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Gene Information
Gene symbol: LIPE
Gene name: lipase, hormone-sensitive
HGNC ID: 6621
Synonyms: HSL
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1528859 | Western blotting of adipocyte homogenate fractions with polyclonal antiserum raised against HSL showed that the enzyme shifted quantitatively from the supernatant of control cells to the floating "fat cake" of lipolytically stimulated cells. |
| 2 | 1528859 | We propose that upon lipolytic activation of adipocytes and phosphorylation of HSL by cAMP-dependent protein kinase, the critical event is not an increase in catalytic activity (i.e., turnover number) but a translocation of the lipase to its substrate at the surface of the lipid storage droplet. |
| 3 | 1528859 | Western blotting of adipocyte homogenate fractions with polyclonal antiserum raised against HSL showed that the enzyme shifted quantitatively from the supernatant of control cells to the floating "fat cake" of lipolytically stimulated cells. |
| 4 | 1528859 | We propose that upon lipolytic activation of adipocytes and phosphorylation of HSL by cAMP-dependent protein kinase, the critical event is not an increase in catalytic activity (i.e., turnover number) but a translocation of the lipase to its substrate at the surface of the lipid storage droplet. |
| 5 | 1542265 | Physiological actions of insulin include suppression of fat mobilization from adipose tissue and activation of adipose tissue lipoprotein lipase. |
| 6 | 1542265 | Here, we report measurements of adipose tissue hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action in vivo in 10 normal and eight obese subjects, with the latter group having varying degrees of glucose intolerance. |
| 7 | 1542265 | HSL and LPL actions (per gram of adipose tissue) were similar in the two groups, after an overnight fast. |
| 8 | 1542265 | In the normal subjects, HSL action was suppressed after a meal (by 75% +/- 6% between 60 to 300 minutes, P less than .01), and the action of LPL was increased (clearance of circulating triacylglycerol [TAG] increased by 140% +/- 57% at 300 minutes, P less than .05). |
| 9 | 1542265 | In obese subjects, adipose tissue HSL and LPL fail to respond to immunoreactive insulin postprandially, which may be an important maladaptation in terms of lipoprotein metabolism and risk of coronary heart disease. |
| 10 | 1542265 | Physiological actions of insulin include suppression of fat mobilization from adipose tissue and activation of adipose tissue lipoprotein lipase. |
| 11 | 1542265 | Here, we report measurements of adipose tissue hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action in vivo in 10 normal and eight obese subjects, with the latter group having varying degrees of glucose intolerance. |
| 12 | 1542265 | HSL and LPL actions (per gram of adipose tissue) were similar in the two groups, after an overnight fast. |
| 13 | 1542265 | In the normal subjects, HSL action was suppressed after a meal (by 75% +/- 6% between 60 to 300 minutes, P less than .01), and the action of LPL was increased (clearance of circulating triacylglycerol [TAG] increased by 140% +/- 57% at 300 minutes, P less than .05). |
| 14 | 1542265 | In obese subjects, adipose tissue HSL and LPL fail to respond to immunoreactive insulin postprandially, which may be an important maladaptation in terms of lipoprotein metabolism and risk of coronary heart disease. |
| 15 | 1542265 | Physiological actions of insulin include suppression of fat mobilization from adipose tissue and activation of adipose tissue lipoprotein lipase. |
| 16 | 1542265 | Here, we report measurements of adipose tissue hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action in vivo in 10 normal and eight obese subjects, with the latter group having varying degrees of glucose intolerance. |
| 17 | 1542265 | HSL and LPL actions (per gram of adipose tissue) were similar in the two groups, after an overnight fast. |
| 18 | 1542265 | In the normal subjects, HSL action was suppressed after a meal (by 75% +/- 6% between 60 to 300 minutes, P less than .01), and the action of LPL was increased (clearance of circulating triacylglycerol [TAG] increased by 140% +/- 57% at 300 minutes, P less than .05). |
| 19 | 1542265 | In obese subjects, adipose tissue HSL and LPL fail to respond to immunoreactive insulin postprandially, which may be an important maladaptation in terms of lipoprotein metabolism and risk of coronary heart disease. |
| 20 | 1542265 | Physiological actions of insulin include suppression of fat mobilization from adipose tissue and activation of adipose tissue lipoprotein lipase. |
