observed in conditions with elevated IGFBP-1 and -2. |
| 3594 | 11472078 | IRMA was less affected than UF by added IGFBP-1 and -2, and reductions in free IGF-I were better revealed by UF than IRMA. |
| 3595 | 11479129 | We therefore investigated the relationship between circulating plasma concentrations of leptin and insulin and immunoreactivity in the endocrine pancreas for leptin and leptin receptor (OB-R) in genetically normal rats that were programmed to become obese during adult life. |
| 3596 | 11479129 | At the time of death (125 days of age), UN offspring had elevated (P<0.005) fasting plasma insulin (AD control 1.417+/-0.15 ng/ml, UN control 2.493+/-0.33 ng/ml, AD hypercaloric 1.70+/-0.17 ng/ml, UN hypercaloric 2.608+/-0.41 ng/ml) and leptin (AD control 8.8+/-1.6 ng/ml, UN control 14.32+/-1.9 ng/ml, AD hypercaloric 15.11+/-1.8 ng/ml, UN hypercaloric 30.18+/-5.3 ng/ml) concentrations, which were further increased (P<0.05) by postnatal hypercaloric nutrition. |
| 3597 | 11479129 | The elevated plasma insulin and leptin concentrations were paralleled by increased immunolabeling for leptin in the peripheral cells of the pancreatic islets. |
| 3598 | 11479129 | Dual immunofluorescence histochemistry for somatostatin and leptin revealed that leptin was co-localized in the pancreatic delta-cells. |
| 3599 | 11479129 | Our data suggest that reduced substrate supply during fetal development can trigger permanent dysregulation of the adipoinsular feedback system leading to hyperleptinemia, hyperinsulinism and compensatory leptin production by pancreatic delta-cells in a further attempt to reduce insulin hypersecretion in the progression to adipogenic diabetes. |
| 3600 | 11506994 | Elevated plasma angiotensinogen (AGT) levels have been demonstrated in insulin-resistant states such as obesity and type 2 diabetes mellitus (DM2), conditions that are directly correlated to hypertension. |
| 3601 | 11506994 | We examined whether hyperinsulinemia or hyperglycemia may modulate fat and liver AGT gene expression and whether obesity and insulin resistance are associated with abnormal AGT regulation. |
| 3602 | 11506994 | We studied chronically catheterized lean (approximately 300 g) and obese (approximately 450 g) Sprague-Dawley rats in four clamp studies (n = 3/group), creating physiological hyperinsulinemia (approximately 60 microU/ml, by an insulin clamp), hyperglycemia (approximately 18 mM, by a pancreatic clamp using somatostatin to prevent endogenous insulin secretion), or euglycemia with glucosamine infusion (GlcN; 30 micromol. kg(-1). min(-1)) and equivalent saline infusions (as a control). |
| 3603 | 11506994 | Although insulin infusion suppressed AGT gene expression in fat and liver of lean rats, the obese rats demonstrated resistance to this effect of insulin. |
| 3604 | 11506994 | In contrast, hyperglycemia at basal insulin levels activated AGT gene expression in fat and liver by approximately threefold in both lean and obese rats (P < 0.001). |
| 3605 | 11506994 | Resistance to the suppressive effect of insulin on AGT expression in obese rats may potentiate the effect of nutrients on AGT gene expression. |
| 3606 | 11506994 | We propose that increased AGT gene expression and possibly its production may provide another link between obesity/insulin resistance and hypertension. |
| 3607 | 11507651 | In the islets, staining intensity of both insulin and islet amyloid polypeptide (IAPP) increased slightly till 10 weeks of age and thereafter decreased rapidly. |
| 3608 | 11507651 | In contrast, the staining intensities of glucagon, somatostatin, and pancreatic polypeptide (PP) did not change. |
| 3609 | 11527089 | Modulation of retinal endothelial cell behaviour by insulin-like growth factor I and somatostatin analogues: implications for diabetic retinopathy. |
| 3610 | 11527089 | Evidence suggests the involvement of growth hormone (GH), insulin-like growth factor I (IGF-I) and somatostatin in the pathology associated with diabetic retinopathy. |
| 3611 | 11527089 | We examined the effect of IGF-I on human retinal endothelial cell (HREC) survival following high glucose exposure and serum starvation, examined the signalling pathways mediating the protective effect of IGF-I on HREC, and characterized somatostatin receptor-induced retinal endothelial cell death. |
| 3612 | 11527089 | Incubation of HREC in serum-free medium caused a time-dependent increase in c-Jun N-terminal kinase (JNK) activity, and continuous culture of HREC in the presence of IGF-I or vascular endothelial growth factor (VEGF) prevented JNK activation and arrested apoptosis. |
| 3613 | 11527089 | Both IGF-I and VEGF produced a time- and concentration-dependent increase in the activation of ERK. |
| 3614 | 11527089 | These studies suggest that IGF-I is critical for HREC survival, and that somatostatin analogues acting through the type 3 receptor have direct effects on retinal endothelial cells. |
| 3615 | 11527089 | Modulation of retinal endothelial cell behaviour by insulin-like growth factor I and somatostatin analogues: implications for diabetic retinopathy. |
| 3616 | 11527089 | Evidence suggests the involvement of growth hormone (GH), insulin-like growth factor I (IGF-I) and somatostatin in the pathology associated with diabetic retinopathy. |
| 3617 | 11527089 | We examined the effect of IGF-I on human retinal endothelial cell (HREC) survival following high glucose exposure and serum starvation, examined the signalling pathways mediating the protective effect of IGF-I on HREC, and characterized somatostatin receptor-induced retinal endothelial cell death. |
| 3618 | 11527089 | Incubation of HREC in serum-free medium caused a time-dependent increase in c-Jun N-terminal kinase (JNK) activity, and continuous culture of HREC in the presence of IGF-I or vascular endothelial growth factor (VEGF) prevented JNK activation and arrested apoptosis. |
| 3619 | 11527089 | Both IGF-I and VEGF produced a time- and concentration-dependent increase in the activation of ERK. |
| 3620 | 11527089 | These studies suggest that IGF-I is critical for HREC survival, and that somatostatin analogues acting through the type 3 receptor have direct effects on retinal endothelial cells. |
| 3621 | 11527089 | Modulation of retinal endothelial cell behaviour by insulin-like growth factor I and somatostatin analogues: implications for diabetic retinopathy. |
| 3622 | 11527089 | Evidence suggests the involvement of growth hormone (GH), insulin-like growth factor I (IGF-I) and somatostatin in the pathology associated with diabetic retinopathy. |
| 3623 | 11527089 | We examined the effect of IGF-I on human retinal endothelial cell (HREC) survival following high glucose exposure and serum starvation, examined the signalling pathways mediating the protective effect of IGF-I on HREC, and characterized somatostatin receptor-induced retinal endothelial cell death. |
| 3624 | 11527089 | Incubation of HREC in serum-free medium caused a time-dependent increase in c-Jun N-terminal kinase (JNK) activity, and continuous culture of HREC in the presence of IGF-I or vascular endothelial growth factor (VEGF) prevented JNK activation and arrested apoptosis. |
| 3625 | 11527089 | Both IGF-I and VEGF produced a time- and concentration-dependent increase in the activation of ERK. |
| 3626 | 11527089 | These studies suggest that IGF-I is critical for HREC survival, and that somatostatin analogues acting through the type 3 receptor have direct effects on retinal endothelial cells. |
| 3627 | 11527089 | Modulation of retinal endothelial cell behaviour by insulin-like growth factor I and somatostatin analogues: implications for diabetic retinopathy. |
| 3628 | 11527089 | Evidence suggests the involvement of growth hormone (GH), insulin-like growth factor I (IGF-I) and somatostatin in the pathology associated with diabetic retinopathy. |
| 3629 | 11527089 | We examined the effect of IGF-I on human retinal endothelial cell (HREC) survival following high glucose exposure and serum starvation, examined the signalling pathways mediating the protective effect of IGF-I on HREC, and characterized somatostatin receptor-induced retinal endothelial cell death. |
| 3630 | 11527089 | Incubation of HREC in serum-free medium caused a time-dependent increase in c-Jun N-terminal kinase (JNK) activity, and continuous culture of HREC in the presence of IGF-I or vascular endothelial growth factor (VEGF) prevented JNK activation and arrested apoptosis. |
| 3631 | 11527089 | Both IGF-I and VEGF produced a time- and concentration-dependent increase in the activation of ERK. |
| 3632 | 11527089 | These studies suggest that IGF-I is critical for HREC survival, and that somatostatin analogues acting through the type 3 receptor have direct effects on retinal endothelial cells. |
| 3633 | 11561557 | Changes in the antral content of VIP, duodenal somatostatin, and colonic galanin in NOD mice with LTD may cause low intestinal secretion and, together with rapid GI, give rise to diarrhoea, which is a common symptom in diabetes. |
| 3634 | 11573134 | However, this transcriptional machinery containing pax8 seems to require contributions from the neighboring cis-acting element that is similar to CRE/AP-1 consensus sequences. |
| 3635 | 11573134 | Modification of this putative CRE/AP-1 site not only represses the NUE transcriptional activities by 90% in FRTL-5 cells, but also nullifies the synergistic effect of PKA on pax8-mediated transactivation in HeLa cells. |
| 3636 | 11573134 | In this report, we have further characterized the putative CRE/AP-1 site within the NIS upstream enhancer using gel mobility shift assay. |
| 3637 | 11573134 | An oligonucleotide probe with NIS CRE/AP-1 sequence produced complex binding patterns in both FRTL-5 and HeLa cell, reflecting the presence of diverse classes of binding factors. |
| 3638 | 11573134 | When compared with CRE or AP-1 elements in other genes, the mobility shift pattern of NIS CRE/AP-1 was similar to those of collagenase TRE, c-Jun TRE, and somatostatin CRE, but the relative intensities of the binding complexes were quite different. |
| 3639 | 11673332 | At 2 months, sensory neurones had no detectable alterations in their calibre or gene expression, assessed using quantitative in situ hybridization studies for mRNA markers that included alpha CGRP, beta CGRP, NFM, t alpha 1-tubulin, SP, VIP, B50 (GAP43), galanin, somatostatin, PACAP, HSP27, c-jun, SNAP 25, p75, TrkA, TrkB and TrkC. |
| 3640 | 11673332 | By 12 months, however, diabetics had developed neurone perikaryal and distal axon atrophy, accompanied by generalized downregulation of mRNA expression, particularly of CGRP transcripts, PACAP, SP, NFM, p75, trkA and trkC. |
| 3641 | 11673332 | With the exception of HSP-27, no elevation in mRNAs that increase after injury, such as VIP, galanin, CCK, PACAP, B50 and t alpha 1-tubulin, was observed and constitutive levels, when detectable, trended towards lower rather than increased levels. |
| 3642 | 11733868 | In order to do this, we administered indomethacin to 5 patients with type 2 diabetes during continuous infusion of somatostatin to block endogenous insulin and glucagon secretion and infusion of basal concentrations of insulin and glucagon in a placebo-controlled study. |
| 3643 | 11733868 | Endogenous glucose production was measured 3 hours after the start of the somatostatin, insulin and glucagon infusion, for 4 hours after administration of placebo/indomethacin, by primed, continuous infusion of [6,6-(2)H(2)] glucose. |
| 3644 | 11733868 | In order to do this, we administered indomethacin to 5 patients with type 2 diabetes during continuous infusion of somatostatin to block endogenous insulin and glucagon secretion and infusion of basal concentrations of insulin and glucagon in a placebo-controlled study. |
| 3645 | 11733868 | Endogenous glucose production was measured 3 hours after the start of the somatostatin, insulin and glucagon infusion, for 4 hours after administration of placebo/indomethacin, by primed, continuous infusion of [6,6-(2)H(2)] glucose. |
| 3646 | 11755928 | We examined whether acute in vivo increases in either plasma glucose or insulin concentrations stimulate PAI-1 gene expression in fat tissue. |
| 3647 | 11755928 | Hyperglycemia (approximately 18mM) was induced for 3 h by glucose infusion during a pancreatic clamp (somatostatin inhibited endogenous insulin secretion). |
| 3648 | 11762360 | For instance, the well-known Zollinger-Ellison syndrome is gastrin-mediated. |
| 3649 | 11762360 | The best general markers are chromogranin A (CgA) and pancreatic polypeptide (PP). |
| 3650 | 11762360 | Specific markers for endocrine tumors include insulin, gastrin, glucagon, vaso intestinal polypeptide (VIP), somatostatin and the primary cathabolic product of serotonin, 5-hydroxyndoleacetic acid (5-HIAA). |
| 3651 | 11762360 | Localisation procedures commonly applied, in the diagnosis of endocrine tumours include ultrasound (US), computed tomography (CT) and somatostatin receptor scintigraphy (SRS). |
| 3652 | 11762360 | For instance, the well-known Zollinger-Ellison syndrome is gastrin-mediated. |
| 3653 | 11762360 | The best general markers are chromogranin A (CgA) and pancreatic polypeptide (PP). |
| 3654 | 11762360 | Specific markers for endocrine tumors include insulin, gastrin, glucagon, vaso intestinal polypeptide (VIP), somatostatin and the primary cathabolic product of serotonin, 5-hydroxyndoleacetic acid (5-HIAA). |
| 3655 | 11762360 | Localisation procedures commonly applied, in the diagnosis of endocrine tumours include ultrasound (US), computed tomography (CT) and somatostatin receptor scintigraphy (SRS). |
| 3656 | 11834421 | Pancreas duodenum homeobox-1 (PDX-1) (also known as insulin promoter factor-1, islet/duodenum homeobox-1, somatostatin transactivating factor-1, insulin upstream factor-1 and glucose-sensitive factor) is a transcription factor encoded by a Hox-like homeodomain gene. |
| 3657 | 11834421 | In adult subjects, PDX-1 is essential for normal pancreatic islet function as suggested by its regulatory action on the expression of a number of pancreatic genes, including insulin, somatostatin, islet amyloid polypeptide, the glucose transporter type 2 and glucokinase. |
| 3658 | 11834421 | Pancreas duodenum homeobox-1 (PDX-1) (also known as insulin promoter factor-1, islet/duodenum homeobox-1, somatostatin transactivating factor-1, insulin upstream factor-1 and glucose-sensitive factor) is a transcription factor encoded by a Hox-like homeodomain gene. |
| 3659 | 11834421 | In adult subjects, PDX-1 is essential for normal pancreatic islet function as suggested by its regulatory action on the expression of a number of pancreatic genes, including insulin, somatostatin, islet amyloid polypeptide, the glucose transporter type 2 and glucokinase. |
| 3660 | 11872657 | Glucose fluxes ([3-(3)H]glucose) were measured during euglycemia (5 mmol/l) and after abrupt onset of hyperglycemia (10 mmol/l; variable dextrose infusion) under fixed hormonal conditions (somatostatin infusion for 6 h with basal insulin/glucagon/growth hormone replacement). |
| 3661 | 11874712 | Inhibition of circulating and renal IGF-I by long-acting somatostatin analogues reduces renal and glomerular growth and urinary albumin excretion in diabetic rats. |
| 3662 | 11874712 | The aim of the present study was to examine renal and glomerular growth in early experimental diabetes in mice along with changes in the GH/IGF-I axis following treatment with the somatostatin analogue octreotide. |
| 3663 | 11874712 | In conclusion, this new diabetic mouse model mimicking human type 1 diabetes is characterised by GH hypersecretion and the somatostatin analogue octreotide is able to prevent renal and glomerular growth, probably mediated through changes in circulating GH and local kidney IGF-I levels. |
| 3664 | 11874712 | Inhibition of circulating and renal IGF-I by long-acting somatostatin analogues reduces renal and glomerular growth and urinary albumin excretion in diabetic rats. |
| 3665 | 11874712 | The aim of the present study was to examine renal and glomerular growth in early experimental diabetes in mice along with changes in the GH/IGF-I axis following treatment with the somatostatin analogue octreotide. |
| 3666 | 11874712 | In conclusion, this new diabetic mouse model mimicking human type 1 diabetes is characterised by GH hypersecretion and the somatostatin analogue octreotide is able to prevent renal and glomerular growth, probably mediated through changes in circulating GH and local kidney IGF-I levels. |
| 3667 | 11874712 | Inhibition of circulating and renal IGF-I by long-acting somatostatin analogues reduces renal and glomerular growth and urinary albumin excretion in diabetic rats. |
| 3668 | 11874712 | The aim of the present study was to examine renal and glomerular growth in early experimental diabetes in mice along with changes in the GH/IGF-I axis following treatment with the somatostatin analogue octreotide. |
| 3669 | 11874712 | In conclusion, this new diabetic mouse model mimicking human type 1 diabetes is characterised by GH hypersecretion and the somatostatin analogue octreotide is able to prevent renal and glomerular growth, probably mediated through changes in circulating GH and local kidney IGF-I levels. |
| 3670 | 11880930 | This study investigates the effects of the islet hormones insulin (Ins), glucagon (Glu), and somatostatin (Som) with nerve stimulation (EFS) acetylcholine (ACh) and cholecytokinin-octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration [Ca(2+)](i) in the pancreas of age-matched control and diabetic rats. |
| 3671 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 3672 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 3673 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 3674 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 3675 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 3676 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 3677 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 3678 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 3679 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 3680 | 11961490 | Endogenous somatostatin inhibits interaction of insulin and cholecystokinin on exocrine secretion of isolated, perfused rat pancreas. |
| 3681 | 12021104 | IL-1beta expression in islet cells of the NOD mouse and its spatial relationship to beta cells and inducible nitric oxide synthase. |
| 3682 | 12021104 | At day 0 (Cy group), IL-1beta was expressed in selective intraislet macrophages but showed an increase from day 7 onwards in macrophages, a few beta cells, and somatostatin cells. |
| 3683 | 12021104 | In the Cy group a proportion of macrophages coexpressed IL-1beta and inducible nitric oxide synthase (iNOS). |
| 3684 | 12067858 | We investigated seven healthy young male volunteers after an overnight fast on two occasions by means of microdialysis and palmitate turnover in a placebo-controlled manner with a pancreatic pituitary clamp involving inhibition with somatostatin and substitution of growth hormone, glucagon, and insulin at basal levels. |
| 3685 | 12086948 | Fixed hormonal conditions were attained by infusing somatostatin for 6 h with replacement of basal insulin, glucagon, and growth hormone. |
| 3686 | 12110051 | Sections of paraffin-embedded tissues were evaluated for amyloid with hematoxylin and eosin (HE) and congo red (CR) staining, and using immunohistochemistry for human islet amyloid polypeptide (IAPP), calcitonin gene-related peptide (CGRP), glucagon, pancreatic polypeptide (PP), somatostatin (SS), and porcine insulin. |
| 3687 | 12110051 | Islet amyloid was positive with HE in 40 baboons, with CR in 39 baboons, and with IAPP and CGRP in 35 baboons. |
| 3688 | 12110051 | IAPP and CGRP only stained islet amyloid. |
| 3689 | 12110051 | PP, SS, glucagon, and porcine insulin did not stain amyloid. |
| 3690 | 12114794 | A case of somatostatin-producing pancreatic tumor associated with severe insulin-dependent diabetes mellitus and ketoacidotic coma is reported. |
| 3691 | 12130560 | The somatostatin analog octreotide inhibits GH-stimulated, but not IGF-I-stimulated, bone growth in hypophysectomized rats. |
| 3692 | 12130560 | In the present study we investigated whether the somatostatin analog octreotide blunts the stimulatory effects of GH and/or IGF-I on bone growth in hypophysectomized rats infused for 6 d with vehicle, GH, or IGF-I. |
| 3693 | 12130560 | The somatostatin analog octreotide inhibits GH-stimulated, but not IGF-I-stimulated, bone growth in hypophysectomized rats. |
| 3694 | 12130560 | In the present study we investigated whether the somatostatin analog octreotide blunts the stimulatory effects of GH and/or IGF-I on bone growth in hypophysectomized rats infused for 6 d with vehicle, GH, or IGF-I. |
| 3695 | 12134168 | We identified a cocrystal composition comprising 75% C8-HI and 25% human insulin that exhibits near-ideal basal pharmacodynamics in somatostatin-treated beagle dogs. |
| 3696 | 12145399 | Insulin (5/5), glucagon (3/5), and somatostatin (3/5) immunohistochemistry revealed that most cells stained positively for insulin diffusely in their cytoplasm (5/5) (staining restricted to the vascular pole of b-cells in the control). |
| 3697 | 12200754 | Eight T2DM and 9 age-, weight-, and gender-matched nondiabetic subjects received a 4-hour glucagon infusion at the rates of 0.2, 0.5, 2, 6, and 8 ng. kg(-1). min(-1) while maintaining the plasma insulin concentration constant at the basal level with exogenous infusions of somatostatin and insulin. |
| 3698 | 12235021 | Insulin concentrations in all instances were maintained at approximately 65 pmol/l by means of continuous infusions of somatostatin and insulin. |
| 3699 | 12242483 | Immunohistochemically, small cells are positive for PDX-1, synaptophysin, insulin, glucagon, somatostatin, pancreatic polypeptide, alpha-fetaprotein and Bcl-2 and negative for cytokeratin 19 and nestin. |
| 3700 | 12354124 | Currently available data suggest that somatostatin analogues might inhibit angiogenesis directly through somatostatin receptors present on endothelial cells and also indirectly through the inhibition of growth factor secretion such as IGF-I and vascular endothelial growth factor (VEGF) and reducing monocyte chemotaxis. |
| 3701 | 12365794 | Fas and Fas ligand immunolocalization in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes. |