| 21 | 1542265 | Here, we report measurements of adipose tissue hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action in vivo in 10 normal and eight obese subjects, with the latter group having varying degrees of glucose intolerance. |
| 22 | 1542265 | HSL and LPL actions (per gram of adipose tissue) were similar in the two groups, after an overnight fast. |
| 23 | 1542265 | In the normal subjects, HSL action was suppressed after a meal (by 75% +/- 6% between 60 to 300 minutes, P less than .01), and the action of LPL was increased (clearance of circulating triacylglycerol [TAG] increased by 140% +/- 57% at 300 minutes, P less than .05). |
| 24 | 1542265 | In obese subjects, adipose tissue HSL and LPL fail to respond to immunoreactive insulin postprandially, which may be an important maladaptation in terms of lipoprotein metabolism and risk of coronary heart disease. |
| 25 | 7476301 | A halfmark is mobilization of lipids, which involves an inhibition of lipoprotein lipase activity in adipose tissue and activation of the hormone sensitive lipase. |
| 26 | 7476301 | The nitrogen-retaining effects of GH seem to involve a direct stimulation of protein synthesis in addition to secondary effects such as generation of insulin-like growth factor-I (IGF-I), hyperinsulinemia, and promotion of lipolysis. |
| 27 | 7476301 | Thus, during periods of substrate affluence, GH acts in concert with insulin and IGF-I to promote protein anabolism. |
| 28 | 7476323 | This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. |
| 29 | 7476323 | Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. |
| 30 | 7476323 | HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. |
| 31 | 7476323 | Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. |
| 32 | 7476323 | In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue. |
| 33 | 7476323 | This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. |
| 34 | 7476323 | Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. |
| 35 | 7476323 | HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. |
| 36 | 7476323 | Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. |
| 37 | 7476323 | In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue. |
| 38 | 7476323 | This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. |
| 39 | 7476323 | Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. |
| 40 | 7476323 | HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. |
| 41 | 7476323 | Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. |
| 42 | 7476323 | In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue. |
| 43 | 7476323 | This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. |
| 44 | 7476323 | Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. |
| 45 | 7476323 | HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. |
| 46 | 7476323 | Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. |
| 47 | 7476323 | In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue. |
| 48 | 7476323 | This study was designed to examine the effects of insulin deficiency on the regulation of HSL in isolated adipocytes. |
| 49 | 7476323 | Compared with levels in control rats, 10 days of insulin deficiency increased HSL activity twofold (P < .05), as assayed for neutral cholesterol esterase activity, and insulin treatment returned HSL activity to normal. |
| 50 | 7476323 | HSL protein was increased twofold (P < .05) in streptozotocin-induced diabetic rats, as estimated by immunoblotting, but remained elevated after insulin treatment. |
| 51 | 7476323 | Levels of HSL mRNA assessed by Northern blot analysis also increased twofold (P < .01) in adipose cells isolated from streptozotocin-induced diabetic rats, and remained elevated after insulin treatment. |
| 52 | 7476323 | In conclusion, our studies suggest that 10 days of insulin deficiency increases HSL expression via pretranslational mechanisms and short-term insulin treatment returns HSL activity to normal via posttranslational mechanisms in adipose tissue. |
| 53 | 8397127 | Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. |
| 54 | 8397127 | When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. |
| 55 | 8397127 | The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. |
| 56 | 8397127 | Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. |
| 57 | 8397127 | Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. |
| 58 | 8397127 | When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. |
| 59 | 8397127 | The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. |
| 60 | 8397127 | Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. |