| 3702 | 12365794 | Here, dual-label immunohistochemistry was employed to examine the intra-islet expression, distribution and cellular sources of Fas and FasL in the NOD mouse, during spontaneous diabetes (days 21, 40 and 90) and following acceleration of diabetes with cyclophosphamide (days 0, 4, 7, 11 and 14 after cyclophosphamide administration). |
| 3703 | 12365794 | FasL was expressed constitutively in most beta cells but not in glucagon or somatostatin cells or islet inflammatory cells and paralleled the loss of insulin immunolabelling with advancing disease. |
| 3704 | 12365794 | During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than CD4 and CD8 T cells, concomitant with advancing insulitis. |
| 3705 | 12365794 | In cyclophosphamide-treated mice, the proportion of Fas-positive intra-islet CD4 and CD8 T cells at day 14 (with and without diabetes) was considerably higher than at days 0, 4, 7 and 11. |
| 3706 | 12365794 | Our results show constitutive expression of FasL in beta cells in the NOD mouse and predominant expression of Fas in intra-islet macrophages and to a lesser extent in T cells prior to diabetes onset. |
| 3707 | 12365794 | Interleukin-1beta in intra-islet macrophages may induce Fas and inducible nitric oxide synthase expression in an autocrine and paracrine manner and mediate beta cell destruction or even death of some macrophages and T cells. |
| 3708 | 12377295 | The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. |
| 3709 | 12377295 | CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. |
| 3710 | 12377295 | They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. |
| 3711 | 12397533 | Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. |
| 3712 | 12397533 | GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. |
| 3713 | 12397533 | Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. |
| 3714 | 12397533 | GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. |
| 3715 | 12401705 | To investigate this possibility, we used a glycogen phosphorylase inhibitor (BAY R3401) to inhibit glycogen breakdown in the overnight-fasted dog, and the effects of complete insulin deficiency or a fourfold rise in the plasma insulin level were assessed during a 5-h experimental period. |
| 3716 | 12401705 | Hormone levels were controlled using somatostatin with portal insulin and glucagon infusion. |
| 3717 | 12453890 | On each occasion, they received an infusion of 0.1 mg. kg(-1). min(-1) somatostatin to suppress endogenous insulin production. |
| 3718 | 12475779 | Arginine-stimulated insulin and somatostatin release is enhanced by the sulfonylurea gliclazide. |
| 3719 | 12501980 | To our knowledge, this is the first report of such a distinct differential behaviour of blood glucose and insulin requirements with different somatostatin analogs, and is worth recalling when starting an insulin-treated diabetic patient on this treatment. |
| 3720 | 12501980 | It may be related to a preferential binding of LAR-octreotide to subtype 2 somatostatin receptors in the pancreas, while lanreotide preferentially binds to subtype 5, not expressed in this tissue; this would explain the fall in glucagon, in parallel to the decrease in insulin requirements after LAR-octreotide; however, a contribution of differences in the effect of both somatostatin analogues on postreceptor signalling systems and/or intestinal carbohydrate absorption cannot be entirely ruled out. |
| 3721 | 12501980 | To our knowledge, this is the first report of such a distinct differential behaviour of blood glucose and insulin requirements with different somatostatin analogs, and is worth recalling when starting an insulin-treated diabetic patient on this treatment. |
| 3722 | 12501980 | It may be related to a preferential binding of LAR-octreotide to subtype 2 somatostatin receptors in the pancreas, while lanreotide preferentially binds to subtype 5, not expressed in this tissue; this would explain the fall in glucagon, in parallel to the decrease in insulin requirements after LAR-octreotide; however, a contribution of differences in the effect of both somatostatin analogues on postreceptor signalling systems and/or intestinal carbohydrate absorption cannot be entirely ruled out. |
| 3723 | 12502488 | Plasma ghrelin concentrations are not regulated by glucose or insulin: a double-blind, placebo-controlled crossover clamp study. |
| 3724 | 12502488 | We hypothesized that insulin or glucose could regulate ghrelin secretion by a feedback mechanism. |
| 3725 | 12502488 | Ghrelin plasma concentration was studied during concomitant exogenous hyperinsulinemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control, respectively. |
| 3726 | 12502488 | Elevated glucose concentrations increased circulating insulin to 612 +/- 85 pmol/l (P < 0.01), but they did not affect ghrelin concentrations. |
| 3727 | 12502488 | Prolonged hyperinsulinemia by exogenous infusion resulted in circulating insulin of 1,602 +/- 261 pmol/l (P < 0.01) and suppressed plasma ghrelin to 49.6% of baseline (P < 0.01). |
| 3728 | 12502488 | During administration of somatostatin, insulin concentration remained constant, but an even greater decrease in ghrelin to 39.5% of baseline was noted (P < 0.01). |
| 3729 | 12502488 | Hyperglycemia does not decrease ghrelin, and a reduction in ghrelin is only seen at supraphysiological insulin concentrations. |
| 3730 | 12502488 | Plasma ghrelin concentrations are not regulated by glucose or insulin: a double-blind, placebo-controlled crossover clamp study. |
| 3731 | 12502488 | We hypothesized that insulin or glucose could regulate ghrelin secretion by a feedback mechanism. |
| 3732 | 12502488 | Ghrelin plasma concentration was studied during concomitant exogenous hyperinsulinemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control, respectively. |
| 3733 | 12502488 | Elevated glucose concentrations increased circulating insulin to 612 +/- 85 pmol/l (P < 0.01), but they did not affect ghrelin concentrations. |
| 3734 | 12502488 | Prolonged hyperinsulinemia by exogenous infusion resulted in circulating insulin of 1,602 +/- 261 pmol/l (P < 0.01) and suppressed plasma ghrelin to 49.6% of baseline (P < 0.01). |
| 3735 | 12502488 | During administration of somatostatin, insulin concentration remained constant, but an even greater decrease in ghrelin to 39.5% of baseline was noted (P < 0.01). |
| 3736 | 12502488 | Hyperglycemia does not decrease ghrelin, and a reduction in ghrelin is only seen at supraphysiological insulin concentrations. |
| 3737 | 12535226 | Teleost fish islets, like mammalian islets, are composed primarily of cells producing insulin, glucagon or somatostatin; however, teleost fish have two different populations of somatostatin (SST) producing delta cells, one producing SST-14, a 14 amino acid SST identical to mammalian SST, which is derived from the pre-proSST-I gene which is present in all vertebrates, and the other a "large" (i.e. 22 to 28 amino acid) SST derived from a pre-proSST-II gene, which is not found in mammals. |
| 3738 | 12547550 | A tumour that secretes glucagon-like peptide-1 and somatostatin in a patient with reactive hypoglycaemia and diabetes. |
| 3739 | 12547550 | We report an instance of a 45-year-old woman with a GLP-1 and somatostatin secreting neuroendocrine tumour who presented with reactive hypoglycaemia and hyperglycaemia, but who was subsequently cured by surgery. |
| 3740 | 12547550 | A tumour that secretes glucagon-like peptide-1 and somatostatin in a patient with reactive hypoglycaemia and diabetes. |
| 3741 | 12547550 | We report an instance of a 45-year-old woman with a GLP-1 and somatostatin secreting neuroendocrine tumour who presented with reactive hypoglycaemia and hyperglycaemia, but who was subsequently cured by surgery. |
| 3742 | 12569088 | Arteriovenous difference and tracer ([3-(3)H]glucose) techniques were used in 42-h-fasted conscious dogs to identify any insulin-like effects of intraportally administered glucagon-like peptide 1-(7-36)amide (GLP-1). |
| 3743 | 12569088 | Each study consisted of an equilibration, a basal, and three 90-min test periods (P1, P2, and P3) during which somatostatin, intraportal insulin (3-fold basal) and glucagon (basal), and peripheral glucose were infused. |
| 3744 | 12572378 | [Effect of jianpi wenshen decoction on serum gastrin, plasma motilin and somatostatin in patients of diabetic diarrhea]. |
| 3745 | 12582462 | Somatostatin analogues such as octreotide have shown promise as a safe and effective treatment for severe proliferative diabetic retinopathy by blocking the local and systemic production of growth hormone and insulin-like growth factor type 1 associated with angiogenesis and endothelial cell proliferation. |
| 3746 | 12582462 | SSTR2 and SSTR3 are the most important receptor subtypes mediating growth hormone secretion and endothelial cell cycle arrest, retinal endothelial cell apoptosis and release of insulin. |
| 3747 | 12586550 | Pancreatic islets from HD transgenic mice express reduced levels of the pancreatic islet hormones insulin, somatostatin, and glucagon and exhibit intrinsic defects in insulin production. |
| 3748 | 12586550 | HD transgenic mice develop an age-dependent reduction of insulin mRNA expression and diminished expression of key regulators of insulin gene transcription, including the pancreatic homeoprotein PDX-1, E2A proteins, and the coactivators CBP and p300. |
| 3749 | 12586550 | Disrupted expression of a subset of transcription factors in pancreatic beta cells by a polyglutamine expansion tract in the huntingtin protein selectively impairs insulin gene expression to result in insulin deficiency and diabetes. |
| 3750 | 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. |
| 3751 | 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. |
| 3752 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 3753 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 3754 | 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. |
| 3755 | 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. |
| 3756 | 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. |
| 3757 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 3758 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 3759 | 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. |
| 3760 | 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. |
| 3761 | 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. |
| 3762 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 3763 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 3764 | 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. |
| 3765 | 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. |
| 3766 | 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. |
| 3767 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 3768 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 3769 | 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. |
| 3770 | 12602782 | Whereas the contents of peptide YY (PYY) and somatostatin were higher in obese diabetic mice, the contents of substance P and VIP were lower. |
| 3771 | 12602782 | The changes in the colonic contents of PYY, VIP and somatostatin may cause low intestinal secretion and, together with slow GIT, give rise to constipation, which is a common symptom in diabetes. |
| 3772 | 12602782 | Whereas the contents of peptide YY (PYY) and somatostatin were higher in obese diabetic mice, the contents of substance P and VIP were lower. |
| 3773 | 12602782 | The changes in the colonic contents of PYY, VIP and somatostatin may cause low intestinal secretion and, together with slow GIT, give rise to constipation, which is a common symptom in diabetes. |
| 3774 | 12621360 | GH feedback occurs through the hypothalamus and involves neuropeptides such as somatostatin, GH-releasing hormone, GH-releasing peptides and neuropeptide Y. |
| 3775 | 12625507 | Instead, a more convenient and valid insulin sensitivity test involving suppression of insulin secretion with somatostatin and a single insulin injection was used. |
| 3776 | 12670298 | Symptomatic control can be achieved by lowering insulin-like growth factor-I (IGF-I) concentrations to within the age-adjusted normal range, and survival can be improved to match that of the general population. |
| 3777 | 12670298 | However, even with optimal surgery and current medical therapies (dopamine agonists, somatostatin analogues), 30% to 50% of patients do not achieve target concentrations of IGF-I and GH. |
| 3778 | 12686458 | PACAP is expressed in secretory granules of insulin and glucagon cells in human and rodent pancreas. |
| 3779 | 12686458 | Insulin and cyclic adenosine monophosphate (cAMP) generation induced by PACAP were investigated in islets isolated from the spontaneously diabetic Goto-Kakizaki (GK) rat. |
| 3780 | 12686458 | PACAP immunoreactivity was observed in virtually all insulin and glucagon cells in both species, but not in somatostatin or pancreatic polypeptide (PP) cells; this co-localization pattern was unaltered in diabetic pancreata. |
| 3781 | 12686458 | In normal human pancreas, PACAP was further localized ultrastructurally to the secretory granules of insulin and glucagon cells. |
| 3782 | 12686458 | PACAP significantly potentiated glucose-stimulated insulin release in isolated islets of normal but not of GK rats. |
| 3783 | 12686458 | In conclusion, using improved immunocytochemistry techniques and electron microscopy (EM), PACAP was shown to be expressed both in normal and diabetic islet cells and localized to secretory granules of insulin and glucagon cells. |
| 3784 | 12704384 | To explore induced islet neogenesis in the liver as a strategy for the treatment of diabetes, we used helper-dependent adenovirus (HDAD) to deliver the pancreatic duodenal homeobox-1 gene (Ipf1; also known as Pdx-1) to streptozotocin (STZ)-treated diabetic mice. |
| 3785 | 12704384 | The diabetes of STZ mice was partially reversed by HDAD-mediated transfer of NeuroD (Neurod), a factor downstream of Ipf1, and completely reversed by a combination of Neurod and betacellulin (Btc), without producing hepatitis. |
| 3786 | 12704384 | We detected in the liver insulin and other islet-specific transcripts, including proinsulin-processing enzymes, beta-cell-specific glucokinase and sulfonylurea receptor. |
| 3787 | 12704384 | Immunocytochemistry detected the presence of insulin, glucagon, pancreatic polypeptide and somatostatin-producing cells organized into islet clusters; immuno-electron microscopy showed typical insulin-containing granules. |
| 3788 | 12716747 | Recent reports have shown that ES cells can differentiate into insulin-producing cells in response to the transient expression of the pdx-1 gene, after the removal of feeder cells. |
| 3789 | 12716747 | Glucose-responsive insulin-producing cells, derived from our feeder-free ES cells, expressed insulin 2, pdx-1, Pax4, and Isl1 and also the glucagon, somatostatin, and PP genes. |
| 3790 | 12716749 | Exogenously administered somatostatin (SST) inhibits secretion of insulin and glucagon. |
| 3791 | 12716749 | In rodents, SST inhibits the release of glucagon, but not that of insulin, via SSTR2. |
| 3792 | 12716749 | Exogenously administered somatostatin (SST) inhibits secretion of insulin and glucagon. |
| 3793 | 12716749 | In rodents, SST inhibits the release of glucagon, but not that of insulin, via SSTR2. |
| 3794 | 12765947 | The subjects were randomized into six groups and were studied at baseline and during infusions of saline (group 1), insulin (0.5 mU. kg(-1). min(-1)) (group 2), insulin plus replacement of AAs (group 3) insulin plus high-dose AAs (group 4), or somatostatin and baseline replacement doses of insulin, glucagon and GH plus high dose of AAs (group 5) or saline (group 6). |
| 3795 | 12837760 | Neurogenin3 and hepatic nuclear factor 1 cooperate in activating pancreatic expression of Pax4. |
| 3796 | 12837760 | During fetal development, paired/homeodomain transcription factor Pax4 controls the formation of the insulin-producing beta cells and the somatostatin-producing delta cells in the islets of Langerhans in the pancreas. |
| 3797 | 12837760 | This short sequence contains binding sites for homeodomain transcription factors PDX1 and hepatic nuclear factor (HNF)1, nuclear receptor HNF4alpha, and basic helix-loop-helix factor Neurogenin3. |
| 3798 | 12837760 | In the current study we demonstrate that the HNF1alpha and Neurogenin3 binding sites are critical for activity of the region through synergy between the two proteins. |
| 3799 | 12837760 | Furthermore, exogenous expression of Neurogenin3 is sufficient to induce expression of the endogenous pax4 gene in the mouse pancreatic ductal cell line mPAC, which already expresses HNF1alpha, whereas expression of both Neurogenin3 and HNF1alpha are necessary to activate the pax4 gene in the fibroblast cell line NIH3T3. |
| 3800 | 12837760 | These data demonstrate how Neurogenin3 and HNF1alpha activate the pax4 gene during the cascade of gene expression events that control pancreatic endocrine cell development. |
| 3801 | 12850289 | The expression of the nucleotide receptors P2X1, P2X2, P2X7, P2Y1, P2Y2 and P2Y4, in the pancreas of the streptozotocin-induced diabetic rat was investigated using immunohistochemistry. |
| 3802 | 12850289 | Double-labelling experiments, using antibodies raised against insulin, somatostatin and glucagon, showed, for the first time, an increase in immunostaining for P2X7 receptors on islet glucagon-containing alpha cells (which had migrated to the interior), while no P2X7 receptors were found in beta and delta cells. |
| 3803 | 12850289 | P2Y1 receptors were present in intra-islet capillaries, while P2Y4 receptors were found on both alpha and beta cells. |
| 3804 | 12850289 | P2Y1 and P2Y2 receptor expression was also found in pancreatic duct cells and P2X1, P2X2, P2Y1 and P2Y2 receptors were identified in small blood vessels. |
| 3805 | 12855013 | Mediators of growth and inflammation, including insulin-like growth factor-1 (IGF-1) and somatostatin (SST) have been implicated in its pathogenesis. |
| 3806 | 12871244 | The expression of somatostatin receptor subtypes (SSTRs) 1 and 2 was studied in benign, pre-malignant and malignant laryngeal specimens. |
| 3807 | 12882918 | ES cells were evaluated for their ability to differentiate into pancreatic and islet lineage-restricted stages including pancreatic duodenal homeobox 1 (PDX1)-positive pancreatic precursor cells, early endocrine cell progenitors, and islet hormone-producing cells. |
| 3808 | 12882918 | Following growth and differentiation in nonselective medium containing serum, murine ES cells spontaneously differentiated into cells individually expressing each of the four major islet hormones: insulin, glucagon, somatostatin, and pancreatic polypeptide. |
| 3809 | 12882918 | Hormone-positive cells appeared within focal clusters of cells coexpressing PDX1 and the nonclassical hormone markers peptide YY (YY) and islet amyloid polypeptide (IAPP) in combination with the definitive hormones, characteristic of endocrine cells appearing during early pancreaticogenesis. |
| 3810 | 12900379 | The plasma insulin concentration and the insulin content were significantly higher in mice treated with 0.1 and 0.2 microg/g BTC. |
| 3811 | 12900379 | BTC treatment significantly increased the number of beta-cells in each islet as well as the number of insulin-positive islets. |
| 3812 | 12900379 | Within islets, the numbers of 5-bromo-2-deoxyuridine/somatostatin-positive cells and pancreatic duodenal homeobox-1/somatostatin-positive cells were significantly increased by BTC. |
| 3813 | 12900379 | These results indicate that BTC improved hyperglycemia induced by a high dose of STZ by promoting neoformation of beta-cells, mainly from somatostatin-positive islet cells. |
| 3814 | 12900379 | The plasma insulin concentration and the insulin content were significantly higher in mice treated with 0.1 and 0.2 microg/g BTC. |
| 3815 | 12900379 | BTC treatment significantly increased the number of beta-cells in each islet as well as the number of insulin-positive islets. |
| 3816 | 12900379 | Within islets, the numbers of 5-bromo-2-deoxyuridine/somatostatin-positive cells and pancreatic duodenal homeobox-1/somatostatin-positive cells were significantly increased by BTC. |
| 3817 | 12900379 | These results indicate that BTC improved hyperglycemia induced by a high dose of STZ by promoting neoformation of beta-cells, mainly from somatostatin-positive islet cells. |
| 3818 | 12915685 | In contrast, most islet cells expressing insulin, glucagon, or somatostatin showed considerably weaker levels of menin expression; however, a subpopulation of pancreatic polypeptide-positive cells exhibited a signal comparable with that detected in adjacent exocrine cells. |
| 3819 | 12918465 | On admission, the hemoglobin level was 8.3g/dl, but the levels of serum iron, vitamin B12, and erythropoietin and, the number of reticulocytes were within normal limits. |
| 3820 | 12918465 | The serum glucagon level was very high (2360 pg/ml), but the levels of other hormones such as somatostatin or gastrin were within normal limits, while insulin was low. |
| 3821 | 12958610 | Plasma insulin concentrations were kept constant at approximately 35 pmol/l by intravenous somatostatin-insulin infusions and there was no significant change in plasma glucose levels during any of the study protocols. |
| 3822 | 12958610 | While tissue plasminogen activator (tPA) and adipsin, an adipocyte derived protease, were unaffected by LIP, changes in soluble vascular cell adhesion molecule-1 (sVCAM-1) were significantly correlated (p = 0.02) with those seen for PAI-1. |
| 3823 | 12958610 | This suggests that hyperlipidemia independent of insulin and plasma glucose levels stimulates vascular tissue and in turn might induce an increase in plasma PAI-1. |
| 3824 | 12970312 | Seven normal subjects were examined on four occasions during a 37-h fast with infusion of somatostatin, insulin, and glucagon for the final 15 h: 1) with GH replacement, 2) with GH replacement and antilipolysis with acipimox, 3) without GH and with antilipolysis, and 4) with GH replacement, antilipolysis, and infusion of intralipid. |
| 3825 | 12974503 | In particular, untreated coeliacs, when compared to controls, showed low postprandial cholecystokinin and increased fasting somatostatin levels. |
| 3826 | 14557451 | A reappraisal of the utility of somatostatin receptor scintigraphy in patients with ectopic adrenocorticotropin Cushing's syndrome. |
| 3827 | 14557451 | The diagnostic utility of somatostatin receptor scintigraphy (SRS) in EAS has been studied in a limited number of patients with conflicting results. |