| 61 | 8397127 | Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. |
| 62 | 8397127 | When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. |
| 63 | 8397127 | The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. |
| 64 | 8397127 | Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. |
| 65 | 8680486 | Lipid hydrolysis in these cells is initiated by cAMP, which leads to phosphorylation of hormone-sensitive lipase in adipocytes and cholesteryl esterase in steroidogenic cells by protein kinase A. |
| 66 | 8690802 | Acute regulation by insulin of phosphatidylinositol-3-kinase, Rad, Glut 4, and lipoprotein lipase mRNA levels in human muscle. |
| 67 | 8690802 | Using reverse transcription-competitive PCR, we have measured the mRNAs encoding the two insulin receptor variants, the insulin receptor substrate-1, the p85alpha subunit of phosphatidylinositol-3-kinase, Ras associated to diabetes (Rad), the glucose transporter Glut 4, glycogen synthase, 6-phosphofructo-l-kinase, lipoprotein lipase, and the hormone-sensitive lipase. |
| 68 | 8690802 | Insulin infusion induced a significant increase in the mRNA level of Glut 4 (+56 +/- 13%), Rad (+96 +/- 25%), the p85alpha subunit of phosphatidylinositol-3-kinase (+92 +/- 18%) and a decrease in the lipoprotein lipase mRNA level (-49 +/- 5%), while the abundance of the other mRNAs was unaffected. |
| 69 | 8690802 | These results demonstrate an acute coordinated regulation by insulin of the expression of genes coding key proteins involved in its action in human skeletal muscle and suggest that Rad and the p85alpha regulatory subunit of phosphatidylinositol-3-kinase can be added to the list of the genes controlled by insulin. |
| 70 | 8692022 | To investigate whether mutations in the HSL gene are associated with non-insulin-dependent diabetes mellitus (NIDDM), we screened for mutations of this gene using single-stranded conformation polymorphism (SSCP) in 35 Japanese subjects with NIDDM. |
| 71 | 8858214 | The lipolytic effects of noradrenaline (major endogenous lipolytic agent), isoprenaline (a non-selective beta-adrenoceptor agonist), forskolin (a direct activator of adenylyl cyclase) and dibutyryl cyclic AMP (activating protein kinase and thereby hormone-sensitive lipase) were reduced by about 50% (p from 0.001 to 0.01). |
| 72 | 8858214 | Thus, lipolytic catecholamine resistance in fat cells, at least partly due to impaired function of hormone-sensitive lipase, is an adipocyte abnormality associated with a family tendency to obesity. |
| 73 | 8858214 | The lipolytic effects of noradrenaline (major endogenous lipolytic agent), isoprenaline (a non-selective beta-adrenoceptor agonist), forskolin (a direct activator of adenylyl cyclase) and dibutyryl cyclic AMP (activating protein kinase and thereby hormone-sensitive lipase) were reduced by about 50% (p from 0.001 to 0.01). |
| 74 | 8858214 | Thus, lipolytic catecholamine resistance in fat cells, at least partly due to impaired function of hormone-sensitive lipase, is an adipocyte abnormality associated with a family tendency to obesity. |
| 75 | 9224423 | High levels of adipose tissue-derived tumor necrosis factor-alpha (AT-TNF) mRNA and protein have previously been associated with genetic models of obesity and insulin resistance. |
| 76 | 9224423 | Since TNF has been shown to affect several key genes in tissue culture, mRNA for lipoprotein lipase, hormone-sensitive lipase, and Glut4 were measured. |
| 77 | 9329383 | To identify molecular defects responsible for this disease, we tested the implication of 14 candidate genes coding for proteins involved either in insulin action, i.e. insulin receptor, insulin receptor substrate 1, insulin-like growth factor I receptor, diabetes-associated ras-like protein (Rad), and glycogen synthase, or in lipid metabolism, i.e. lipoprotein lipase; apolipoproteins CII, AII, and CIII; hepatic lipase; hormone-sensitive lipase; the beta 3-adrenergic receptor; leptin; and fatty acid-binding protein 2. |
| 78 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 79 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 80 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 81 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 82 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 83 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 84 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 85 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 86 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 87 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 88 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 89 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 90 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 91 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 92 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 93 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 94 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 95 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 96 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 97 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 98 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 99 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 100 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 101 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 102 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 103 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 104 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 105 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 106 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 107 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 108 | 9351402 | Adipose tissue lipoprotein lipase and hormone-sensitive lipase. |
| 109 | 9351402 | The enzymes lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) are rate-limiting steps for the turnover of fatty acids in adipose tissue, because they hydrolyze extracellular triglycerides in lipoproteins (LPL) and intracellular triglycerides in adipocytes (HSL). |
| 110 | 9351402 | The present study was undertaken to simultaneously determine the activities of LPL and HSL in subcutaneous adipose tissue from male patients with FCHL and IRS. |
| 111 | 9351402 | LPL and HSL activity was investigated in 10 nonobese FCHL patients and compared with 10 matched healthy nonobese subjects, and in 8 essentially normolipidemic IRS patients (who did not have overt diabetes mellitus) and compared with 9 nonobese matched control subjects. |
| 112 | 9351402 | LPL activity was 43% lower in patients with IRS (P < .0005), as compared with control subjects, but HSL activity was not significantly different in the two groups, On the other hand, HSL activity was decreased by 45% in FCHL patients (P < .01), as compared with control subjects, but LPL activity was not significantly different in FCHL patients and the control group. |
| 113 | 9351402 | However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. |
| 114 | 9421381 | No difference in mRNA expression between omental and subcutaneous adipose tissue was observed for hormone sensitive lipase, lipoprotein lipase, 6-phosphofructo-1-kinase, insulin receptor substrate 1, p85alpha regulatory subunit of phosphatidylinositol-3-kinase, and Rad. |
| 115 | 9421381 | Perhaps consistent with a less efficient insulin signaling, a twofold reduction in GLUT4, glycogen synthase, and leptin mRNA expression was observed in omental adipose tissue. |
| 116 | 9568706 | BRL 49653 blocks the lipolytic actions of tumor necrosis factor-alpha: a potential new insulin-sensitizing mechanism for thiazolidinediones. |
| 117 | 9568706 | Adipocyte production of TNF-alpha is proposed to play a role in the development of insulin resistance, and because BRL 49653 has been shown to antagonize some of the effects of TNF-alpha, we examined the effects of TNF-alpha and BRL 49653 on adipocyte lipolysis. |
| 118 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 119 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 120 | 9726225 | In contrast to the marked site-related expression of leptin, genes encoding lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and adipsin were not consistently differentially expressed. |
| 121 | 9726225 | Of note, a highly significant inverse correlation between adipocyte PPAR-gamma expression and BMI (r = -0.7, P = 0.0005) was found. |
| 122 | 9726225 | Because cIAP2 may be involved in the regulation of TNF-alpha signaling, this raises the possibility that depot-specific differences may exist in the regulation of adipocyte apoptosis. |
| 123 | 9726225 | Given the importance of PPAR-gamma in adipocyte development and insulin sensitivity, the inverse correlation between adipocyte PPAR-gamma mRNA levels and adiposity may represent a local regulatory mechanism restraining fat accumulation and/or may be related to the reduction of insulin sensitivity that occurs with increasing fat mass. |
| 124 | 9892250 | Because HSL in adipocytes is activated by cAMP-dependent protein kinase (PKA), PKA-regulated triglyceride hydrolysis in beta-cells may participate in the regulation of insulin secretion, possibly by providing a lipid-derived signal, e.g., long-chain acyl-CoA and diacylglycerol. |