| 3828 | 14557451 | A reappraisal of the utility of somatostatin receptor scintigraphy in patients with ectopic adrenocorticotropin Cushing's syndrome. |
| 3829 | 14557451 | The diagnostic utility of somatostatin receptor scintigraphy (SRS) in EAS has been studied in a limited number of patients with conflicting results. |
| 3830 | 14578293 | Glucose levels were raised from 5 to 10 mmol/l while maintaining fixed hormonal conditions by infusing somatostatin with basal insulin, glucagon, and growth hormone. |
| 3831 | 14583439 | Insulin concentrations were maintained at approximately 65 pmol/l by means of a somatostatin and "basal" insulin infusion. |
| 3832 | 14600073 | A pancreatic-pituitary clamp was maintained with somatostatin infusion and replacement of GH, insulin, and glucagon at baseline levels. |
| 3833 | 14693692 | During the experimental period, somatostatin, fourfold basal intraportal insulin, basal intraportal glucagon, and peripheral glucose (to double the hepatic glucose load) were infused. |
| 3834 | 14693692 | Intraportal 5-HT enhances NHGU but blunts nonhepatic glucose uptake, raising the possibility that hepatic-targeted 5-HT or 5-HT receptor agonists might reduce postprandial hyperglycemia. |
| 3835 | 14693695 | During periods 1 and 2, somatostatin, basal intraportal insulin and glucagon, portal glucose (21.3 micromol.kg(-1).min(-1)), peripheral glucose (to double the hepatic glucose load), and peripheral nicotinic acid (1.5 mg.kg(-1).min(-1)) were infused. |
| 3836 | 14715864 | In vitro data have recently suggested that sulfonylureas (SUs) enhance GH secretion by modulating the effects of GHRH and somatostatin in pituitary cells. |
| 3837 | 14715864 | Subsequently, GH concentrations were measured regularly after stimulation with GHRH (bolus 0.1 micro g/kg) alone and during concomitant infusion with somatostatin (7 ng.kg(-1).min(-1)). |
| 3838 | 14715864 | In vitro data have recently suggested that sulfonylureas (SUs) enhance GH secretion by modulating the effects of GHRH and somatostatin in pituitary cells. |
| 3839 | 14715864 | Subsequently, GH concentrations were measured regularly after stimulation with GHRH (bolus 0.1 micro g/kg) alone and during concomitant infusion with somatostatin (7 ng.kg(-1).min(-1)). |
| 3840 | 14718149 | A diagnosis of metastatic glucagonoma was established and therapy with streptozocin, 5-FU, insulin and synthetic somatostatin analogs was initiated. |
| 3841 | 14747277 | Somatostatin was infused and glucagon and insulin were replaced in the portal vein to achieve basal arterial and portal vein levels at rest and simulated levels during the first 60 min of exercise. |
| 3842 | 14751362 | Combination of LHRH analog with somatostatin analog and dexamethasone versus chemotherapy in hormone-refractory prostate cancer: a randomized phase II study. |
| 3843 | 14767880 | Lys9 for Glu9 substitution in glucagon-like peptide-1(7-36)amide confers dipeptidylpeptidase IV resistance with cellular and metabolic actions similar to those of established antagonists glucagon-like peptide-1(9-36)amide and exendin (9-39). |
| 3844 | 14767880 | Its effects, mediated through the regulation of insulin, glucagon, and somatostatin, are glucose-dependent and contribute to the tight control of glucose levels. |
| 3845 | 14983031 | We detected in diabetic mice proinsulin- and insulin-positive cells in the liver, adipose tissue, spleen, bone marrow, and thymus; many cells also produced glucagon, somatostatin, and pancreatic polypeptide. |
| 3846 | 14984323 | To assess a possible influence of short-term administration of somatostatin on remission development in adult patients with newly diagnosed diabetes mellitus type 1, the somatostatin analog octreotide was given for two weeks after the establishment of the diagnosis at the daily dose of 150 microg subcutaneously in addition to the regular insulin and metabolic therapy. |
| 3847 | 14988244 | In the present study, we used neonatal rats treated with streptozotocin (STZ) to investigate the effects of activin A and BTC on regeneration of pancreatic beta-cells. |
| 3848 | 14988244 | One-day-old Sprague-Dawley rats were injected with STZ (85 micro g/g) and then administered for 7 days with activin A and/or BTC. |
| 3849 | 14988244 | Treatment with activin A and BTC significantly reduced the plasma glucose concentration and the plasma glucose response to intraperitoneal glucose loading. |
| 3850 | 14988244 | The pancreatic insulin content and beta-cell mass in rats treated with activin A and BTC were significantly increased compared with the control group on day 8 and at 2 months. |
| 3851 | 14988244 | Treatment with activin A and BTC significantly increased the DNA synthesis in preexisting beta-cells, ductal cells, and delta-cells. |
| 3852 | 14988244 | The number of islet cell-like clusters (ICCs) and islets was significantly increased by treatment with activin A and BTC. |
| 3853 | 14988244 | In addition, the number of insulin/somatostatin-positive cells and pancreatic duodenal homeobox-1/somatostatin-positive cells was significantly increased. |
| 3854 | 14988244 | These results indicate that, in neonatal STZ-treated rats, a combination of activin A and BTC promoted regeneration of pancreatic beta-cells and improved glucose metabolism in adults. |
| 3855 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 3856 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 3857 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 3858 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 3859 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 3860 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 3861 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 3862 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 3863 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 3864 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 3865 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 3866 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 3867 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 3868 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 3869 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 3870 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 3871 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 3872 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 3873 | 15007609 | Somatostatin analogues are a therapeutic option in patients with chronic overproduction of growth hormone (GH) and insulin-like growth factor 1 (IGF-1). |
| 3874 | 15016242 | GLP-1 regulates blood glucose via actions on gastric emptying and islet hormones, including the regulation of insulin, glucagon, and somatostatin secretion. |
| 3875 | 15016242 | GLP-1 action is essential for beta-cell function, because the disruption of GLP-1 signaling results in reduced insulin secretion, decreased islet cyclic adenosine monophosphate, and abnormal intracellular calcium oscillations. |
| 3876 | 15028942 | The transcription factor pancreatic duodenal homeobox 1 (PDX-1) is uniformly expressed in early pancreatic buds of embryos as well as the beta and delta cells of the islets of Langerhans. |
| 3877 | 15028942 | It has been shown that PDX-1 is required for maintaining the pancreatic islet functions by activating gene transcriptions including insulin, somatostatin (SST), islet amyloid polypeptide, glucose transporter type 2, and glucokinase. |
| 3878 | 15034596 | These aggregates showed endocrine gene expression for insulin (I and II), glucagon, somatostatin and pancreatic polypeptide. |
| 3879 | 15034596 | Immunohistochemistry also confirmed that these aggregates were positive for insulin, somatostatin, pancreatic polypeptide and C-peptide. |
| 3880 | 15034596 | These aggregates showed endocrine gene expression for insulin (I and II), glucagon, somatostatin and pancreatic polypeptide. |
| 3881 | 15034596 | Immunohistochemistry also confirmed that these aggregates were positive for insulin, somatostatin, pancreatic polypeptide and C-peptide. |
| 3882 | 15047618 | Regulated expression of pdx-1 promotes in vitro differentiation of insulin-producing cells from embryonic stem cells. |
| 3883 | 15047618 | The results showed that pdx-1 expression clearly enhanced the expression of the insulin 2, somatostatin, Kir6.2, glucokinase, neurogenin3, p48, Pax6, PC2, and HNF6 genes in the resulting differentiated cells. |
| 3884 | 15047618 | Thus, exogenous expression of pdx-1 should provide a promising approach for efficiently producing insulin-secreting cells from human ES cells for future therapeutic use in diabetic patients. |
| 3885 | 15047619 | Basal and glucose-stimulated secretion of insulin and somatostatin were unaffected by SR95531. |
| 3886 | 15053988 | Somatostatin was infused, and glucagon and insulin were replaced to basal levels. |
| 3887 | 15056499 | Somatostatin agonists may also exert their anti-angiogenic activity indirectly by inhibition of growth factors like vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis or through its immunomodulatory effects. |
| 3888 | 15077918 | Somatostatin is a natural peptide hormone that affects the release of a number of other hormones, such as growth hormone, glucagon, insulin and gastrin. |
| 3889 | 15077918 | This compound has been shown to block the local and systemic production of insulin-like growth factor 1 and growth hormone, which promote the angiogenesis and endothelial cell proliferation associated with proliferative retinopathy. |
| 3890 | 15077918 | Several studies have confirmed that using somatostatin analogs to block insulin-like growth factor 1 production is effective in reducing neovascularization and preventing disease progression to proliferative stage of diabetic retinopathy. |
| 3891 | 15077918 | Somatostatin is a natural peptide hormone that affects the release of a number of other hormones, such as growth hormone, glucagon, insulin and gastrin. |
| 3892 | 15077918 | This compound has been shown to block the local and systemic production of insulin-like growth factor 1 and growth hormone, which promote the angiogenesis and endothelial cell proliferation associated with proliferative retinopathy. |
| 3893 | 15077918 | Several studies have confirmed that using somatostatin analogs to block insulin-like growth factor 1 production is effective in reducing neovascularization and preventing disease progression to proliferative stage of diabetic retinopathy. |
| 3894 | 15125025 | The immunohistochemical data showed that, among the established islet hormones, insulin was present in more than 50% of cells, whereas glucagon and somatostatin occurred only sporadically. |
| 3895 | 15125025 | Though cells positive for pancreatic polypeptide (PP) were not found, PP-related peptides (NPY and PYY) however could be detected in a minority of cells. |
| 3896 | 15125025 | The great majority of RINm5F cells were immunoreactive for chromogranin B (CgB), followed by insulin, chromogranin A (CgA), and serotonin (5-HT). |
| 3897 | 15153604 | Embryoid bodies were first cultured and plated in insulin-transferrin-selenium-fibronectin medium, followed by medium supplemented with N2, B27, and basic fibroblast growth factor (bFGF). |
| 3898 | 15153604 | In addition to insulin, most cells also coexpressed glucagon or somatostatin, indicating a similarity to immature pancreatic cells. |
| 3899 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3900 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3901 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3902 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3903 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3904 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3905 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3906 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3907 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3908 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3909 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3910 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3911 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3912 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3913 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3914 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3915 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3916 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3917 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3918 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3919 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3920 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3921 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3922 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3923 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3924 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3925 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3926 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3927 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3928 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3929 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3930 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3931 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3932 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3933 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3934 | 15161757 | Regulation of rat pancreatic CCKB receptor and somatostatin expression by insulin. |
| 3935 | 15161757 | The cholecystokinin B receptor (CCK(B)R) is localized on pancreatic endocrine somatostatin delta-cells. |
| 3936 | 15161757 | Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK(B)R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK(B)R in islets was measured. |
| 3937 | 15161757 | Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. |
| 3938 | 15161757 | Gland and islet CCK(B)R mRNA and protein almost disappeared during diabetes; CCK(B) mRNA reappeared in response to insulin, but the protein did not. |
| 3939 | 15161757 | Confocal microscopy confirmed data obtained on somatostatin and CCK(B)R as established biochemically in the course of the treatments. |
| 3940 | 15161757 | In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK(B)R mRNA; the CCK(B)R protein appears to be delayed. |
| 3941 | 15161771 | Among the many known actions of TZDs, increased circulating levels of the high molecular weight (HMW) multimer of adiponectin may be an important insulin-sensitizing mechanism. |
| 3942 | 15161771 | Glucose fluxes ([3-(3)H]glucose infusion) were measured during 6-h euglycemic (5 mmol/l) "pancreatic clamp" studies (somatostatin/glucagon/growth hormone) with stepped insulin levels. |
| 3943 | 15161771 | Increased abundance of the HMW adiponectin multimer may contribute to the hepatic insulin-sensitizing effects of these agents. |
| 3944 | 15180566 | Deficient insulin release causes hyperglycemia and diabetes, whereas excessive insulin release can give rise to serious metabolic disorders, such as nesidioblastosis (Persistent Hyperinsulinemic Hypoglycemia of Infancy, PHHI) and might also be closely associated with development of type 2 diabetes and obesity. |
| 3945 | 15180566 | Thus, insulin release is regulated by e.g. somatostatin receptors, GLP-1 receptors, muscarinic receptors, cholecystokinin receptors and adrenergic receptors. |
| 3946 | 15190448 | Abdominal ultrasound (US), computed tomography (CT), magnetic resonance tomography (MRT) and somatostatin receptor scintigraphy (SRS) are used for localisation of the primary tumour and metastasis. |
| 3947 | 15209756 | A literature review on medical therapies for diabetic retinopathy has been performed, and the following classes of drugs are discussed: blockers of the renin-angiotensin system, protein kinase C-beta inhibitors, glitazones, somatostatin analogues, lipid-lowering drugs and anti-inflammatory drugs. |
| 3948 | 15220198 | A novel variant of ionotropic glutamate receptor regulates somatostatin secretion from delta-cells of islets of Langerhans. |
| 3949 | 15220198 | Somatostatin from delta-cells, considered a local inhibitor of islet function, reduces insulin and glucagon secretion by activating somatostatin receptors in islet cells. |
| 3950 | 15220198 | Somatostatin secretion from delta-cells is increased by high glucose via glucose metabolism in a similar way to insulin secretion from beta-cells. |
| 3951 | 15220198 | In this study, we showed that delta-cells express GluR4c-flip, a newly identified splicing variant of GluR4, an (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type ionotropic glutamate receptor of rat. |
| 3952 | 15220198 | A novel variant of ionotropic glutamate receptor regulates somatostatin secretion from delta-cells of islets of Langerhans. |
| 3953 | 15220198 | Somatostatin from delta-cells, considered a local inhibitor of islet function, reduces insulin and glucagon secretion by activating somatostatin receptors in islet cells. |
| 3954 | 15220198 | Somatostatin secretion from delta-cells is increased by high glucose via glucose metabolism in a similar way to insulin secretion from beta-cells. |
| 3955 | 15220198 | In this study, we showed that delta-cells express GluR4c-flip, a newly identified splicing variant of GluR4, an (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type ionotropic glutamate receptor of rat. |
| 3956 | 15220198 | A novel variant of ionotropic glutamate receptor regulates somatostatin secretion from delta-cells of islets of Langerhans. |
| 3957 | 15220198 | Somatostatin from delta-cells, considered a local inhibitor of islet function, reduces insulin and glucagon secretion by activating somatostatin receptors in islet cells. |
| 3958 | 15220198 | Somatostatin secretion from delta-cells is increased by high glucose via glucose metabolism in a similar way to insulin secretion from beta-cells. |
| 3959 | 15220198 | In this study, we showed that delta-cells express GluR4c-flip, a newly identified splicing variant of GluR4, an (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type ionotropic glutamate receptor of rat. |
| 3960 | 15231824 | We have previously reported, by means of photobleaching fluorescence resonance energy transfer (pbFRET) microscopy and fluorescence correlation spectroscopic analysis in live cells, that human somatostatin receptor (hSSTR) 5 could both homodimerize and heterodimerize with hSSTR1 in the presence of the agonist SST-14. |
| 3961 | 15247250 | We have previously reported by means of photobleaching fluorescence resonance energy transfer (pbFRET) microscopy and fluorescence correlation spectroscopic (FCS) analysis in live cells, that human somatostatin receptor (hSSTR) 5 could both homodimerize and heterodimerize with hSSTR1 in the presence of the agonist SST-14. |
| 3962 | 15247250 | In an effort to elucidate the role of ligand and receptor subtypes in heterodimerization, we have employed both pb-FRET microscopy and Western blot on cells stably co-expressing hSSTR1 and hSSTR5 treated with subtype-specific agonists. |
| 3963 | 15247250 | Here we provide evidence that activation of hSSTR5 but not hSSTR1 is necessary for heterodimeric assembly. |
| 3964 | 15247250 | Finally, we demonstrate that heterodimerization is subtype-selective involving ligand-induced conformational changes in hSSTR5 but not hSSTR1 and could be attributed to molecular events occurring at the C-tail. |
| 3965 | 15281344 | It is likely that an interaction between gene expression (such as pituitary tumour transforming gene), hormonal stimuli including oestrogens, corticosteroids, dopamine, 16-kDa fragments of prolactin and growth hormone, somatostatin analogues, and pro- and anti-angiogenic growth factors (e.g. vascular endothelial growth factor and fibroblast growth factor), determine the final angiogenic phenotype of pituitary tumours, and thus subsequent tumour behaviour. |
| 3966 | 15315909 | During EXP, somatostatin, fourfold basal intraportal insulin, basal intraportal glucagon, and peripheral glucose (to double the hepatic glucose load) were infused. |
| 3967 | 15321003 | Real-time polymerase chain reaction confirmed the identification of various islet-specific genes detected by microarray analysis, but also showed that such genes as pancreatic duodenal homeobox 1 protein and glucagon-like peptide 1 receptor, which were not detected by gene array, can be readily identified and quantified. |
| 3968 | 15321003 | Indeed, the abundance of mRNA for insulin when compared with the level of somatostatin mRNA was not as different as one would have predicated based on the classic knowledge of islet physiology. |
| 3969 | 15364160 | Association of serum apolipoprotein C III levels and apolipoprotein C III gene Sst I polymorphism with carotid intima-media thickness in Chinese type 2 diabetic patients. |
| 3970 | 15364160 | Apolipoprotein C III (apo C III) plays a central role in regulating plasma metabolism of triglyceride-rich lipoprotein (TRL). |
| 3971 | 15494355 | Comparison between somatostatin analogues and ACE inhibitor in the NOD mouse model of diabetic kidney disease. |
| 3972 | 15502648 | Diabetes mellitus influences the degree of colocalization of calcitonin gene-related peptide with insulin and somatostatin in the rat pancreas. |
| 3973 | 15561914 | To address this, six patients with type 2 diabetes and six age- and BMI-matched normal subjects received a combined 3-h insulin and somatostatin clamp to decrease beta-cell secretory demand. |
| 3974 | 15561928 | Interestingly, somatostatin receptor (sstr1) expression was increased by SREBP1c, whereas AMPK induced the expression of peptide YY, the early endocrine pancreas marker. |
| 3975 | 15561932 | At the onset of exercise, somatostatin was infused into a peripheral vein, and insulin and glucagon were infused in the portal vein to maintain basal levels (EX-Basal) or simulate the response to exercise (EX-Sim). |
| 3976 | 15624122 | Increased levels of SST were also found in antigen-presenting cells and are associated with a significant increase of CD8 expression levels on CD4(+)/CD8(+) immature thymocytes. |
| 3977 | 15629153 | They also contain cells expressing the other major islet hormones (glucagon, somatostatin, and pancreatic polypeptide). |
| 3978 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 3979 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 3980 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 3981 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 3982 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 3983 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 3984 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 3985 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 3986 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 3987 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 3988 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 3989 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 3990 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 3991 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 3992 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 3993 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 3994 | 15765120 | TC islets contained cells stained positive for insulin, glucagon, somatostatin, pancreatic polypeptide, as well as PDX-1, chromogranin, and hepatocyte-derived growth factor receptor, c-met. |
| 3995 | 15765120 | Duct-like cells in TC of BBdp rats expressed markers of committed endocrine precursors: PDX-1, neurogenin 3 and protein gene product 9.5. |
| 3996 | 15778893 | Twelve healthy volunteers consecutively underwent a hyperglycaemic experiment (HYPER), with the plasma glucose level maintained at 20 mmol.l(-1) for 6 h by combined infusion of somatostatin, insulin and glucose; and a normoglycaemic experiment (NORMO), with similar infusions but with the plasma glucose maintained at fasting level. |
| 3997 | 15778893 | In an age- and weight matched group, fasting and 6-h sympathetic activity was measured without infusion of somatostatin and insulin (CONTROL). |
| 3998 | 15778893 | Twelve healthy volunteers consecutively underwent a hyperglycaemic experiment (HYPER), with the plasma glucose level maintained at 20 mmol.l(-1) for 6 h by combined infusion of somatostatin, insulin and glucose; and a normoglycaemic experiment (NORMO), with similar infusions but with the plasma glucose maintained at fasting level. |
| 3999 | 15778893 | In an age- and weight matched group, fasting and 6-h sympathetic activity was measured without infusion of somatostatin and insulin (CONTROL). |
| 4000 | 15809016 | Progression of diabetic retinopathy during improved metabolic control may be treated with reduced insulin dosage and/or somatostatin analogue administration -- a case report. |
| 4001 | 15809016 | Serum concentrations of IGF-I, IGFBP-3, insulin, cystatin C, creatinine, endogenous creatinine clearance and HbA1c-levels were assessed by routine laboratory methods; serum IGF-I bioactivity was estimated by a highly specific kinase receptor activation assay. |
| 4002 | 15961235 | In AD cortical brain region, somatostatin and neuropeptide-Y-positive neurons decreased (>70%), and glial fibrillary acidic protein-positive astrocytes significantly increased (>130%) in comparison to control brain. |
| 4003 | 15961235 | SSTR2 and 4 were the predominant subtypes followed by SSTR1, 3 and 5. |
| 4004 | 15961235 | AD cortex showed a marked reduction in neuronal expression of SSTR4 and 5 and a modest decrease in SSTR2-like immunoreactivity without any changes in SSTR1 immunoreactive neurons. |
| 4005 | 15961235 | In AD cortex, SSTR1-, 3- and 4-like immunoreactivities were strongly expressed in glial cells but not SSTR2 and 5. |
| 4006 | 15961235 | These findings suggest the differential loss of immunoreactivity of SSTR2, 4 and 5 but not SSTR1, and increased SSTR3 in frontal cortex of AD brain as well as subtype-selective glial expression in AD brain. |
| 4007 | 16024998 | Interestingly, EGFP mRNA-negative and protein-positive cells expressed insulin, glucagon, somatostatin and pancreatic polypeptide, pancreatic endocrine markers. |
| 4008 | 16123357 | Somatostatin-insulin-glucose clamps created conditions of low peripheral hyperinsulinemia ( approximately 100 pmol/l, 0-180 min) and prandial-like peripheral hyperinsulinemia ( approximately 430 pmol/l, 180-360 min). |
| 4009 | 16123357 | Furthermore, amino acid infusion increased the inhibitory insulin receptor substrate-1 phosphorylation at Ser312 and Ser636/639 and decreased insulin-induced phosphoinositide 3-kinase activity. |
| 4010 | 16123357 | However, plasma amino acid elevation failed to reduce insulin-induced Akt/protein kinase B and glycogen synthase kinase 3alpha phosphorylation. |
| 4011 | 16181081 | Low levels of neuropeptide Y, somatostatin and corticotropin-releasing factor, described in Alzheimer disease (AD), were related to a defect in proteolytic processing of their protein precursors. |
| 4012 | 16200462 | Histopathological changes in insulin, glucagon and somatostatin cells in the islets of NOD mice during cyclophosphamide-accelerated diabetes: a combined immunohistochemical and histochemical study. |
| 4013 | 16200462 | The cyclophosphamide model of accelerated diabetes in the NOD mouse is a useful model of insulin-dependent diabetes mellitus (IDDM). |
| 4014 | 16223861 | The expression levels of cyclin-dependent kinase 2 and cyclin A, as well as cyclin-dependent kinase 1 and cyclin B, were decreased by TH, and after withdrawal not only did these regulators of Rb phosphorylation and mitosis increase in their expression but so too did the D1 and D3 cyclins. |
| 4015 | 16223861 | Because somatostatin can arrest growth by activating MAPK pathways, we examined these pathways in TtT-97 tumors and found that the ERK pathway and several of its upstream and downstream effectors, including cAMP response element binding protein, were activated with TH treatment and deactivated after its withdrawal. |
| 4016 | 16223861 | This led to the hypothesis that TH, acting through increased type 5 somatostatin receptor, could activate the ERK pathway leading to cAMP response element binding protein-dependent decreased expression of critical cell cycle proteins, specifically cyclin A, resulting in hypophosphorylation of Rb and its subsequent arrest of S-phase progression. |
| 4017 | 16223861 | The expression levels of cyclin-dependent kinase 2 and cyclin A, as well as cyclin-dependent kinase 1 and cyclin B, were decreased by TH, and after withdrawal not only did these regulators of Rb phosphorylation and mitosis increase in their expression but so too did the D1 and D3 cyclins. |
| 4018 | 16223861 | Because somatostatin can arrest growth by activating MAPK pathways, we examined these pathways in TtT-97 tumors and found that the ERK pathway and several of its upstream and downstream effectors, including cAMP response element binding protein, were activated with TH treatment and deactivated after its withdrawal. |
| 4019 | 16223861 | This led to the hypothesis that TH, acting through increased type 5 somatostatin receptor, could activate the ERK pathway leading to cAMP response element binding protein-dependent decreased expression of critical cell cycle proteins, specifically cyclin A, resulting in hypophosphorylation of Rb and its subsequent arrest of S-phase progression. |
| 4020 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 4021 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 4022 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 4023 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 4024 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 4025 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 4026 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 4027 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 4028 | 16250324 | Several research centers carried out collaborative studies of the nucleotide sequences of human and animal proopiomelanocortin (lipotropin precursor) and prolactin cDNA. |
| 4029 | 16250324 | Researchers constructed genetic engineering producers of human pre-proinsulin and somatostatin, identified structural genes expressed in pancreatic beta-cells, studied antigenic properties of glutamic acid decarboxylase (GAD), which determine insulin-dependent diabetes, and identified the cholesterase determinant. |
| 4030 | 16250324 | They revealed mutations in the genes of proopiomelanocortin and melanocortin receptors (MC4-P), which inhibit leptin regulation of appetite and are associated with human obesity. |
| 4031 | 16306340 | Dense core vesicle proteins IA-2 and IA-2beta: metabolic alterations in double knockout mice. |
| 4032 | 16306340 | IA-2 and IA-2beta are members of the transmembrane protein tyrosine phosphatase family located in dense core vesicles of neuroendocrine cells, including the beta-cells of pancreatic islets. |
| 4033 | 16306340 | In the present study, by mating C57BL/6Nci IA-2(+/-) with IA-2beta(+/-) mice, we generated double knockout mice (IA-2(-/-)/IA-2beta(-/-)) to study the effect of the combined deletion of these two proteins on insulin secretion and blood glucose levels. |
| 4034 | 16306340 | Histological examination and immunostaining for insulin, glucagon, somatostatin, and pancreatic polypeptide revealed no difference between the double knockout and wild-type mice. |
| 4035 | 16306340 | No evidence of insulin resistance was observed nor were there alterations in fasting blood glucose, insulin, or leptin levels in the double knockout mice maintained on a high-fat diet compared with the wild-type mice maintained on the same diet. |
| 4036 | 16306340 | In addition, to determine whether the combined deletion of IA-2 and IA-2beta played any role in the development of diabetes in NOD mice, we generated double knockout mice on the NOD/LtJ background. |
| 4037 | 16306340 | Taken together, our experiments show that the dense core vesicle proteins IA-2 and IA-2beta, alone or in combination, are involved in insulin secretion, but neither alone nor in combination are they required for the development of diabetes in NOD mice. |
| 4038 | 16345100 | Specifically, through RT-PCR analyses and functionality assays, we show that cells within the population expressed all four of the endocrine hormone genes and proteins (insulin, glucagon, somatostatin, pancreatic polypeptide). |
| 4039 | 16405075 | RT-PCR analysis revealed that a series of transcriptional factors involved in differentiation of pancreatic endocrine cells was induced by the treatment with sodium butyrate and betacellulin. mRNAs for insulin, pancreatic polypeptide, and somatostatin were also observed. |
| 4040 | 16405075 | Immunoreactive pancreatic polypeptide, somatostatin, and insulin were detected in sodium butyrate and betacellulin-treated HSL cells. |
| 4041 | 16405075 | RT-PCR analysis revealed that a series of transcriptional factors involved in differentiation of pancreatic endocrine cells was induced by the treatment with sodium butyrate and betacellulin. mRNAs for insulin, pancreatic polypeptide, and somatostatin were also observed. |
| 4042 | 16405075 | Immunoreactive pancreatic polypeptide, somatostatin, and insulin were detected in sodium butyrate and betacellulin-treated HSL cells. |
| 4043 | 16443761 | At high glucose, CART potentiated cAMP-enhanced insulin secretion via the cAMP/protein kinase A-dependent pathway. |
| 4044 | 16443761 | In the absence of cAMP-elevating agents, CART was without effect on INS-1 cells but modestly inhibited secretion of insulin, glucagon, and somatostatin from isolated islets. |
| 4045 | 16460677 | Human adipose tissue-derived mesenchymal stem cells differentiate into insulin, somatostatin, and glucagon expressing cells. |
| 4046 | 16460677 | During the proliferation period, the cells expressed the stem cell markers nestin, ABCG2, SCF, Thy-1 as well as the pancreatic endocrine transcription factor Isl-1. |
| 4047 | 16460677 | Using quantitative PCR a down-regulation of ABCG2 and up-regulation of pancreatic developmental transcription factors Isl-1, Ipf-1, and Ngn3 were observed together with induction of the islet hormones insulin, glucagon, and somatostatin. |
| 4048 | 16461552 | As previously reported, HI STZ resulted in a decrease in circulating GH and IGF-I levels which was associated with a rise in hypothalamic neuropeptide Y (NPY) mRNA (355% of vehicle-treated controls) and a fall in GH-releasing hormone (GHRH) mRNA (45% of vehicle-treated controls) levels. |
| 4049 | 16461552 | Changes in hypothalamic neuropeptide expression were reflected by an increase in immunoreactive NPY within the arcuate and paraventricular nuclei and a decrease in GHRH immunoreactivity in the arcuate nucleus, as assessed by immunohistochemistry. |
| 4050 | 16461552 | However, pituitary receptor mRNA levels for GHRH and ghrelin increased and those for somatostatin (sst2, sst3 and sst5) decreased following HI STZ treatment. |
| 4051 | 16461552 | Specifically, LO STZ treatment did suppress circulating IGF-I levels to the same extent as HI STZ treatment; however, the impact on hypothalamic NPY mRNA levels was less dramatic (158% of vehicle-treated controls) where NPY immunoreactivity was increased only within the paraventricular nucleus. |
| 4052 | 16461897 | Insulin-immunoreactive beta cells, glucagon-immunoreactive alpha cells, and somatostatin-containing delta cells were found scattered throughout the human islet. |
| 4053 | 16498061 | Efficacy of 12-month treatment with the GH receptor antagonist pegvisomant in patients with acromegaly resistant to long-term, high-dose somatostatin analog treatment: effect on IGF-I levels, tumor mass, hypertension and glucose tolerance. |
| 4054 | 16505218 | Tomosyn is expressed in beta-cells and negatively regulates insulin exocytosis. |
| 4055 | 16505218 | Tomosyn, a syntaxin-binding protein, is capable of dissociating mammalian homolog of the Caenorhabditis elegans unc-18 gene from syntaxin and is involved in the regulation of exocytosis. |
| 4056 | 16505218 | Western blotting revealed a 130-kDa protein corresponding to tomosyn in insulin-secreting beta-cell lines. |
| 4057 | 16505218 | Immunohistochemistry revealed punctate tomosyn immunoreactivity in the cytoplasm of insulin-, glucagon-, pancreatic polypeptide-, and somatostatin-containing islet cells. |
| 4058 | 16505218 | Syntaxin 1 coimmunoprecipitated with tomosyn in extracts of insulin-secreting cells. |
| 4059 | 16505218 | Hence, in the pancreatic beta-cell, tomosyn negatively regulates insulin exocytosis. |
| 4060 | 16519802 | Colocalization of somatostatin receptors and epidermal growth factor receptors in breast cancer cells. |
| 4061 | 16549322 | We already characterised 1 phagotope (CH1p), as an epitope of human osteopontin, an autoantigen expressed within the somatostatin cells of human islets. |
| 4062 | 16599577 | The resulting population consisted of single cells and many islet-like aggregates that contained all of the endocrine cell types (including insulin-positive, glucagon-positive, somatostatin-positive, and pancreatic polypeptide-positive cells). |
| 4063 | 16750430 | Foxd3 is expressed in most beta cells and infrequently in alpha and PP cells but is not expressed in somatostatin cells. |
| 4064 | 16793952 | Effects of the long-acting somatostatin analogue Lanreotide Autogel on glucose tolerance and insulin resistance in acromegaly. |
| 4065 | 16804060 | Insulin-positive cells and pancreatic duodenal homeobox 1 (PDX1)-positive cells both were clearly increased in the older compared with the younger transgenic mice. |
| 4066 | 16804060 | In addition, a subset of the DBA-labeled cells was positive for PDX1, insulin, glucagon, somatostatin, or pancreatic polypeptide. |
| 4067 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4068 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4069 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4070 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4071 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4072 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4073 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4074 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4075 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4076 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4077 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4078 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4079 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4080 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4081 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4082 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4083 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4084 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4085 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4086 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4087 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4088 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4089 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4090 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4091 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4092 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4093 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4094 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4095 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4096 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4097 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4098 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4099 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4100 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4101 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4102 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4103 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4104 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4105 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4106 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4107 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4108 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4109 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4110 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4111 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4112 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4113 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4114 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4115 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 4116 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 4117 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 4118 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 4119 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 4120 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 4121 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 4122 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 4123 | 16842887 | In adult rats the intra-islet expression of CART is limited to the somatostatin producing delta-cells, while in adult mice CART is mainly expressed in nerve fibers. |
| 4124 | 16842887 | During development islet CART is upregulated; in rats in almost all types of islet endocrine cells, including the insulin-producing beta-cells, and in mice mainly in the alpha-cells. |
| 4125 | 16842887 | While CART inhibits glucose stimulated insulin secretion from rat islets it augments insulin secretion amplified by cAMP. |
| 4126 | 16857751 | Somatostatin inhibits both glucagon and insulin secretion. |
| 4127 | 16857751 | Despite its function in the inhibition of glucagon secretion, somatostatin fails to reduce hyperglycemia in type 2 diabetes, due to a parallel suppression of insulin secretion. |
| 4128 | 16857751 | Somatostatin inhibits both glucagon and insulin secretion. |
| 4129 | 16857751 | Despite its function in the inhibition of glucagon secretion, somatostatin fails to reduce hyperglycemia in type 2 diabetes, due to a parallel suppression of insulin secretion. |
| 4130 | 16925587 | However, hypothalamic atrophy occurs at early stages of HD with loss of orexin- and somatostatin-containing cell populations. |
| 4131 | 16926384 | When pancreatic acinar cells of streptozotocin-treated mice were cultured in suspension in the presence of epidermal growth factor and nicotinamide under low-serum condition, expressions of insulin genes gradually increased. |
| 4132 | 16926384 | In addition, expressions of other pancreatic hormones, including glucagon, somatostatin, and pancreatic polypeptide, were also induced. |
| 4133 | 16982847 | However, at E14.5, Nkx6.1 immunoreactivity marks the nuclei of all epithelial cells of the ventral and dorsal pancreatic buds and the only endocrine cell types found at this time point are glucagon and PYY. |
| 4134 | 16982847 | At E18.5 the pancreas is well branched and both glucagon- and ghrelin-positive cells are scattered or found in clusters, whereas insulin-positive cells are not found. |
| 4135 | 16982847 | Ghrelin-, glucagon-, PYY-, gastrin-, somatostatin (SS)-, pancreatic polypeptide (PP)-, and insulin-immunoreactive cells are found scattered or in small groups within or lining the developing ductal epithelium as marked by cytokeratin 19. |
| 4136 | 16982850 | There is a lack of agreement on the distribution of islet amyloid polypeptide (IAPP) in the pancreases of healthy and diabetic subjects. |
| 4137 | 16982850 | Therefore, a detailed morphometrical and immunohistochemical study was performed to obtain information on the distribution of cells expressing insulin, glucagon, somatostatin, pancreatic polypeptide (PP), and IAPP in the pancreases of non-diabetic (n=4) and diabetic individuals (n=6). |
| 4138 | 16990588 | The islet-like clusters showed endocrine gene expression typical for pancreatic beta-cell development and function, such as insulin (I and II), glucagon, somatostatin, GLUT-2, pancreatic duodenal homeobox-1 (PDX-1), and Pax 4. |
| 4139 | 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. |
| 4140 | 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. |
| 4141 | 17047390 | Somatostatin analogs control GH/insulin-like growth factor (IGF)-1 excess, induce tumor shrinkage in a high proportion of patients, improve symptoms of acromegaly with relatively limited side effects and are successfully administered in patients not suitable for surgery. |
| 4142 | 17047390 | Furthermore, preoperative somatostatin analogs have been suggested to improve outcome for tumors with limited invasiveness, while surgical tumor debulking in cases that are, at least partially, somatostatin resistant, increases the achievement of normal IGF-1 levels by postoperative somatostatin analog treatment. |
| 4143 | 17047390 | Somatostatin analogs improve insulin sensitivity, exerting, however, a concomitant direct inhibitory effect on insulin secretion, with a net balance leaning towards a deterioration in glucose homeostasis. |
| 4144 | 17047390 | As a result, oral insulin secretagogues (and/or insulin) should probably be preferred to insulin sensitizers in acromegalic patients developing diabetes while on somatostatin analogs. |