| 125 | 10334320 | These included cholecystokinin A and B receptors (CCK-AR and CCK-BR), glucagon-like peptide 1 receptor (GLP-1R), the LIM/homeodomain islet-1 gene (Isl-1), the caudal-type homeodomain 3 (CDX-3), the uncoupling protein 1 (UCP-1), the beta3-adrenoceptor (beta3-AR), the fatty acid-binding protein 2 (FABP-2), the hormone-sensitive lipase (HSL), the lipoprotein lipase (LPL), the apoprotein-C2 (apo-C2), the insulin receptor substrate-1 (IRS-1), the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and the liver carnitine palmitoyltransferase-1 (CPT-1). |
| 126 | 10334320 | Phenotypes related to obesity such as BMI, adult life body weight gain, fasting leptin, insulin, fasting glycerol, and free fatty acids were used for nonparametric sib-pair analyses. |
| 127 | 10334320 | Moreover, a suggestive indication for linkage was found between the Isl-1 locus and BMI and leptin values (P = 0.001 and 0.0003, respectively) and leptin adjusted for BMI (P = 0.0001). |
| 128 | 10334320 | Multipoint analyses for leptin trait with Isl-1 and two flanking markers (D5S418 and D5S407) showed that the logarithm of odds (LOD) score is 1.73, coinciding with the Isl-1 locus. |
| 129 | 10334320 | Although marginally positive indications for linkage in subgroups of families were found with IRS-1, CPT-1, and HSL loci, our data suggested that these genes are not major contributors to obesity. |
| 130 | 10334320 | These included cholecystokinin A and B receptors (CCK-AR and CCK-BR), glucagon-like peptide 1 receptor (GLP-1R), the LIM/homeodomain islet-1 gene (Isl-1), the caudal-type homeodomain 3 (CDX-3), the uncoupling protein 1 (UCP-1), the beta3-adrenoceptor (beta3-AR), the fatty acid-binding protein 2 (FABP-2), the hormone-sensitive lipase (HSL), the lipoprotein lipase (LPL), the apoprotein-C2 (apo-C2), the insulin receptor substrate-1 (IRS-1), the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and the liver carnitine palmitoyltransferase-1 (CPT-1). |
| 131 | 10334320 | Phenotypes related to obesity such as BMI, adult life body weight gain, fasting leptin, insulin, fasting glycerol, and free fatty acids were used for nonparametric sib-pair analyses. |
| 132 | 10334320 | Moreover, a suggestive indication for linkage was found between the Isl-1 locus and BMI and leptin values (P = 0.001 and 0.0003, respectively) and leptin adjusted for BMI (P = 0.0001). |
| 133 | 10334320 | Multipoint analyses for leptin trait with Isl-1 and two flanking markers (D5S418 and D5S407) showed that the logarithm of odds (LOD) score is 1.73, coinciding with the Isl-1 locus. |
| 134 | 10334320 | Although marginally positive indications for linkage in subgroups of families were found with IRS-1, CPT-1, and HSL loci, our data suggested that these genes are not major contributors to obesity. |
| 135 | 10480596 | Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose. |
| 136 | 10480596 | We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO). |
| 137 | 10480596 | However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h. |
| 138 | 10480596 | Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased. |
| 139 | 10480596 | Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis. |
| 140 | 10480596 | We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL. |
| 141 | 10480596 | Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose. |
| 142 | 10480596 | We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO). |
| 143 | 10480596 | However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h. |
| 144 | 10480596 | Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased. |
| 145 | 10480596 | Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis. |
| 146 | 10480596 | We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL. |
| 147 | 10480596 | Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose. |
| 148 | 10480596 | We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO). |
| 149 | 10480596 | However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h. |
| 150 | 10480596 | Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased. |
| 151 | 10480596 | Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis. |
| 152 | 10480596 | We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL. |
| 153 | 10480596 | Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose. |
| 154 | 10480596 | We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO). |
| 155 | 10480596 | However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h. |
| 156 | 10480596 | Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased. |
| 157 | 10480596 | Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis. |
| 158 | 10480596 | We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL. |