| 4145 | 17047390 | Nevertheless, glucose tolerance remains normal in most of the nondiabetic acromegalic patients, while diabetic acromegalic patients on insulin are at risk for hypoglycemia during initiation of somatostatin analog therapy. |
| 4146 | 17047390 | Somatostatin analogs control GH/insulin-like growth factor (IGF)-1 excess, induce tumor shrinkage in a high proportion of patients, improve symptoms of acromegaly with relatively limited side effects and are successfully administered in patients not suitable for surgery. |
| 4147 | 17047390 | Furthermore, preoperative somatostatin analogs have been suggested to improve outcome for tumors with limited invasiveness, while surgical tumor debulking in cases that are, at least partially, somatostatin resistant, increases the achievement of normal IGF-1 levels by postoperative somatostatin analog treatment. |
| 4148 | 17047390 | Somatostatin analogs improve insulin sensitivity, exerting, however, a concomitant direct inhibitory effect on insulin secretion, with a net balance leaning towards a deterioration in glucose homeostasis. |
| 4149 | 17047390 | As a result, oral insulin secretagogues (and/or insulin) should probably be preferred to insulin sensitizers in acromegalic patients developing diabetes while on somatostatin analogs. |
| 4150 | 17047390 | Nevertheless, glucose tolerance remains normal in most of the nondiabetic acromegalic patients, while diabetic acromegalic patients on insulin are at risk for hypoglycemia during initiation of somatostatin analog therapy. |
| 4151 | 17047390 | Somatostatin analogs control GH/insulin-like growth factor (IGF)-1 excess, induce tumor shrinkage in a high proportion of patients, improve symptoms of acromegaly with relatively limited side effects and are successfully administered in patients not suitable for surgery. |
| 4152 | 17047390 | Furthermore, preoperative somatostatin analogs have been suggested to improve outcome for tumors with limited invasiveness, while surgical tumor debulking in cases that are, at least partially, somatostatin resistant, increases the achievement of normal IGF-1 levels by postoperative somatostatin analog treatment. |
| 4153 | 17047390 | Somatostatin analogs improve insulin sensitivity, exerting, however, a concomitant direct inhibitory effect on insulin secretion, with a net balance leaning towards a deterioration in glucose homeostasis. |
| 4154 | 17047390 | As a result, oral insulin secretagogues (and/or insulin) should probably be preferred to insulin sensitizers in acromegalic patients developing diabetes while on somatostatin analogs. |
| 4155 | 17047390 | Nevertheless, glucose tolerance remains normal in most of the nondiabetic acromegalic patients, while diabetic acromegalic patients on insulin are at risk for hypoglycemia during initiation of somatostatin analog therapy. |
| 4156 | 17047390 | Somatostatin analogs control GH/insulin-like growth factor (IGF)-1 excess, induce tumor shrinkage in a high proportion of patients, improve symptoms of acromegaly with relatively limited side effects and are successfully administered in patients not suitable for surgery. |
| 4157 | 17047390 | Furthermore, preoperative somatostatin analogs have been suggested to improve outcome for tumors with limited invasiveness, while surgical tumor debulking in cases that are, at least partially, somatostatin resistant, increases the achievement of normal IGF-1 levels by postoperative somatostatin analog treatment. |
| 4158 | 17047390 | Somatostatin analogs improve insulin sensitivity, exerting, however, a concomitant direct inhibitory effect on insulin secretion, with a net balance leaning towards a deterioration in glucose homeostasis. |
| 4159 | 17047390 | As a result, oral insulin secretagogues (and/or insulin) should probably be preferred to insulin sensitizers in acromegalic patients developing diabetes while on somatostatin analogs. |
| 4160 | 17047390 | Nevertheless, glucose tolerance remains normal in most of the nondiabetic acromegalic patients, while diabetic acromegalic patients on insulin are at risk for hypoglycemia during initiation of somatostatin analog therapy. |
| 4161 | 17047390 | Somatostatin analogs control GH/insulin-like growth factor (IGF)-1 excess, induce tumor shrinkage in a high proportion of patients, improve symptoms of acromegaly with relatively limited side effects and are successfully administered in patients not suitable for surgery. |
| 4162 | 17047390 | Furthermore, preoperative somatostatin analogs have been suggested to improve outcome for tumors with limited invasiveness, while surgical tumor debulking in cases that are, at least partially, somatostatin resistant, increases the achievement of normal IGF-1 levels by postoperative somatostatin analog treatment. |
| 4163 | 17047390 | Somatostatin analogs improve insulin sensitivity, exerting, however, a concomitant direct inhibitory effect on insulin secretion, with a net balance leaning towards a deterioration in glucose homeostasis. |
| 4164 | 17047390 | As a result, oral insulin secretagogues (and/or insulin) should probably be preferred to insulin sensitizers in acromegalic patients developing diabetes while on somatostatin analogs. |
| 4165 | 17047390 | Nevertheless, glucose tolerance remains normal in most of the nondiabetic acromegalic patients, while diabetic acromegalic patients on insulin are at risk for hypoglycemia during initiation of somatostatin analog therapy. |
| 4166 | 17053790 | We have developed a differentiation process that converts human embryonic stem (hES) cells to endocrine cells capable of synthesizing the pancreatic hormones insulin, glucagon, somatostatin, pancreatic polypeptide and ghrelin. |
| 4167 | 17065334 | We measured brain glucose metabolism, using [(18)F]fluorodeoxyglucose positron emission tomography, in seven insulin-sensitive (homeostasis model assessment of insulin resistance [HOMA-IR] = 1.3) and seven insulin-resistant (HOMA-IR = 6.3) men, during suppression of endogenous insulin by somatostatin, with and without an insulin infusion that elevated insulin to 24.6 +/- 5.2 and 23.2 +/- 5.8 mU/l (P = 0.76), concentrations similar to fasting levels of the resistant subjects and approximately threefold above those of the insulin-sensitive subjects. |
| 4168 | 17070443 | Blood glucose, plasma insulin, somatostatin (SS), and GH levels were determined. |
| 4169 | 17130474 | A total of 13 type 2 diabetic and 17 nondiabetic subjects were studied on two separate occasions while maintaining similar insulin and glucose levels in both groups by 7-h infusions of somatostatin, low- or high-dose insulin (0.25 and 1.5 mU/kg of fat-free mass per min, respectively), and glucose. |
| 4170 | 17130474 | The lack of MAPR increment in response to high-dose insulin in type 2 diabetic patients occurred in association with reduced glucose disposal and expression of peroxisome proliferator-activated receptor-gamma coactivator 1alpha, citrate synthase, and cytochrome c oxidase I. |
| 4171 | 17137336 | As expected, the three major islet hormones (insulin, glucagon, and somatostatin) were detected, as well as various beta-cell enriched secretory products, ion channels, and transcription factors. |
| 4172 | 17137336 | In addition, significant proteome coverage of metabolic enzymes and cellular pathways was observed, including the integrin signaling cascade and the MAP kinase, NF-kappa beta, and JAK/STAT pathways. |
| 4173 | 17168853 | The role of growth hormone, insulin-like growth factor and somatostatin in diabetic retinopathy. |
| 4174 | 17168853 | Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are implicated in the aberrant cell growth and pathological neovascularization that characterises proliferative diabetic retinopathy. |
| 4175 | 17168853 | IGF-I may exert its cell growth promoting properties by stimulating a number of pathways including protein-kinase B (Akt), nuclear factor kB (NF-kappaB)/AP-1 and hypoxic-inducible factor-1alpha (HIF-1alpha). |
| 4176 | 17168853 | In addition, other growth factors may participate in IGF-I induced cell growth including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF). |
| 4177 | 17168853 | GH receptor antagonists, GH receptor antisense oligonucleotides, somatostatin analogues and receptor neutralising antibodies to IGF-I reduce hypoxic-induced retinal neovascularization. |
| 4178 | 17168853 | The role of growth hormone, insulin-like growth factor and somatostatin in diabetic retinopathy. |
| 4179 | 17168853 | Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are implicated in the aberrant cell growth and pathological neovascularization that characterises proliferative diabetic retinopathy. |
| 4180 | 17168853 | IGF-I may exert its cell growth promoting properties by stimulating a number of pathways including protein-kinase B (Akt), nuclear factor kB (NF-kappaB)/AP-1 and hypoxic-inducible factor-1alpha (HIF-1alpha). |
| 4181 | 17168853 | In addition, other growth factors may participate in IGF-I induced cell growth including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF). |
| 4182 | 17168853 | GH receptor antagonists, GH receptor antisense oligonucleotides, somatostatin analogues and receptor neutralising antibodies to IGF-I reduce hypoxic-induced retinal neovascularization. |
| 4183 | 17172056 | The proportion of insulin-producing cells differentiated from Pdx-1+BMSCs was 28.23% +/- 2.56%, higher than that from BMSCs transfected with vacant vector and Pdx-1-BMSCs (7.23% +/- 1.56% and 4.08% +/- 2.69% respectively) by flow cytometry. |
| 4184 | 17172056 | Immunocytochemical examination also testified the expression of multiple beta-cells-specific genes such as insulin, glucagons, somatostatin in differentiated BMSCs. |
| 4185 | 17172056 | Glucose-induced insulin secretion from Pdx-1+BMSCs in 5 mmol/L and 25 mmol/L glocuse was (56.61 +/- 4.82) microU/mL and (115.29 +/- 2.56) microU/mL respectively, which were much higher than those from Pdx-1-BMSCs ((25.53 +/- 6.49) microU/mL and (53.26 +/- 7.56) microU/mL respectively). |
| 4186 | 17178896 | Peroxisome proliferator-activated receptor gamma is a Zac target gene mediating Zac antiproliferation. |
| 4187 | 17178896 | Zac is a C2H2 zinc finger protein, which regulates apoptosis and cell cycle arrest through DNA binding and transactivation. |
| 4188 | 17178896 | Here, applying genome-wide expression analysis, we identify peroxisome proliferator-activated receptor gamma (PPARgamma) as a new bona fide Zac target gene, which is induced by direct Zac binding to the proximal PPARgamma1 promoter. |
| 4189 | 17178896 | We show that in human colon carcinoma cells, ZAC activates expression of PPARgamma target genes in a PPARgamma-dependent manner. |
| 4190 | 17178896 | Moreover, we show that treatment of pituitary tumor cells with octreotide, a somatostatin analogue, leads to Zac induction and subsequent Zac-dependent up-regulation of PPARgamma, which thereupon mediates part of the antiproliferative activity of Zac. |
| 4191 | 17178896 | Our work provides a first step toward elucidating a functional relationship between Zac and PPARgamma that could be relevant to the understanding of tumorigenesis and diabetes as well. |
| 4192 | 17179205 | Other endocrine cell types (producing somatostatin and pancreatic polypeptide) are also found in close association with the bile-duct-derived beta cells, but exocrine pancreatic tissue is not present. |
| 4193 | 17218353 | This pancreatic RAS has been proposed to have important endocrine and exocrine roles in the pancreas, regulating local blood flow, duct cell sodium bicarbonate secretion, acinar cell digestive enzyme secretion, islet beta-cell (pro)insulin biosynthesis, and thus, glucose-stimulated insulin release, delta-cell somatostatin secretion, and pancreatic cell proliferation and differentiation. |
| 4194 | 17259389 | This study investigated the impact of tolbutamide on the glucose dependence of the GLP-1-mediated effects on insulin, glucagon, and somatostatin secretion in the in situ perfused rat pancreas. |
| 4195 | 17259389 | At 3 mmol/l glucose, GLP-1 alone did not augment insulin secretion, whereas tolbutamide alone caused a rapid increase in insulin secretion. |
| 4196 | 17259389 | However, when GLP-1 and tolbutamide were administered simultaneously, insulin secretion increased significantly to 43.7 +/- 6.2 pmol/min (means +/- SE), exceeding the sum of the responses to GLP-1 (2.0 +/- 0.6 pmol/min; P = 0.019) and tolbutamide (11.3 +/- 3.8; P = 0.005) alone by a factor of 3.3. |
| 4197 | 17259389 | At 11 mmol/l glucose, co-infusion of GLP-1 and tolbutamide augmented insulin secretion to 141.7 +/- 10.3 vs. 115.36 +/- 14.1 (GLP-1) and 42.5 +/- 7.3 pmol/min (tolbutamide). |
| 4198 | 17259389 | Interestingly, increases in somatostatin secretion, both by glucose and GLP-1, were consistently paralleled by suppression of glucagon release. |
| 4199 | 17259389 | This study investigated the impact of tolbutamide on the glucose dependence of the GLP-1-mediated effects on insulin, glucagon, and somatostatin secretion in the in situ perfused rat pancreas. |
| 4200 | 17259389 | At 3 mmol/l glucose, GLP-1 alone did not augment insulin secretion, whereas tolbutamide alone caused a rapid increase in insulin secretion. |
| 4201 | 17259389 | However, when GLP-1 and tolbutamide were administered simultaneously, insulin secretion increased significantly to 43.7 +/- 6.2 pmol/min (means +/- SE), exceeding the sum of the responses to GLP-1 (2.0 +/- 0.6 pmol/min; P = 0.019) and tolbutamide (11.3 +/- 3.8; P = 0.005) alone by a factor of 3.3. |
| 4202 | 17259389 | At 11 mmol/l glucose, co-infusion of GLP-1 and tolbutamide augmented insulin secretion to 141.7 +/- 10.3 vs. 115.36 +/- 14.1 (GLP-1) and 42.5 +/- 7.3 pmol/min (tolbutamide). |
| 4203 | 17259389 | Interestingly, increases in somatostatin secretion, both by glucose and GLP-1, were consistently paralleled by suppression of glucagon release. |
| 4204 | 17303805 | To define the effects of acute hyperglycemia per se (i.e., without the confounding effect of hyperinsulinemia) in human tissues in vivo, we performed global gene expression analysis using microarrays in vastus lateralis muscle and subcutaneous abdominal adipose tissue of seven healthy men during a hyperglycemic-euinsulinemic clamp with infusion of somatostatin to inhibit endogenous insulin release. |
| 4205 | 17308040 | In P2, somatostatin, basal intraportal insulin, and 5-fold basal intraportal glucagon (2.5 ng/kg/min) were infused. |
| 4206 | 17329620 | An amino acid mixture was infused to activate mTOR, and somatostatin-insulin-glucose clamps created conditions of low peripheral hyperinsulinemia (approximately 100 pmol/l, 0-180 min) and prandial-like peripheral hyperinsulinemia (approximately 450 pmol/l, 180-360 min). |
| 4207 | 17329620 | In conclusion, rapamycin stimulates insulin-mediated glucose uptake in man under conditions known to activate the mTOR/S6K pathway. |
| 4208 | 17364502 | This study examined the expression of P2X7 receptors in pancreatic islets of the non-obese diabetic (NOD) mouse model of human autoimmune insulin-dependent diabetes mellitus, to determine whether they are involved in islet cell destruction during early- and late-developing diabetes. |
| 4209 | 17364502 | Pancreatic cells containing glucagon (alpha-cells), insulin (beta-cells) and somatostatin (delta-cells) were co-localized with P2X7 receptors. |
| 4210 | 17369816 | In addition to insulin-producing beta-cells and glucagon-secreting alpha-cells, the islets contain somatostatin-releasing delta-cells. |
| 4211 | 17369816 | Somatostatin is a powerful inhibitor of insulin and glucagon secretion. |
| 4212 | 17369816 | In addition to insulin-producing beta-cells and glucagon-secreting alpha-cells, the islets contain somatostatin-releasing delta-cells. |
| 4213 | 17369816 | Somatostatin is a powerful inhibitor of insulin and glucagon secretion. |
| 4214 | 17371386 | The 'light' (or B) islets were composed of insulin-immunoreactive cells, completed perhaps by a few somatostatin-immunoreactive cells occurring on the periphery. |
| 4215 | 17371386 | In morphometric analysis, volume density of insulin-, glucagon-, and somatostatin-immunoreactive cells was measured, and ratios were calculated between particular components. |
| 4216 | 17371386 | The 'light' (or B) islets were composed of insulin-immunoreactive cells, completed perhaps by a few somatostatin-immunoreactive cells occurring on the periphery. |
| 4217 | 17371386 | In morphometric analysis, volume density of insulin-, glucagon-, and somatostatin-immunoreactive cells was measured, and ratios were calculated between particular components. |
| 4218 | 17379930 | GLP-1 stimulates the production and secretion of insulin, the release of somatostatin, glucose utilisation by increasing insulin sensitivity and in animal studies also beta-cell function and expansion (proliferation). |
| 4219 | 17380065 | Experimental and clinical evidence suggests that pharmacological compounds like somatostatin analogues and protein kinase C (PKC) inhibitors may be effective in the treatment of diabetic retinopathy. |
| 4220 | 17380065 | Chronic overproduction of growth hormone and insulin-like growth factor 1 play an important role in the pathogenesis of diabetic retinopathy. |
| 4221 | 17409288 | Accordingly, this review ends with a discussion of the status and therapeutic potential of glucagon receptor antagonists, alpha-cell selective somatostatin agonists, glucagon-like peptide-1 agonists, and dipeptidyl peptidase-IV inhibitors. |
| 4222 | 17578804 | Somatostatin analogues had an effect on cAMP accumulation, chromogranin A secretion and MAP kinase activity in the cell line. |
| 4223 | 17578804 | Treatment of rat pancreatic islets with somatostatin analogues with selective receptor affinity was not sufficient to induce an inhibition of insulin and glucagon secretion. |
| 4224 | 17578804 | Somatostatin analogues had an effect on cAMP accumulation, chromogranin A secretion and MAP kinase activity in the cell line. |
| 4225 | 17578804 | Treatment of rat pancreatic islets with somatostatin analogues with selective receptor affinity was not sufficient to induce an inhibition of insulin and glucagon secretion. |
| 4226 | 17685870 | There are two therapeutic strategies for blocking retinal angiogenesis in PDR: systemic drug administration (protein kinase C inhibitors and somatostatin analogs) or local therapies (anti-vascular endothelial growth factor strategies, anti-inflammatory agents, gene therapy and stem cell therapy). |
| 4227 | 17693389 | Attenuation of insulin secretion by insulin-like growth factor binding protein-1 in pancreatic beta-cells. |
| 4228 | 17693389 | Incubation of dispersed mouse beta-cells with IGFBP-1 for 30min inhibited insulin secretion stimulated by glucose, glucagon-like peptide 1 (GLP-1) or tolbutamide without changes in basal release of insulin and in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and NAD(P)H evoked by glucose. |
| 4229 | 17693389 | In contrast, IGFBP-1 augmented glucose-stimulated insulin secretion in intact islets, associated with a reduced somatostatin secretion. |
| 4230 | 17693389 | These results suggest a suppressive action of IGFBP-1 on insulin secretion in isolated beta-cells through a mechanism distal to energy generating steps and not involving regulation of [Ca(2+)](i). |
| 4231 | 17693389 | In contrast, IGFBP-1 amplifies glucose-stimulated insulin secretion in intact islets, possibly by suppressing somatostatin secretion. |
| 4232 | 17693389 | These direct modulatory influences of IGFBP-1 on insulin secretion may imply an important regulatory role of IGFBP-1 in vivo and in the pathogenesis of type 2 diabetes, in which loss of insulin release is an early pathogenetic event. |
| 4233 | 17693389 | Attenuation of insulin secretion by insulin-like growth factor binding protein-1 in pancreatic beta-cells. |
| 4234 | 17693389 | Incubation of dispersed mouse beta-cells with IGFBP-1 for 30min inhibited insulin secretion stimulated by glucose, glucagon-like peptide 1 (GLP-1) or tolbutamide without changes in basal release of insulin and in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and NAD(P)H evoked by glucose. |
| 4235 | 17693389 | In contrast, IGFBP-1 augmented glucose-stimulated insulin secretion in intact islets, associated with a reduced somatostatin secretion. |
| 4236 | 17693389 | These results suggest a suppressive action of IGFBP-1 on insulin secretion in isolated beta-cells through a mechanism distal to energy generating steps and not involving regulation of [Ca(2+)](i). |
| 4237 | 17693389 | In contrast, IGFBP-1 amplifies glucose-stimulated insulin secretion in intact islets, possibly by suppressing somatostatin secretion. |
| 4238 | 17693389 | These direct modulatory influences of IGFBP-1 on insulin secretion may imply an important regulatory role of IGFBP-1 in vivo and in the pathogenesis of type 2 diabetes, in which loss of insulin release is an early pathogenetic event. |
| 4239 | 17891462 | Pancreata from female NOD mice at diagnosis and at 1, 2, 3 and 4 weeks thereafter were analysed immunohistochemically for insulin, glucagon and somatostatin cells and glucose transporter-2 (glut2) and correlated with the degree of insulitis and islet immune cell phenotypes. |
| 4240 | 17891462 | During this period, beta cells also declined sharply whereas glucagon and somatostatin cells increased, with occasional islet cells co-expressing insulin and glucagon. |
| 4241 | 17891462 | Glut2 was absent in insulin-containing cells from 1 week onwards. |
| 4242 | 17891462 | CD4 and CD8 T cells and macrophages persisted until 4 weeks, in islets with residual beta cells or extensive insulitis. |
| 4243 | 17891462 | Pancreata from female NOD mice at diagnosis and at 1, 2, 3 and 4 weeks thereafter were analysed immunohistochemically for insulin, glucagon and somatostatin cells and glucose transporter-2 (glut2) and correlated with the degree of insulitis and islet immune cell phenotypes. |
| 4244 | 17891462 | During this period, beta cells also declined sharply whereas glucagon and somatostatin cells increased, with occasional islet cells co-expressing insulin and glucagon. |
| 4245 | 17891462 | Glut2 was absent in insulin-containing cells from 1 week onwards. |
| 4246 | 17891462 | CD4 and CD8 T cells and macrophages persisted until 4 weeks, in islets with residual beta cells or extensive insulitis. |
| 4247 | 17901402 | Transcripts for insulin, glucagon, and somatostatin in recovered ECC grafts increased with time in vivo, reaching levels approximately 1% of those in adult islets. |
| 4248 | 17901402 | We show that hIPCs are mesenchymal stromal cells (MSCs) that adhere to plastic, express CD73, CD90, and CD105, and can differentiate in vitro into adipocytes, chondrocytes, and osteocytes. |
| 4249 | 17901402 | Moreover, we find a minor population of CD105(+)/CD73(+)/CD90(+) cells in adult human islets (prior to incubation in vitro) that express insulin mRNA at low levels. |
| 4250 | 17996499 | Expression of HNF-4alpha (MODY1), HNF-1beta (MODY5), and HNF-1alpha (MODY3) proteins in the developing mouse pancreas. |
| 4251 | 17996499 | The type 1, 3, and 5 forms of maturity-onset diabetes of the young (MODY) are caused by mutations of the genes encoding hepatocyte nuclear factor (HNF)-4alpha, HNF-1alpha, and HNF-1beta, respectively [Yamagata, K., Oda, N., Kaisaki, P.J., Menzel, S., Furuta, H., Vaxillaire, M., et al., 1996a. |
| 4252 | 17996499 | Mutation in hepatocyte nuclear factor-1beta gene (TCF2) associated with MODY. |
| 4253 | 17996499 | We performed an immunohistochemical study to investigate its expression in comparison with the expression of HNF-1alpha and HNF-1beta. |
| 4254 | 17996499 | HNF-4alpha and HNF-1beta were initially expressed by Pdx1(+) common progenitor cells and neurogenin3(+) (Ngn3(+)) endocrine precursor cells during the first transition, but expression of HNF-1beta and either HNF-4alpha or HNF-1alpha became complementary around the end of the second transition (E15.5). |
| 4255 | 17996499 | In the mature pancreas, HNF-4alpha was expressed by glucagon-positive alpha-cells, insulin-positive beta-cells, somatostatin-positive delta-cells, and pancreatic polypeptide-positive PP-cells, as well as by pancreatic exocrine cells and ductal cells. |
| 4256 | 17996499 | Most of the HNF-4alpha(+) cells were also positive for HNF-1alpha, but HNF-4alpha expression in some non-beta-cells was remarkably high, and this was not paralleled by high HNF-1alpha expression. |
| 4257 | 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. |
| 4258 | 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. |
| 4259 | 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. |
| 4260 | 18020966 | GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis. |
| 4261 | 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. |
| 4262 | 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. |
| 4263 | 18095239 | To test whether a similar mechanism could explain the enhanced Growth Hormone (GH) secretory response to GH-Releasing Hormone (GHRH), which is seen in human LC, we studied the effect of the cholinesterase inhibitor pyridostigmine (PD), which is able to reduce the release of hypothalamic somatostatin (SS), on the GHRH-stimulated GH secretion. |
| 4264 | 18202127 | Insulin stimulates primary beta-cell proliferation via Raf-1 kinase. |
| 4265 | 18202127 | Elevating glucose from 5-15 mm did not significantly increase beta-cell replication. beta-Cell proliferation was inhibited by somatostatin as well as inhibitors of insulin signaling. |
| 4266 | 18202127 | Interestingly, inhibiting Raf-1 kinase blocked proliferation stimulated by low, but not high (superphysiological), insulin doses. |
| 4267 | 18202127 | Insulin-stimulated mouse insulinoma cell proliferation was dependent on both phosphatidylinositol 3-kinase/Akt and Raf-1/MAPK kinase pathways. |
| 4268 | 18202127 | Overexpression of Raf-1 was sufficient to increase proliferation in the absence of insulin, whereas a dominant-negative Raf-1 reduced proliferation in the presence of 200-pm insulin. |
| 4269 | 18202127 | Together, these results demonstrate for the first time that insulin, at levels that have been measured in vivo, can directly stimulate beta-cell proliferation and that Raf-1 kinase is involved in this process. |
| 4270 | 18220619 | Other growth factors or cytokines such as insulin-like growth factor I (IGF-1), hepatocyte growth factor (HGF), basic fibroblast growth factor (b-FGF), platelet derived growth factor (PDGF), pro-inflammatory cytokines and angiopoetins, are also involved in the pathogenesis of PDR. |
| 4271 | 18220619 | The main antiangiogenic factor is the pigment epithelium derived factor (PEDF) but the transforming growth factor beta (TGF-beta), thrombospondin (TSP) and somatostatin are also among the intraocullary synthesized antiangiogenic factors. |
| 4272 | 18220620 | The failure of laser treatment and the destructive nature of the therapy has forced researchers to pursue new alternatives including vitrectomy with or without internal limiting membrane peels, the use of proteinkinase C inhibitors, intravitreal injections of antibodies that inhibit the vascular endothelial growth factor, somatostatin analog, or the intravitreal injection with corticosteroids. |
| 4273 | 18374064 | For LSC, cell preparations (n = 9) were stained for insulin (beta-cells), glucagon (alpha-cells), somatostatin (delta cells), and pancreatic polypeptide (ppp cells). |
| 4274 | 18375050 | In the pancreas, SST is a potent regulator of insulin and glucagon secretion. |
| 4275 | 18406800 | Homeodomain protein IDX-1: a master regulator of pancreas development and insulin gene expression. |
| 4276 | 18406800 | In the adult endocrine pancreas, IDX-1 is primarily expressed in beta cells, where it is a key factor in the upregulation of insulin gene transcription and appears to have a role in the regulation of the somatostatin, glucokinase, glucose transporter-2, and islet amyloid polypeptide genes. |
| 4277 | 18406800 | The observed functions of IDX-1 and its downregulation in parallel with insulin in glucose-toxicity models implicate IDX-1 as a potential factor contributing to the pathogenesis of diabetes mellitus. |
| 4278 | 18583199 | Overnight beta-cell rest, e.g. during somatostatin administration, improves the disordered pulsatile insulin secretion in type 2 diabetes. |
| 4279 | 18653781 | Using both coimmunoprecipitation and photobleaching fluorescence resonance energy transfer microscopy techniques, we determined that SSTR2 and SSTR5 heterodimerize. |
| 4280 | 18653781 | Surprisingly, selective activation of SSTR2 and not SSTR5, or their costimulation, modulates the association. |
| 4281 | 18653781 | The SSTR2-selective agonist L-779,976 is more efficacious at inhibiting adenylate cyclase, activating ERK1/2, and inducing the cyclin-dependent kinase inhibitor p27(Kip1) in cells expressing both SSTR2 and SSTR5 compared with SSTR2 alone. |
| 4282 | 18653781 | Given that SST analogs show preferential binding to SSTR2, these data provide a mechanism for their effectiveness in controlling pituitary tumors and the absence of tolerance seen in patients undergoing long-term administration. |
| 4283 | 18683496 | The sensitivity of components of the adenylate cyclase signaling system (heterotrimer G proteins and adenylate cyclase enzyme) to the regulatory effects of hormones mediated through G proteins (stimulatory effect of isoproterenol and relaxin and inhibitory effects of somatostatin) was decreased in the myocardium of hyperglycemic rats under conditions of transitory hyperglycemia caused by intravenous glucose and in hyperglycemia associated with insulin insufficiency in 24-h type 1 streptozotocin-induced diabetes mellitus. |
| 4284 | 18766168 | Additional metabolic effects of adding GH receptor antagonist to long-acting somatostatin analog in patients with active acromegaly. |
| 4285 | 18845907 | MIN6 cells excreted insulin, glucagon, somatostatin and ghrelin. |
| 4286 | 18845907 | They expressed mRNAs of insulin I and II, proglucagon, somatostatin, pancreatic polypeptide (PP) and ghrelin which were shown in the mouse pancreatic islet core and periphery obtained by LCM. |
| 4287 | 18845907 | Glucagon, somatostatin and ghrelin were detectable in the culture medium. |
| 4288 | 18845907 | MIN6 cells excreted insulin, glucagon, somatostatin and ghrelin. |
| 4289 | 18845907 | They expressed mRNAs of insulin I and II, proglucagon, somatostatin, pancreatic polypeptide (PP) and ghrelin which were shown in the mouse pancreatic islet core and periphery obtained by LCM. |
| 4290 | 18845907 | Glucagon, somatostatin and ghrelin were detectable in the culture medium. |
| 4291 | 18845907 | MIN6 cells excreted insulin, glucagon, somatostatin and ghrelin. |
| 4292 | 18845907 | They expressed mRNAs of insulin I and II, proglucagon, somatostatin, pancreatic polypeptide (PP) and ghrelin which were shown in the mouse pancreatic islet core and periphery obtained by LCM. |
| 4293 | 18845907 | Glucagon, somatostatin and ghrelin were detectable in the culture medium. |
| 4294 | 19098161 | Somatostatin was infused to prevent insulin secretion, and glucagon was infused to replace basal plasma levels of the hormone. |
| 4295 | 19117123 | The aim of this study was to investigate the effects of zinc supplementation on somatostatin and insulin peptide expressions and biochemical parameters. |
| 4296 | 19135250 | However, in addition to insulin/c-peptide, most cells also coexpressed PDX-1 (pancreas duodenum homeobox-1), glucagon, somatostatin or pancreatic polypeptide. |
| 4297 | 19147599 | Long-term treatment of acromegalic patients resistant to somatostatin analogues with the GH receptor antagonist pegvisomant: its efficacy in relation to gender and previous radiotherapy. |
| 4298 | 19322513 | Conversely, insulin-like growth factor 1 (IGF-I) enhances insulin sensitivity primarily on skeletal muscles. |
| 4299 | 19322513 | However, in acromegaly, increased IGF-I levels are unable to counteract the insulin-resistance status determined by GH excess. |
| 4300 | 19322513 | Therapy with somatostatin analogues (SSAs) induce control of GH and IGF-I excess in the majority of patients, but their inhibitory effect on pancreatic insulin secretion might complicate the overall effect of this treatment on glucose tolerance. |
| 4301 | 19322513 | In patients with neuroendocrine tumours (NETs) the occurrence of altered glucose tolerance may be due to a decreased insulin secretion, like it happens in patients who underwent pancreatic surgery and in those with pheochromocytoma, or to an altered counterbalance between hormones, such as in patients with glucagonoma and somatostatinoma. |
| 4302 | 19324939 | Association of SSTR2 polymorphisms and glucose homeostasis phenotypes: the Insulin Resistance Atherosclerosis Family Study. |
| 4303 | 19324939 | OBJECTIVE This study evaluated the influence of somatostatin receptor type 2 (SSTR2) polymorphisms on measures of glucose homeostasis in the Insulin Resistance Atherosclerosis Family Study (IRASFS). |
| 4304 | 19324939 | SSTR2 is a G-protein-coupled receptor that, in response to somatostatin, mediates inhibition of insulin, glucagon, and growth hormone release and thus may affect glucose homeostasis. |
| 4305 | 19324939 | Association of SSTR2 polymorphisms and glucose homeostasis phenotypes: the Insulin Resistance Atherosclerosis Family Study. |
| 4306 | 19324939 | OBJECTIVE This study evaluated the influence of somatostatin receptor type 2 (SSTR2) polymorphisms on measures of glucose homeostasis in the Insulin Resistance Atherosclerosis Family Study (IRASFS). |
| 4307 | 19324939 | SSTR2 is a G-protein-coupled receptor that, in response to somatostatin, mediates inhibition of insulin, glucagon, and growth hormone release and thus may affect glucose homeostasis. |
| 4308 | 19326481 | During P1 and P2 somatostatin (to inhibit insulin and glucagon secretion), 4x basal intraportal insulin, basal intraportal glucagon, and peripheral glucose (2x hepatic glucose load) were infused. |
| 4309 | 19373755 | The prospective study included 30 patients with acromegaly (mean age 53+/-14 year; 16 females, 14 males; BMI 28.1+/-3.6 kg/m (2); mean+/-SD), 12 patients had active disease (IGF-1 751+/-338 microg/L; GH 25.6+/-36.4 microg/L), 9 were well-controlled (IGF-1 157+/-58 microg/L; GH 1.8+/-1.1 microg/L) under somatostatin analogue octreotide (n=5), dopamine agonists (n=2), and the GH receptor antagonist pegvisomant (n=2; GH levels were not determined in this subgroup) and 9 were cured IGF-1 (148+/-57 microg/L; GH 0.5+/-0.2 microg/L). |
| 4310 | 19521525 | Neurogenin 3 (ngn3) is a basic helix loop helix transcription factor that is transiently expressed in the developing mouse pancreas with peak expression around E15. |
| 4311 | 19521525 | Within the pancreas EGFP was localized in close proximity to cells that stained positive for ngn3, insulin, and glucagon, but was absent from regions of the pancreas that stained positive for amylase. |
| 4312 | 19521525 | RT/PCR analysis confirmed that the purified cells expressed EGFP, ngn3, insulin, glucagon, somatostatin and pancreatic polypeptide. |
| 4313 | 19587243 | Fasting hyperglycemia is not associated with increased expression of PEPCK or G6Pc in patients with Type 2 Diabetes. |
| 4314 | 19587243 | Fasting hyperglycemia in patients with type 2 diabetes mellitus (T2DM) is attributed to increased hepatic gluconeogenesis, which has been ascribed to increased transcriptional expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase, catalytic (G6Pc). |
| 4315 | 19587243 | In a second model, control and HFF rats were infused with somatostatin, followed by portal vein infusion of insulin and glucagon. |
| 4316 | 19587243 | Surprisingly, the expression of PEPCK or G6Pc was not increased. |
| 4317 | 19587243 | However, PEPCK and G6Pc expression remained unchanged. |
| 4318 | 19587243 | Finally, in patients with T2DM, hepatic expression of PEPCK or G6Pc was not increased. |
| 4319 | 19587243 | Thus, in contrast to current dogma, these data demonstrate that increased transcriptional expression of PEPCK1 and G6Pc does not account for increased gluconeogenesis and fasting hyperglycemia in patients with T2DM. |
| 4320 | 19620250 | Men1(+/-) mice with parathyroid neoplasms were hypercalcaemic and hypophosphataemic, with inappropriately normal serum parathyroid hormone concentrations. |
| 4321 | 19620250 | Pancreatic and pituitary tumours expressed chromogranin A (CgA), somatostatin receptor type 2 and vascular endothelial growth factor-A. |
| 4322 | 19620250 | Serum CgA concentrations in Men1(+/-) mice were not elevated. |
| 4323 | 19622615 | Effects of initial therapy for five years with somatostatin analogs for acromegaly on growth hormone and insulin-like growth factor-I levels, tumor shrinkage, and cardiovascular disease: a prospective study. |
| 4324 | 19668479 | A number of drugs may play a role in DR therapy in the coming few years; eg, somatostatin agonists (sandostatin), corticosteroids (triamcinolone, dexamethasone, fluocinolone), vascular endothelial growth factor inhibitors (pegaptanib, ranibizumab), hyaluronidase and plasmin enzyme. |
| 4325 | 19763127 | Combination treatment with somatostatin analogs and pegvisomant (a growth-hormone-receptor antagonist) is, however, highly effective at normalizing the level of insulin-like growth factor I in over 90% of patients and might also have a favorable effect on quality of life in those with biochemically controlled acromegaly. |
| 4326 | 19767827 | Glucagon-like peptide-1 (GLP-1) ameliorates the symptoms of diabetes through stimulation of insulin secretion. |
| 4327 | 19767827 | With exendin-4 treatment on diabetic mice, the following results were noted: (i) exendin-4 suppressed the increase in plasma glucose and inhibited somatostatin expression induced by STZ, (ii) reduction of insulin prevalence was inhibited, while expression of p75 neurotrophin receptor (p75NTR), pancreatic nerve growth factor (NGF), and NGF-positive islet cell prevalence increased, (iii) there were no alterations in the severity of proliferated cell nuclear antigen positive or apoptotic beta cells in pancreatic islets, and (iv) pancreatic catalase, glutathione peroxidase, and superoxide dismutase activities significantly increased. |
| 4328 | 19767827 | In conclusion, these data suggest that exendin-4 might exert its actions through the NGF/p75NTR system and decrease somatostatin expression. |
| 4329 | 19767827 | Glucagon-like peptide-1 (GLP-1) ameliorates the symptoms of diabetes through stimulation of insulin secretion. |
| 4330 | 19767827 | With exendin-4 treatment on diabetic mice, the following results were noted: (i) exendin-4 suppressed the increase in plasma glucose and inhibited somatostatin expression induced by STZ, (ii) reduction of insulin prevalence was inhibited, while expression of p75 neurotrophin receptor (p75NTR), pancreatic nerve growth factor (NGF), and NGF-positive islet cell prevalence increased, (iii) there were no alterations in the severity of proliferated cell nuclear antigen positive or apoptotic beta cells in pancreatic islets, and (iv) pancreatic catalase, glutathione peroxidase, and superoxide dismutase activities significantly increased. |
| 4331 | 19767827 | In conclusion, these data suggest that exendin-4 might exert its actions through the NGF/p75NTR system and decrease somatostatin expression. |
| 4332 | 19915842 | Studies on the mechanism and localization demonstrate that renal uptake of radiolabelled somatostatin analogues largely depends on the megalin/cubulin system in the proximal tubule cells. |
| 4333 | 20122988 | Confocal microscopy revealed abounden GPR30 expression in insulin, glucagon and somatostatin cells. |
| 4334 | 20122988 | Dose-response studies of G-1 vs 17beta-estradiol in isolated islets at 1 or 12 mM glucose showed an almost identical pattern in that both compounds increased insulin and inhibited glucagon and somatostatin secretion. |
| 4335 | 20122988 | ICI-182,780 and EM-652, potent antagonists of the 17beta-estradiol receptors (ER alpha and ER beta) did not influence the amplifying effect of G-1 or 17beta-estradiol on cAMP content or insulin secretion from isolated islets. |
| 4336 | 20122988 | Cytokine-induced (IL-1 beta+TNFalpha+INF gamma) apoptosis in islets, cultured for 24h at 5mM glucose, was almost abolished by G-1 or 17beta-estradiol treatment. |
| 4337 | 20122988 | Confocal microscopy revealed abounden GPR30 expression in insulin, glucagon and somatostatin cells. |
| 4338 | 20122988 | Dose-response studies of G-1 vs 17beta-estradiol in isolated islets at 1 or 12 mM glucose showed an almost identical pattern in that both compounds increased insulin and inhibited glucagon and somatostatin secretion. |
| 4339 | 20122988 | ICI-182,780 and EM-652, potent antagonists of the 17beta-estradiol receptors (ER alpha and ER beta) did not influence the amplifying effect of G-1 or 17beta-estradiol on cAMP content or insulin secretion from isolated islets. |
| 4340 | 20122988 | Cytokine-induced (IL-1 beta+TNFalpha+INF gamma) apoptosis in islets, cultured for 24h at 5mM glucose, was almost abolished by G-1 or 17beta-estradiol treatment. |
| 4341 | 20126668 | Work in cell lines has suggested that the most abundant and ubiquitously expressed granins, chromogranin A and B (CgA and CgB), are involved in granulogenesis and protein sorting. |
| 4342 | 20126668 | Stimulated secretion of insulin, glucagon and somatostatin was reduced in CgB-ko islets, in parallel with somewhat impaired glucose clearance and reduced insulin release, but normal insulin sensitivity in vivo. |
| 4343 | 20158571 | MafA promotes the reprogramming of placenta-derived multipotent stem cells into pancreatic islets-like and insulin+ cells. |
| 4344 | 20158571 | MafA is a pancreatic transcriptional factor that controls β-cell-specific transcription of the insulin gene. |
| 4345 | 20158571 | In this study, we investigate the role of MafA in placenta-derived multipotent stem cells (PDMSCs) that constitutively expressed Oct-4 and Nanog. |
| 4346 | 20158571 | Our results showed that overexpression of MafA in PDMSCs significantly up-regulated the expression of pancreatic development-related genes (Sox17, Foxa2, Pdx1 and Ngn3). |
| 4347 | 20158571 | MafA increased the expression levels of the mRNAs of NKx2.2, Glut2, insulin, glucagons and somatostatin, and further facilitated the differentiation of PDMSCs into insulin(+) cells. |
| 4348 | 20158571 | The glucose-stimulated responses to insulin and c-peptide production in MafA-overexpressing PDMSCs were significantly higher than in PDMSCs with vector control. |
| 4349 | 20158571 | Importantly, the expression of MafA in PDMSCs xenotransplanted into immunocompromised mice improved the restoration of blood insulin levels to control values and greatly prolonged the survival of graft cells in immunocompromised mice with STZ-induced diabetes. |
| 4350 | 20158571 | In summary, these data suggest that MafA plays a novel role in the reprogramming of stem cells into pancreatic β-progenitors, promotes the islet-like characteristics of PDMSCs, as well as functionally enhances insulin production to restore the regulation of blood glucose levels in transplanted grafts. |
| 4351 | 20159854 | Inactive cortisone is converted to active cortisol within the liver by 11 beta-hydroxysteroid dehydrogenase-1 (11 beta-HSD1), and impaired regulation of this process may be related to increased hepatic glucose production (HGP) in individuals with type 2 diabetes. |
| 4352 | 20159854 | The primary aim of this study was to investigate the effect of acute 11 beta-HSD1 inhibition on HGP and fat metabolism during insulin deficiency. |
| 4353 | 20159854 | Somatostatin was infused to create insulin deficiency, and the animals were treated with a specific 11 beta-HSD1 inhibitor (compound 531) or placebo for 5 h. 11 beta-HSD1 inhibition completely suppressed hepatic cortisol production, and this attenuated the increase in HGP that occurred during insulin deficiency. |
| 4354 | 20159854 | PEPCK and glucose-6-phosphatase expression were decreased when 11 beta-HSD1 was inhibited, but gluconeogenic flux was unchanged, implying an effect on glycogenolysis. |
| 4355 | 20159854 | Since inhibition of hepatic cortisol production reduces HGP during insulin deficiency, 11 beta-HSD1 is a potential therapeutic target for the treatment of excess glucose production that occurs in diabetes. |
| 4356 | 20396697 | Sensitivity of the adenylate cyclase signaling system to the regulatory effect of human chorionic gonadotropin and PACAP (pituitary adenylyl cyclase-activating polypeptide) was significantly reduced. |
| 4357 | 20396697 | Somatostatin, acting through inhibitory G proteins, produced less pronounced effect on the adenylate cyclase signaling system. |
| 4358 | 20396697 | The increase in the duration of diabetes was accompanied by a decrease in the stimulatory effects of human chorionic gonadotropin and PACAP on adenylate cyclase. |