| 159 | 10567009 | Skeletal muscle uncoupling protein 2 and 3 (UCP-2 and UCP-3) mRNA levels are increased during calorie restriction in lean and nondiabetic obese subjects. |
| 160 | 10567009 | In this work, we have investigated the effect of a 5-day hypocaloric diet (1,045 kJ/day) on UCP-2 and UCP-3 gene expression in the skeletal muscle of type-2 diabetic obese patients. |
| 161 | 10567009 | Before the diet, UCP-2 and UCP-3 mRNA levels were more abundant in diabetic than in nondiabetic subjects. |
| 162 | 10567009 | Calorie restriction induced a two- to threefold increase in UCP-2 and UCP-3 mRNA levels in nondiabetic patients. |
| 163 | 10567009 | Variations in plasma nonesterified fatty acid level were positively correlated with changes in skeletal muscle UCP-3(L) (r = 0.6, P < 0.05) and adipose tissue hormone-sensitive lipase (r = 0.9, P < 0.001) mRNA levels. |
| 164 | 10634941 | Hormonal stimulation of cAMP formation and the activation of cAMP-dependent protein kinase leads to the phosphorylation of hormone-sensitive lipase and a large increase in lipolysis in adipocytes. |
| 165 | 10724087 | The effects of tolbutamide on lipoproteins, lipoprotein lipase and hormone-sensitive lipase. |
| 166 | 10889791 | Among these, the genes for beta 3-adrenergic receptor, hormone-sensitive lipase, lipoprotein lipase, IRS-1, PC-1, skeletal muscle glycogen synthase, etc. appear to increase the risk of the metabolic syndrome. |
| 167 | 11016888 | In addition adipose tissue lipoprotein lipase (LPL) activity was increased in masoprocol-treated rats and adipose tissue hormone-sensitive lipase (HSL) activity was decreased. |
| 168 | 11220283 | There are a number of potential thrifty genes, including those that regulate lipolysis or code for the beta3-adrenergic receptor, the hormone-sensitive lipase, and lipoprotein lipase. |
| 169 | 11272142 | Gene expression of sn-glycerol-3-phosphate acyltransferase (GPAT), diacylglycerol acyltransferase (DGAT), and hormone-sensitive lipase (HSL), three key enzymes of lipid metabolism, was detected in isolated rat islets. |
| 170 | 11334438 | Insulin and leptin acutely regulate cholesterol ester metabolism in macrophages by novel signaling pathways. |
| 171 | 11334438 | Leptin also stimulates both phosphoinositide 3-kinase (PI 3-kinase) activity and tyrosine phosphorylation of JAK2 and STAT3 in these cells. |
| 172 | 11334438 | We investigated the effects of leptin on hormone-sensitive lipase (HSL), which acts as a neutral cholesterol esterase in macrophages and is a rate-limiting step in cholesterol ester breakdown. |
| 173 | 11334438 | Leptin significantly increased HSL activity in J774.2 macrophages, and these effects were additive with the effects of cAMP and were blocked by PI 3-kinase inhibitors. |
| 174 | 11334438 | Conversely, insulin inhibited HSL in macrophages, but unlike adipocytes, this effect did not require PI 3-kinase. |
| 175 | 11334438 | These results indicate that leptin and insulin regulate cholesterol-ester homeostasis in macrophages and, therefore, defects in this process caused by leptin and/or insulin resistance could contribute to the increased incidence of atherosclerosis found associated with obesity and type 2 diabetes. |
| 176 | 11334438 | Insulin and leptin acutely regulate cholesterol ester metabolism in macrophages by novel signaling pathways. |
| 177 | 11334438 | Leptin also stimulates both phosphoinositide 3-kinase (PI 3-kinase) activity and tyrosine phosphorylation of JAK2 and STAT3 in these cells. |
| 178 | 11334438 | We investigated the effects of leptin on hormone-sensitive lipase (HSL), which acts as a neutral cholesterol esterase in macrophages and is a rate-limiting step in cholesterol ester breakdown. |
| 179 | 11334438 | Leptin significantly increased HSL activity in J774.2 macrophages, and these effects were additive with the effects of cAMP and were blocked by PI 3-kinase inhibitors. |
| 180 | 11334438 | Conversely, insulin inhibited HSL in macrophages, but unlike adipocytes, this effect did not require PI 3-kinase. |
| 181 | 11334438 | These results indicate that leptin and insulin regulate cholesterol-ester homeostasis in macrophages and, therefore, defects in this process caused by leptin and/or insulin resistance could contribute to the increased incidence of atherosclerosis found associated with obesity and type 2 diabetes. |
| 182 | 11334438 | Insulin and leptin acutely regulate cholesterol ester metabolism in macrophages by novel signaling pathways. |
| 183 | 11334438 | Leptin also stimulates both phosphoinositide 3-kinase (PI 3-kinase) activity and tyrosine phosphorylation of JAK2 and STAT3 in these cells. |