| 4359 | 20396697 | Our results indicate that changes in hormonal regulation of the adenylate cyclase signaling system and functional activity of cAMP-dependent signaling cascades are important factors for dysfunction of spermatogenesis and steroidogenesis during insulin-independent diabetes. |
| 4360 | 20501667 | We speculated that hyperinsulinemia minimized glucose-mediated VLDL changes and performed hyperglycemic-hypoinsulinemic clamp studies in which insulin was clamped near fasting levels with somatostatin (17 mm blood glucose, 0.25 mU/kg . min insulin). |
| 4361 | 20501667 | Under low-insulin conditions, serum VLDL levels were increased 4.7-fold after hyperglycemia, and forkhead box O1 (FoxO1) was not excluded from the nucleus of liver cells. |
| 4362 | 20501667 | We tested the extent that impaired inactivation of FoxO1 by insulin was sufficient for glucose to promote increased serum VLDL. |
| 4363 | 20501667 | We found that, when the ability of insulin to inactivate FoxO1 is blocked after adenoviral delivery of constitutively active FoxO1, glucose increased serum VLDL triglyceride when given both by ip glucose tolerance testing (3.5-fold increase) and by a hyperglycemic clamp (4.6-fold). |
| 4364 | 20501667 | Under both experimental conditions in which insulin signaling to FoxO1 was impaired, we found increased activation of carbohydrate response element binding protein. |
| 4365 | 20501667 | These data suggest that glucose more potently promotes increased serum VLDL when insulin action is impaired, with either low insulin levels or disrupted downstream signaling to the transcription factor FoxO1. |
| 4366 | 20558893 | CT scan of the chest showed two nodular lesions in the right lung (S5, S7), while a mild uptake was noted only in S5 lesion by FDG-PET, but positive uptake was only in S7 lesion by somatostatin receptor scintigraphy (SRS). |
| 4367 | 20558893 | Inferior petrosal sinus sampling revealed a gradient of plasma ACTH after CRH stimulation, consistent with the diagnosis of Cushing' s disease. |
| 4368 | 20558893 | This was a diagnostic challenging case with ectopic ACTH syndrome indistinguishable from Cushing' s disease by various endocrine and imaging tests, among which SRS successfully localized the tumor responsible for ectopic ACTH secretion. |
| 4369 | 20606719 | Emerging reports on the organization of the different hormone-secreting cell types (alpha, glucagon; beta, insulin; and delta, somatostatin) in human islets have emphasized the distinct differences between human and mouse islets, raising questions about the relevance of studies of mouse islets to human islet physiology. |
| 4370 | 20718077 | The role of glucagon- and somatostatin-secreting cells in the regulation of insulin release and beta-cell function in heterotypic pseudoislets. |
| 4371 | 20812342 | The usual methods to surmount the problem of distinguishing between endogenous and exogenous human insulin include evaluation in subjects with no or little endogenous insulin, hyper-insulinemic clamp studies or the administration of somatostatin to suppress endogenous insulin secretion. |
| 4372 | 20812342 | These studies used hyper-insulinemic euglycemic clamps or meal challenges and subjects received insulin or Glucagon-like peptide 1 (GLP-1). |
| 4373 | 20817146 | High plasma calcitonin level was evidenced, with normal chromogranin-A value, and high plasma somatostatin results lately communicated. |
| 4374 | 20823464 | Otherwise, medical therapy is indicated, utilizing somatostatin analogs, dopamine agonists, and pegvisomant, a GH receptor antagonist. |
| 4375 | 20953065 | GH secretion is mainly regulated at the hypothalamus by a dual interplay between growth hormone releasing hormone (GHRH) and somatostatin, which are modulated by various factors. |
| 4376 | 20953065 | We examined the regulatory mechanism of GH secretion in an apparently healthy young man without decreased IGF-1 concentration and nocturnal GH secretion, but who showed low responses to insulin tolerance (ITT) and to GHRP-2 tests. |
| 4377 | 20953065 | However, he had normal secretion of pituitary hormone based on hypothalamic releasing hormone tests combined with CRH, GRH as GHRH, LH-RH and TRH. |
| 4378 | 20953065 | In addition, he had a GH response without paradoxical secretion to TRH stimulation as well as an ACTH response to subcutaneous glucagon stimulation, and AVP secretion responded to 5% hypertonic saline infusion, though it was not adequately stimulated by ITT. |
| 4379 | 21060975 | Furthermore, we showed that hPDMSCs can form islet-like cell clusters (ILCs) on stepwise exposure to serum-free defined media containing specific growth factors and differentiating agents. qRT-PCR showed the expression of insulin, glucagon, and somatostatin in undifferentiated hPDMSCs and in ILCs. |
| 4380 | 21060975 | Differentiated ILCs were found to express human insulin, glucagon, and somatostatin by immunocytochemistry. |
| 4381 | 21060975 | Furthermore, we showed that hPDMSCs can form islet-like cell clusters (ILCs) on stepwise exposure to serum-free defined media containing specific growth factors and differentiating agents. qRT-PCR showed the expression of insulin, glucagon, and somatostatin in undifferentiated hPDMSCs and in ILCs. |
| 4382 | 21060975 | Differentiated ILCs were found to express human insulin, glucagon, and somatostatin by immunocytochemistry. |
| 4383 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4384 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4385 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4386 | 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. |
| 4387 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4388 | 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. |
| 4389 | 21095180 | Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. |
| 4390 | 21095180 | Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. |
| 4391 | 21095180 | In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. |
| 4392 | 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. |
| 4393 | 21095180 | Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. |
| 4394 | 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. |
| 4395 | 21099270 | The basic helix-loop-helix transcription factor neurogenin-3 (Ngn3, Neurog3) is critical for the development of the endocrine cells of the islets. |
| 4396 | 21099270 | The successive waves of Ngn3 expression that occur during the primary and secondary transitions of endocrine cell development temporally determine the four distinct endocrine cell lineages, α, β, PP, and δ cells that express glucagon, insulin, pancreatic polypeptide, and somatostatin, respectively. |
| 4397 | 21099272 | We successfully cloned the Acomys Pdx-1 gene and we demonstrate by immunocytochemistry that the Pdx-1 protein is expressed in the pancreatic insulin immunoreactive cells and in a subset of the somatostatin cells. |
| 4398 | 21099272 | The basic islet structure is very similar to other rodents - with the insulin cells in the center, and glucagon, somatostatin, PP and occasional PYY cells in the periphery. |
| 4399 | 21099272 | Nkx6.1 was localized specifically to the insulin immunoreactive cells, while Nkx2.2 was found in all endocrine cells except the somatostatin immunoreactive cells. |
| 4400 | 21099272 | Both MafA and MafB were expressed in the islets; MafA being specific for the insulin cells, while MafB was primarily in the glucagon cells but also found in some insulin cells. |
| 4401 | 21099272 | We successfully cloned the Acomys Pdx-1 gene and we demonstrate by immunocytochemistry that the Pdx-1 protein is expressed in the pancreatic insulin immunoreactive cells and in a subset of the somatostatin cells. |
| 4402 | 21099272 | The basic islet structure is very similar to other rodents - with the insulin cells in the center, and glucagon, somatostatin, PP and occasional PYY cells in the periphery. |
| 4403 | 21099272 | Nkx6.1 was localized specifically to the insulin immunoreactive cells, while Nkx2.2 was found in all endocrine cells except the somatostatin immunoreactive cells. |
| 4404 | 21099272 | Both MafA and MafB were expressed in the islets; MafA being specific for the insulin cells, while MafB was primarily in the glucagon cells but also found in some insulin cells. |
| 4405 | 21099272 | We successfully cloned the Acomys Pdx-1 gene and we demonstrate by immunocytochemistry that the Pdx-1 protein is expressed in the pancreatic insulin immunoreactive cells and in a subset of the somatostatin cells. |
| 4406 | 21099272 | The basic islet structure is very similar to other rodents - with the insulin cells in the center, and glucagon, somatostatin, PP and occasional PYY cells in the periphery. |
| 4407 | 21099272 | Nkx6.1 was localized specifically to the insulin immunoreactive cells, while Nkx2.2 was found in all endocrine cells except the somatostatin immunoreactive cells. |
| 4408 | 21099272 | Both MafA and MafB were expressed in the islets; MafA being specific for the insulin cells, while MafB was primarily in the glucagon cells but also found in some insulin cells. |
| 4409 | 21099303 | Human umbilical cord matrix stem cells (hUCMSCs) were found to express CD29, CD44, CD73, CD90, CD105, smooth muscle actin, nestin, vimentin, proliferation marker Ki67 and embryonic markers Oct4, SSEA4. |
| 4410 | 21099303 | These were found to be negative for CD33, CD34, CD45 and HLA DR. |
| 4411 | 21099303 | Real time qPCR analysis of newly generated islets further demonstrated abundance of Pdx-1, Ngn3, insulin, glucagon and somatostatin transcripts. |
| 4412 | 21099310 | In these clusters the expression of insulin, glucagon, and somatostatin genes is induced. |
| 4413 | 21099310 | Human IPC lack expression of Von Willebrand Factor, CD31, CD34, CD45, and CK19 and CA19.9, demonstrating that hIPC are neither of hematopoietic, endothelial, nor of ductal origin. |
| 4414 | 21099310 | The mesenchymal stem cells (MSC) markers CD105, CD90, CD73, CD44, CD29, and CD13 are expressed, as well as nestin and vimentin. |
| 4415 | 21099310 | Also hIPC express the pericyte markers CD146, NG2, αSMA and PDGF-Rβ. |
| 4416 | 21099310 | Immunoflowcytometry revealed that human islets contain 2.0 ± 0.8% of CD105/CD90 double-positive cells. |
| 4417 | 21359756 | The majority of cells, which are mainly located in the center of the islet, are the insulin-producing ß;β-cells In the periphery, α-cells and δ-cells synthesizing glucagon and somatostatin, respectively, are found. |
| 4418 | 21395072 | [A decrease of sensitivity of adenylyl cyclase and heterotrimeric G-proteins to chorionic gonadotropin and peptide hormones action in the tissues of reproductive system of the rats in the condition of experimental type 2 diabetes]. |
| 4419 | 21395072 | The aim of the work was the identification of the changes in functioning of human chorionic gonadotropin (hCG)--and peptide hormones-sensitive adenylyl cyclase system (ACS) in the ovary, testes and uterus of rats with neonatal streptozotocin (STZ) diabetes that is similar to the type 2 diabetes in humans. |
| 4420 | 21395072 | The effects of hCG, PACAP-38 and relaxin, realizing their effects via G-protein of the stimulatory type (Gs), and somatostatin, acting via G-protein of the inhibitory type (Gi), on adenylyl cyclase (AC) activity and the GTP binding of the G-proteins were studied. |
| 4421 | 21448141 | Acromegaly is a rare disease characterized by excess secretion of growth hormone (GH) and increased circulating insulin-like growth factor 1 (IGF-1) concentrations. |
| 4422 | 21448141 | The therapeutic options for acromegaly include surgery, radiotherapy and medical therapies, such as dopamine agonists, somatostatin receptor ligands and the GH receptor antagonist pegvisomant. |
| 4423 | 21537428 | Among neuroprotective factors, pigment epithelial derived factor, somatostatin and erythropoietin seem to be the most relevant and these will be considered in this review. |
| 4424 | 21669591 | Somatostatin (SST) may protect organism from overnutrition-induced insulin resistance and oxidative stress by inhibiting pancreatic endocrine and exocrine secretion, gastrointestinal digestion and absorption. |
| 4425 | 21821034 | Antibody staining for insulin, glucagon, somatostatin and Glucagon-like peptide-1 (GLP-1) showed that the distribution pattern of the different cell types within islets was comparable to pig and human islets. |
| 4426 | 21821034 | In all three species protein expression of zinc transporter ZnT8 was detected in most of the insulin producing beta cells whereas Zip14 expression was widely expressed in alpha and beta cells. |
| 4427 | 21821034 | In both human and NWP little or no expression of Glut2 was observed compared to Glut1 and glucokinase at the protein level, however the messenger RNA level of Glut2 was greater than Glut1 and glucokinase. |
| 4428 | 21853126 | No tumors predominantly expressed insulin, pancreatic polypeptide, or somatostatin, although some harbored focal aggregates of tumor cells expressing one of those hormones. |
| 4429 | 21915820 | Enhanced differentiation of human adipose tissue-derived stromal cells into insulin-producing cells with glucagon-like peptide-1. |
| 4430 | 21915820 | Here, we report an efficient approach to induce human adipose-derived stromal cells (hADSCs) to differentiate into insulin-producing cells, with glucagon-like peptide-1 (GLP-1). hADSCs were successfully isolated from the adipose tissue, with adipogenic and osteogenic differentiation potency. |
| 4431 | 21915820 | Reverse transcription polymerase chain reaction analysis showed the expression of the pancreas-related genes in the differentiated cells, such as pdx-1, ngn3, insulin, glucagon, somatostatin, glucokinase n and glut2. |
| 4432 | 21915820 | Immunocytochemical analysis showed that the induced cells co-expressed insulin, C-peptide and PDX-1. |
| 4433 | 21915820 | In addition, flow cytometry analysis and ELISA showed that, in the presence of GLP-1, the percentage of insulin-producing cells was increased from 5.9% to 28.0% and the release of insulin increased from 9.53±0.7 pmol/106 cells to 15.86±1.3 pmol/106 cells. |
| 4434 | 21915820 | These results indicated that hADSCs isolated from adipose tissues can be induced to differentiate into insulin-producing cells, which is further enhanced with the treatment of GLP-1. |
| 4435 | 21940282 | Glucagon responses of isolated α cells to glucose, insulin, somatostatin, and leptin. |
| 4436 | 22002691 | Prominent signals were measured that corresponded to all the main peptide hormones present in islet-endocrine cells: (α-cells) glucagon, glicentin-related polypeptide/GRPP; (β-cells) insulin I, insulin II, C-peptide I, C-peptide II, amylin; (δ-cells) somatostatin-14; and (PP-cells), and pancreatic polypeptide. |
| 4437 | 22138721 | The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin. |
| 4438 | 22138721 | Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group. |
| 4439 | 22138721 | There was no statistically significant difference among the four groups for somatostatin and apelin peptides. |
| 4440 | 22138721 | Caspase-3 signals were not observed only in diabetic group treated with ghrelin. |
| 4441 | 22138721 | Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group. |
| 4442 | 22138721 | Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats. |
| 4443 | 22138721 | The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin. |
| 4444 | 22138721 | Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group. |
| 4445 | 22138721 | There was no statistically significant difference among the four groups for somatostatin and apelin peptides. |
| 4446 | 22138721 | Caspase-3 signals were not observed only in diabetic group treated with ghrelin. |
| 4447 | 22138721 | Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group. |
| 4448 | 22138721 | Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats. |
| 4449 | 22138721 | The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin. |
| 4450 | 22138721 | Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group. |
| 4451 | 22138721 | There was no statistically significant difference among the four groups for somatostatin and apelin peptides. |
| 4452 | 22138721 | Caspase-3 signals were not observed only in diabetic group treated with ghrelin. |
| 4453 | 22138721 | Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group. |
| 4454 | 22138721 | Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats. |
| 4455 | 22154324 | A decreased sensory neuropeptide (SNP) release such as that of substance P, somatostatin, and calcitonin gene-related peptide determined from organ fluid of tracheal preparations subjected to electrical field stimulation also occurred in diabetic animals. |
| 4456 | 22183781 | New criteria that define acromegaly remission are more stringent: normal (age/sex-adjusted) insulin-like growth factor type 1 (IGF-1), growth hormone (GH) random (GHr) <1 μg/L, and a GH nadir (GHn) during oral glucose tolerance test (OGTT) of <0.4 μg/L. |
| 4457 | 22183781 | Discordance between GH and IGF-1 values is often attributed to somatostatin receptor ligands (SRLs) or radiation. |
| 4458 | 22183781 | Fifty-four patients had post-operative GHr and IGF-1 measurements, 28 patients had GHn during OGTT, and 16 patients had 5-point 2-h GH day curve tests. |
| 4459 | 22465973 | In 1998, a well-differentiated 1.2 cm gastric neuroendocrine tumor, immunoreactive for chromogranin A, with a Ki-67 index less than 2% and with infiltration to the submucosal layer was diagnosed and enucleated. |
| 4460 | 22465973 | The patient refused antrectomy and started long-acting somatostatin analog (lanreotide) in 2005 when the Ki-67 index was 7%, but he stopped the treatment after 4 months. |
| 4461 | 22562529 | Insulin-like growth factor-I correlates more closely than growth hormone with insulin resistance and glucose intolerance in patients with acromegaly. |
| 4462 | 22562529 | In normal subjects growth hormone (GH) and insulin-like growth factor-I (IGF-I) have opposing effects on glucose metabolism. |
| 4463 | 22562529 | Active acromegaly is associated with insulin resistance (IR) and glucose intolerance although both GH and IGF-I are elevated. |
| 4464 | 22562529 | Basal serum IGF-I and GH, glucose and insulin during an oral glucose tolerance test were measured in 70 normoglycemic and 44 hyperglycemic acromegalic patients (21 impaired fasting glucose, 11 impaired glucose tolerance and 12 diabetes mellitus) according to American Diabetes Association criteria. 55 patients were assessed before any treatment for acromegaly and 59 after surgery and/or radiotherapy (15 patients had normal IGF-I after treatment). |
| 4465 | 22562529 | Patients treated with somatostatin analogs, GH-receptor antagonists or antidiabetic drugs were excluded. |
| 4466 | 22562529 | Homeostatic Model Assessment 2-Insulin Resistance (HOMA2-IR) index correlated more closely with IGF-I (r = 0.65, p < 0.0001) than nadir (r = 0.23, p = 0.008) or random GH (r = 0.26, p = 0.002). |
| 4467 | 22583133 | These results are fully in accord with earlier evidence from studies with somatostatin analogues which showed that the GH-insulin-like growth factor I (IGF-I)-axis plays a key role in the adrenal diabetic hypertrophy-hyperfunction syndrome. |
| 4468 | 22586489 | Furthermore, Pdx1(+)/Insulin(-) cells were detected following STZ treatment, indicating the involvement of endocrine progenitor cells in the regeneration of these non-β cells. |
| 4469 | 22586489 | This is further confirmed by the detection of Pdx1(+)/glucagon(+) cells and Pdx1(+)/somatostatin(+) cells following STZ treatment. |
| 4470 | 22665046 | The majority of human islets from the pancreas head, body and tail regions are composed of insulin-containing β-cells followed by lower proportions of glucagon-containing α-cells and somatostatin-containing δ-cells. |
| 4471 | 22665046 | Pancreatic polypeptide-containing PP cells and ghrelin-containing epsilon cells are also present but in small numbers. |
| 4472 | 22707198 | Microarray data demonstrated for the first time that overexpression of the genes encoding IL-1 receptor, lipid metabolic enzymes (e.g. |
| 4473 | 22707198 | Mte1, Ptdss1, and Sult2a1), myo-inositol oxygenase, glucagon, and somatostatin as well as down-regulation of olfactory receptor 984 and mitochondrial ribosomal protein, which are highly linked to T1DM etiology. |
| 4474 | 22707198 | The results of the microarray analysis revealed that up-regulation of IL-2, IL12a, and leptin receptor and down-regulation of PIK3 played important physiological roles in the onset of T2DM. |
| 4475 | 22969729 | This review integrates the physiology of glucagon secretion regulating glucose homeostasis in vivo to single α-cell signaling, and how both become perturbed in diabetes. α-cells within the social milieu of the islet micro-organ are regulated not only by intrinsic signaling events but also by paracrine regulation, particularly by adjacent insulin-secreting β-cells and somatostatin-secreting δ-cells. |
| 4476 | 22969729 | Whereas, there are many secretory products released by β- and δ-cells that become deficient or excess in diabetes, we discuss the major ones, including the better known insulin and lesser known somatostatin, which act as putative paracrine on/off switches that very finely regulate α-cell secretory responses in health and diabetes. |
| 4477 | 22969729 | This review integrates the physiology of glucagon secretion regulating glucose homeostasis in vivo to single α-cell signaling, and how both become perturbed in diabetes. α-cells within the social milieu of the islet micro-organ are regulated not only by intrinsic signaling events but also by paracrine regulation, particularly by adjacent insulin-secreting β-cells and somatostatin-secreting δ-cells. |
| 4478 | 22969729 | Whereas, there are many secretory products released by β- and δ-cells that become deficient or excess in diabetes, we discuss the major ones, including the better known insulin and lesser known somatostatin, which act as putative paracrine on/off switches that very finely regulate α-cell secretory responses in health and diabetes. |
| 4479 | 23043302 | The most promising peptidergic pathways for which treatment strategies may be developed at present are stimulation of the somatostatin-related pathway and the pituitary adenylyl cyclase-activating polypeptide-related pathway or inhibition of angiotensinergic mechanisms. |
| 4480 | 23064014 | A major lineage of enteroendocrine cells coexpress CCK, secretin, GIP, GLP-1, PYY, and neurotensin but not somatostatin. |
| 4481 | 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. |
| 4482 | 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. |
| 4483 | 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. |
| 4484 | 23087044 | Islet-associated protein-2 (IA-2) and IA-2β (also known as phogrin) are unique neuroendocrine-specific protein tyrosine phosphatases (PTPs). |
| 4485 | 23087044 | The IA-2 family of PTPs was originally identified from insulinoma cells and discovered to be major autoantigens in type 1 diabetes. |
| 4486 | 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. |
| 4487 | 23087044 | Therefore, we immunohistochemically investigated the expression of the IA-2 family of PTPs in the rat gastrointestinal tract. |
| 4488 | 23087044 | In the stomach, IA-2 and IA-2β were expressed in GECs that secrete serotonin, somatostatin, and cholecystokinin/gastrin-1. |
| 4489 | 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. |
| 4490 | 23087044 | Pancreatic islet cells that secrete gut hormones expressed the IA-2 family of PTPs. |
| 4491 | 23087044 | These results reveal that the IA-2 family of PTPs is expressed in a cell type-specific manner in rat GECs. |
| 4492 | 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. |
| 4493 | 23161216 | The role of voltage-gated potassium channels Kv2.1 and Kv2.2 in the regulation of insulin and somatostatin release from pancreatic islets. |
| 4494 | 23161216 | The voltage-gated potassium channels Kv2.1 and Kv2.2 are highly expressed in pancreatic islets, yet their contribution to islet hormone secretion is not fully understood. |
| 4495 | 23161216 | Pancreatic β-cells from Kv2.1(-/-) mice possess reduced Kv current and display greater glucose-stimulated insulin secretion (GSIS) relative to WT β-cells. |
| 4496 | 23161216 | GxTX-1E and RY796 enhanced somatostatin release in isolated human and mouse islets and in situ perfused pancreata from WT and Kv2.1(-/-) mice. |
| 4497 | 23161216 | Kv2.2 silencing in mouse islets by adenovirus-small hairpin RNA (shRNA) specifically enhanced islet somatostatin, but not insulin, secretion. |
| 4498 | 23161216 | In mice lacking somatostatin receptor 5, GxTX-1E stimulated insulin secretion and improved glucose tolerance. |
| 4499 | 23161216 | Collectively, these data show that Kv2.1 regulates insulin secretion in β-cells and Kv2.2 modulates somatostatin release in δ-cells. |
| 4500 | 23161216 | Development of selective Kv2.1 inhibitors without cross inhibition of Kv2.2 may provide new avenues to promote GSIS for the treatment of type 2 diabetes. |
| 4501 | 23161216 | The role of voltage-gated potassium channels Kv2.1 and Kv2.2 in the regulation of insulin and somatostatin release from pancreatic islets. |
| 4502 | 23161216 | The voltage-gated potassium channels Kv2.1 and Kv2.2 are highly expressed in pancreatic islets, yet their contribution to islet hormone secretion is not fully understood. |
| 4503 | 23161216 | Pancreatic β-cells from Kv2.1(-/-) mice possess reduced Kv current and display greater glucose-stimulated insulin secretion (GSIS) relative to WT β-cells. |
| 4504 | 23161216 | GxTX-1E and RY796 enhanced somatostatin release in isolated human and mouse islets and in situ perfused pancreata from WT and Kv2.1(-/-) mice. |
| 4505 | 23161216 | Kv2.2 silencing in mouse islets by adenovirus-small hairpin RNA (shRNA) specifically enhanced islet somatostatin, but not insulin, secretion. |
| 4506 | 23161216 | In mice lacking somatostatin receptor 5, GxTX-1E stimulated insulin secretion and improved glucose tolerance. |
| 4507 | 23161216 | Collectively, these data show that Kv2.1 regulates insulin secretion in β-cells and Kv2.2 modulates somatostatin release in δ-cells. |
| 4508 | 23161216 | Development of selective Kv2.1 inhibitors without cross inhibition of Kv2.2 may provide new avenues to promote GSIS for the treatment of type 2 diabetes. |
| 4509 | 23161216 | The role of voltage-gated potassium channels Kv2.1 and Kv2.2 in the regulation of insulin and somatostatin release from pancreatic islets. |
| 4510 | 23161216 | The voltage-gated potassium channels Kv2.1 and Kv2.2 are highly expressed in pancreatic islets, yet their contribution to islet hormone secretion is not fully understood. |
| 4511 | 23161216 | Pancreatic β-cells from Kv2.1(-/-) mice possess reduced Kv current and display greater glucose-stimulated insulin secretion (GSIS) relative to WT β-cells. |
| 4512 | 23161216 | GxTX-1E and RY796 enhanced somatostatin release in isolated human and mouse islets and in situ perfused pancreata from WT and Kv2.1(-/-) mice. |
| 4513 | 23161216 | Kv2.2 silencing in mouse islets by adenovirus-small hairpin RNA (shRNA) specifically enhanced islet somatostatin, but not insulin, secretion. |
| 4514 | 23161216 | In mice lacking somatostatin receptor 5, GxTX-1E stimulated insulin secretion and improved glucose tolerance. |
| 4515 | 23161216 | Collectively, these data show that Kv2.1 regulates insulin secretion in β-cells and Kv2.2 modulates somatostatin release in δ-cells. |
| 4516 | 23161216 | Development of selective Kv2.1 inhibitors without cross inhibition of Kv2.2 may provide new avenues to promote GSIS for the treatment of type 2 diabetes. |
| 4517 | 23161216 | The role of voltage-gated potassium channels Kv2.1 and Kv2.2 in the regulation of insulin and somatostatin release from pancreatic islets. |
| 4518 | 23161216 | The voltage-gated potassium channels Kv2.1 and Kv2.2 are highly expressed in pancreatic islets, yet their contribution to islet hormone secretion is not fully understood. |
| 4519 | 23161216 | Pancreatic β-cells from Kv2.1(-/-) mice possess reduced Kv current and display greater glucose-stimulated insulin secretion (GSIS) relative to WT β-cells. |
| 4520 | 23161216 | GxTX-1E and RY796 enhanced somatostatin release in isolated human and mouse islets and in situ perfused pancreata from WT and Kv2.1(-/-) mice. |
| 4521 | 23161216 | Kv2.2 silencing in mouse islets by adenovirus-small hairpin RNA (shRNA) specifically enhanced islet somatostatin, but not insulin, secretion. |
| 4522 | 23161216 | In mice lacking somatostatin receptor 5, GxTX-1E stimulated insulin secretion and improved glucose tolerance. |
| 4523 | 23161216 | Collectively, these data show that Kv2.1 regulates insulin secretion in β-cells and Kv2.2 modulates somatostatin release in δ-cells. |
| 4524 | 23161216 | Development of selective Kv2.1 inhibitors without cross inhibition of Kv2.2 may provide new avenues to promote GSIS for the treatment of type 2 diabetes. |
| 4525 | 23179962 | Anterior pituitary hormones for endocrine dysfunction, histology, Ki-67 labeling index (LI), and p53 positivity of the tumor and pituitary imaging by magnetic resonance imaging were evaluated. |
| 4526 | 23179962 | Sex, Ki-67 LI, p53 positivity, diabetes mellitus, hypertension, somatostatin analogue and anticoagulant use did not predispose to PA whereas cavernous sinus invasion predisposed patients to PA (p < 0.01). |
| 4527 | 23221614 | Vesicular monoamine transporter, type 2 (VMAT2) expression as it compares to insulin and pancreatic polypeptide in the head, body and tail of the human pancreas. |
| 4528 | 23221614 | VMAT2 is also present in the pancreas and is expressed by insulin producing β cells, but not by glucagon or somatostatin expressing islet cells. |
| 4529 | 23228667 | One of the medical treatments used in Cushing's disease is the somatostatin analogue pasireotide, which acts on adrenocorticotropic hormone (ACTH) secretion by the pituitary. |
| 4530 | 23230431 | In particular, virtually all benign insulinomas highly overexpress GLP-1 receptors (GLP-1R). |
| 4531 | 23230431 | Targeting GLP-1R with the stable GLP-1 analogs (111)In-DOTA/DPTA-exendin-4 offers a new approach to successfully localize these small tumors. |
| 4532 | 23230431 | Malignant insulinomas, in contrast to their benign counterparts, express GLP-1R in only one-third of the cases, while they more often express the somatostatin type 2 receptors. |
| 4533 | 23230431 | The GLP-1R overexpression in selected cancers is worth to be kept in mind with regard to the increasing use of GLP-1 analogs for diabetes therapy. |
| 4534 | 23230431 | While the functional role of GLP-1R in neoplasia is not known yet, it may be safe to monitor patients undergoing GLP-1 therapy carefully. |
| 4535 | 23285726 | The brain peptidergic systems regulated by melanocortin receptors agonists, neuropeptide Y, glucagon-like peptide-1, kisspeptins and somatostatin play an important role in the etiology and pathogenesis of DM. |
| 4536 | 23291436 | Although somatostatin analogues are effective medical therapy for acromegaly, the serum insulin-like growth factor-I (IGF-I) levels remain uncontrolled in 35% of patients. |
| 4537 | 23291436 | There were no correlations between the decrease of serum IGF-I levels during combined therapy and the response of GH in a bromocriptine test, random GH, IGF-I, and PRL levels, the tumor volume, and the expression of PRL and dopamine D2 receptor in the tumor. |
| 4538 | 23306763 | Marginal and not validated therapies are cyclosporine, somatostatin analogues, TNF-a inhibitors and rituximab. |
| 4539 | 23326594 | Glucagon-producing cells are almost completely lost in Pax6-null embryos, and insulin-expressing beta and somatostatin-expressing delta cells are reduced. |
| 4540 | 23326678 | The endocrine pancreas consists of functional units organized into cell clusters called islets of Langerhans where insulin-producing cells are found in the core and surrounded by glucagon-, somatostatin-, pancreatic polypeptide-, and ghrelin-producing cells. |
| 4541 | 23431428 | At the end of each period, a somatostatin-insulin-glucose infusion test (SIGIT) was performed to evaluate the insulin sensitivity. |
| 4542 | 23434929 | Selective antagonism of somatostatin receptor type 2 (SSTR2) normalizes glucagon and corticosterone responses to hypoglycemic clamp in diabetic rats. |
| 4543 | 23434929 | Thus, SSTR2 antagonism after recurrent hypoglycemia improves the glucagon and corticosterone responses and largely ameliorates insulin-induced hypoglycemia in diabetic rats. |
| 4544 | 23566555 | Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats. |
| 4545 | 23566555 | The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach. |
| 4546 | 23566555 | Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats. |
| 4547 | 23566555 | Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group. |
| 4548 | 23566555 | Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats. |
| 4549 | 23566555 | Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats. |
| 4550 | 23566555 | The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach. |
| 4551 | 23566555 | Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats. |
| 4552 | 23566555 | Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group. |
| 4553 | 23566555 | Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats. |
| 4554 | 23566555 | Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats. |
| 4555 | 23566555 | The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach. |
| 4556 | 23566555 | Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats. |
| 4557 | 23566555 | Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group. |
| 4558 | 23566555 | Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats. |
| 4559 | 23595987 | cAMP-responsive element-binding protein (CREB)-regulated transcription coactivator 2 (CRTC2) promotes glucagon clearance and hepatic amino acid catabolism to regulate glucose homeostasis. |
| 4560 | 23595987 | cAMP-responsive element-binding protein (CREB)-regulated transcription coactivator 2 (CRTC2) regulates transcription of gluconeogenic genes by specifying targets for the transcription factor CREB in response to glucagon. |
| 4561 | 23595987 | When this phenomenon was prevented with somatostatin or a glucagon-neutralizing antibody, endogenous glucose production was reduced by CRTC2 KD. |
| 4562 | 23606308 | These cells not only expressed MSC-specific markers like Sca-1, CD90.2, CD73, and CD44 but also generated osteocytes, adipocytes, and neurons when induced with specific growth media. |
| 4563 | 23606308 | Upon exposure to islet differentiation serum-free cocktail a significant upregulation of pancreatic markers like Nkx2.2, Nkx6.1, Pdx1, insulin, and somatostatin was seen. |
| 4564 | 23630299 | We hypothesized that hypoglycemia can be prevented in autoimmune T1D by SST receptor type 2 (SSTR2) antagonism of α-cells, which relieve SSTR2 inhibition, thereby increasing glucagon secretion. |
| 4565 | 23630299 | Diabetic and nondiabetic rats underwent a 3-h infusion of vehicle compared with SSTR2 antagonist (SSTR2a) during insulin-induced hypoglycemia clamped at 3 ± 0.5 mmol/L. |
| 4566 | 23694765 | G-protein coupled receptors (GPCRs) regulate hormone secretion from islets of Langerhans, and recently developed therapies for type-2 diabetes target islet GLP-1 receptors. |
| 4567 | 23694765 | We have used this atlas to describe how islet GPCRs interact with their endogenous ligands, regulate islet hormone secretion, and interact with drugs known to target GPCRs, with a focus on drug/receptor interactions that may affect insulin secretion. |
| 4568 | 23694765 | The islet GPCRome consists of 293 GPCRs, a majority of which have unknown effects on insulin, glucagon and somatostatin secretion. |
| 4569 | 23694765 | Islet GPCRs are also the targets of a large number of clinically used drugs, and based on their coupling characteristics and effects on receptor signalling we identified 107 drugs predicted to stimulate and 184 drugs predicted to inhibit insulin secretion. |
| 4570 | 23694765 | The islet GPCRome highlights knowledge gaps in the current understanding of islet GPCR function, and identifies GPCR/ligand/drug interactions that might affect insulin secretion, which are important for understanding the metabolic side effects of drugs. |
| 4571 | 23725211 | Significant expressions of PDX1, neurogenin3 (Ngn3), glucagon, glucose transporter2 (Glut2), and somatostatin were detected by quantitative RT-PCR (P < 0.05). |
| 4572 | 23725211 | PDX1 and insulin proteins were shown by immunocytochemistry analysis. |
| 4573 | 23725211 | Insulin secretion of hUDSCs(PDX1+) in the high-glucose medium was 1.8 μU/mL. |
| 4574 | 23769060 | Additionally, some endocrine transdifferentiation of the liver, with storage of insulin in granules, and expression of some β-cell transcription factors (eg, Pdx1, Neurod1, Neurog3, Nkx2-2, Pax4) and pancreatic hormones in both studies. |
| 4575 | 23769060 | Reverse-transcription polymerase chain reaction analysis of the liver tissue revealed expression of several β-cell transcription factors, including the key factors, Pdx-1 and Neurod1, pancreatic hormones, glucagon, and somatostatin; however, endogenous pig insulin was not expressed. |
| 4576 | 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. |
| 4577 | 23818527 | GLP-1 and GIP promote β-cell proliferation and survival in rodents. |
| 4578 | 23818527 | GLP-1 and GIP exert their actions predominantly through unique G protein-coupled receptors expressed on β-cells and other pancreatic cell types. |
| 4579 | 23897760 | Enrichment of human embryonic stem cell-derived NKX6.1-expressing pancreatic progenitor cells accelerates the maturation of insulin-secreting cells in vivo. |
| 4580 | 23897760 | We previously described a differentiation protocol to generate pancreatic progenitor cells from hESCs, composed of mainly pancreatic endoderm (PDX1/NKX6.1-positive), endocrine precursors (NKX2.2/synaptophysin-positive, hormone/NKX6.1-negative), and polyhormonal cells (insulin/glucagon-positive, NKX6.1-negative). |
| 4581 | 23897760 | However, the relative contributions of NKX6.1-negative versus NKX6.1-positive cell fractions to the maturation of functional β-cells remained unclear. |
| 4582 | 23897760 | Prior to transplant, both populations contained a high proportion of PDX1-expressing cells (~85%-90%) but were distinguished by their relatively high (~80%) or low (~25%) expression of NKX6.1. |
| 4583 | 23897760 | Fasting human C-peptide levels were similar between groups throughout the study, but only NKX6.1-high grafts displayed robust meal-, glucose- and arginine-responsive insulin secretion as early as 3 months post-transplant. |
| 4584 | 23897760 | Theracyte devices from both groups contained almost exclusively pancreatic endocrine tissue, but NKX6.1-high grafts contained a greater proportion of insulin-positive and somatostatin-positive cells, whereas NKX6.1-low grafts contained mainly glucagon-expressing cells. |
| 4585 | 23897760 | Insulin-positive cells in NKX6.1-high, but not NKX6.1-low grafts expressed nuclear MAFA. |
| 4586 | 23911664 | Confocal microscopy of control islets showed expression of GPR40 protein in insulin, glucagon and somatostatin cells. |
| 4587 | 23911664 | GPR40 expression was strongly increased in islets of hyperlipidaemic fa/fa rats and coincided with a concentration-related increase in palmitate-induced release of insulin and glucagon and its inhibition of somatostatin release. |
| 4588 | 23911664 | The palmitate antagonist rosiglitazone promoted reappearance of GPR40 in high-glucose-cultured islets and served as partial agonist in glucose-stimulated insulin release. |
| 4589 | 23911664 | Mild hyperlipidaemia in obesity-prone diabetes creates increased GPR40 expression and increased risk for an exaggerated palmitate-induced insulin response and lipotoxicity, a metabolic situation suitable for GPR40 antagonist treatment. |
| 4590 | 23911664 | Chronic hyperglycaemia creates abrogated GPR40 expression and downregulated insulin release, a metabolic situation suitable for GPR40 agonist treatment to avoid glucotoxicity. |
| 4591 | 23911664 | Confocal microscopy of control islets showed expression of GPR40 protein in insulin, glucagon and somatostatin cells. |
| 4592 | 23911664 | GPR40 expression was strongly increased in islets of hyperlipidaemic fa/fa rats and coincided with a concentration-related increase in palmitate-induced release of insulin and glucagon and its inhibition of somatostatin release. |
| 4593 | 23911664 | The palmitate antagonist rosiglitazone promoted reappearance of GPR40 in high-glucose-cultured islets and served as partial agonist in glucose-stimulated insulin release. |
| 4594 | 23911664 | Mild hyperlipidaemia in obesity-prone diabetes creates increased GPR40 expression and increased risk for an exaggerated palmitate-induced insulin response and lipotoxicity, a metabolic situation suitable for GPR40 antagonist treatment. |
| 4595 | 23911664 | Chronic hyperglycaemia creates abrogated GPR40 expression and downregulated insulin release, a metabolic situation suitable for GPR40 agonist treatment to avoid glucotoxicity. |
| 4596 | 23913443 | Here, we found that selenoprotein T (SelT), a new thioredoxin-like protein of the endoplasmic reticulum, is present at high levels in human and mouse pancreas as revealed by immunofluorescence and quantitative PCR. |
| 4597 | 23913443 | Confocal immunohistochemistry studies revealed that SelT is mostly confined to insulin- and somatostatin-producing cells in mouse and human islets. |
| 4598 | 23913443 | Finally, we found that SelT is up-regulated by pituitary adenylate cyclase-activating polypeptide (PACAP) in β-pancreatic cells and that SelT could act by facilitating a feed-forward mechanism to potentiate insulin secretion induced by the neuropeptide. |
| 4599 | 23939195 | The biochemical utility of chromogranin A, chromogranin B and cocaine- and amphetamine-regulated transcript for neuroendocrine neoplasia. |
| 4600 | 23939195 | The peptides chromogranin A (CgA), chromogranin B (CgB) and cocaine- and amphetamine-regulated transcript (CART) are widely distributed throughout the neuroendocrine system. |
| 4601 | 23939195 | CgA and CgB have been used as general NEN biomarkers for many years, while CART has only recently been identified. |
| 4602 | 23939195 | However, circulating CgA concentrations exhibit considerable intra-individual biological variation, are altered by proton pump inhibitors (PPIs) and somatostatin analogues and are elevated in non-NEN malignancies. |
| 4603 | 23939195 | The effects of treatment and non-NEN conditions on circulating CgB and CART concentrations are less well understood. |
| 4604 | 23939195 | CgB is less affected by impaired renal function and PPIs than CgA; while, circulating CART concentrations lack a diurnal variation in humans and are more reliable markers of pancreatic NEN malignancy than CgA. |
| 4605 | 23939195 | However, the utility of CgB and CART in NEN management is yet to be elucidated. |
| 4606 | 23939195 | Further studies are needed to establish whether CgB and CART are useful alternatives to CgA. |
| 4607 | 16754785 | Target soluble N-ethylmaleimide-sensitive factor attachment protein receptors (t-SNAREs) differently regulate activation and inactivation gating of Kv2.2 and Kv2.1: Implications on pancreatic islet cell Kv channels. |
| 4608 | 16754785 | We have hypothesized that the plasma membrane protein components of the exocytotic soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor (SNARE) complex, syntaxin 1A and SNAP-25, distinctly regulate different voltage-gated K+ (Kv) channels that are differentially distributed. |
| 4609 | 16754785 | Neuroendocrine islet cells (alpha, beta, delta) uniformly contain both syntaxin 1A and SNAP-25. |
| 4610 | 16754785 | However, using immunohistochemistry, we show that the different pancreatic islet cells contain distinct dominant Kv channels, including Kv2.1 in beta cells and Kv2.2 in alpha and delta cells, whose interactions with the SNARE proteins would, respectively regulate insulin, glucagon and somatostatin secretion. |
| 4611 | 16754785 | We therefore examined the regulation by syntaxin 1A and SNAP-25 of these two channels. |
| 4612 | 16754785 | We have shown that Kv2.1 interacts with syntaxin 1A and SNAP-25 and, based on studies in oocytes, suggested a model of two distinct modes of interaction of syntaxin 1A and the complex syntaxin 1A/SNAP-25 with the C terminus of the channel. |
| 4613 | 16754785 | Here, we characterized the interactions of syntaxin 1A and SNAP-25 with Kv2.2 which is highly homologous to Kv2.1, except for the C-terminus. |
| 4614 | 16754785 | Comparative two-electrode voltage clamp analysis in oocytes between Kv2.2 and Kv2.1 shows that Kv2.2 interacts only with syntaxin 1A and, in contrast to Kv2.1, it does not interact with the syntaxin 1A/SNAP-25 complex and hence is not sensitive to the assembly/disassembly state of the complex. |