| 184 | 11334438 | We investigated the effects of leptin on hormone-sensitive lipase (HSL), which acts as a neutral cholesterol esterase in macrophages and is a rate-limiting step in cholesterol ester breakdown. |
| 185 | 11334438 | Leptin significantly increased HSL activity in J774.2 macrophages, and these effects were additive with the effects of cAMP and were blocked by PI 3-kinase inhibitors. |
| 186 | 11334438 | Conversely, insulin inhibited HSL in macrophages, but unlike adipocytes, this effect did not require PI 3-kinase. |
| 187 | 11334438 | These results indicate that leptin and insulin regulate cholesterol-ester homeostasis in macrophages and, therefore, defects in this process caused by leptin and/or insulin resistance could contribute to the increased incidence of atherosclerosis found associated with obesity and type 2 diabetes. |
| 188 | 11375348 | Subcellular localization of insulin receptor substrate family proteins associated with phosphatidylinositol 3-kinase activity and alterations in lipolysis in primary mouse adipocytes from IRS-1 null mice. |
| 189 | 11375348 | To clarify the roles of insulin receptor substrate (IRS) family proteins in phosphatidylinositol (PI) 3-kinase activation and insulin actions in adipocytes, we investigated the intracellular localization of IRS family proteins and PI 3-kinase activation in response to insulin by fractionation of mouse adipocytes from wild-type and IRS-1 null mice. |
| 190 | 11375348 | In adipocytes from wild-type mice, tyrosine-phosphorylated IRS-1 and IRS-2, which were found to associate with PI 3-kinase in response to insulin, were detected in the plasma membrane (PM) and low-density microsome (LDM) fractions. |
| 191 | 11375348 | In adipocytes from IRS-1-null mice, insulin-stimulated PI 3-kinase activity in anti-phosphotyrosine (alphaPY) immunoprecipitates in the LDM fraction was almost exclusively mediated via IRS-2 and was reduced to 25%; however, insulin-stimulated PI 3-kinase activity in the PM fraction was primarily mediated via IRS-3 and was reduced to 60%. |
| 192 | 11375348 | To determine the potential functional impact of the distinct subcellular localization of IRSs and associating PI 3-kinase activity on adipocyte-specific metabolic actions, we examined lipolysis in IRS-1 null mice. |
| 193 | 11375348 | The antilipolytic effect of insulin in IRS-1 null adipocytes, however, was comparable to that in wild-type mice. |
| 194 | 11375348 | Thus, discordance between these two insulin actions as well as the transcriptional and translational effect (HSL mRNA and protein regulation) and the PM effect (antilipolysis) of insulin may be explained by distinct roles of both PI 3-kinase activity associated with IRS-1/IRS-2 and PI 3-kinase activity associated with IRS-3 in insulin actions related to their subcellular localization. |
| 195 | 11522661 | A role for hormone-sensitive lipase in glucose-stimulated insulin secretion: a study in hormone-sensitive lipase-deficient mice. |
| 196 | 11522661 | In addition, hormone-sensitive lipase (HSL) is expressed in beta-cells and may provide fatty acids necessary for the generation of coupling factors linking glucose metabolism to insulin release. |
| 197 | 11522661 | We have recently created HSL-deficient mice that were used to directly assess the role of HSL in insulin secretion and action. |
| 198 | 11522661 | Freshly isolated islets from HSL-deficient mice displayed elevated secretion at low (3 mmol/l) glucose, failed to release insulin in response to high (20 mmol/l) glucose, but had a normal secretion when challenged with elevated KCl. |
| 199 | 11522661 | The results demonstrate an important role of HSL and endogenous beta-cell lipolysis in the coupling mechanism of glucose-stimulated insulin secretion. |
| 200 | 11522661 | A role for hormone-sensitive lipase in glucose-stimulated insulin secretion: a study in hormone-sensitive lipase-deficient mice. |
| 201 | 11522661 | In addition, hormone-sensitive lipase (HSL) is expressed in beta-cells and may provide fatty acids necessary for the generation of coupling factors linking glucose metabolism to insulin release. |
| 202 | 11522661 | We have recently created HSL-deficient mice that were used to directly assess the role of HSL in insulin secretion and action. |
| 203 | 11522661 | Freshly isolated islets from HSL-deficient mice displayed elevated secretion at low (3 mmol/l) glucose, failed to release insulin in response to high (20 mmol/l) glucose, but had a normal secretion when challenged with elevated KCl. |
| 204 | 11522661 | The results demonstrate an important role of HSL and endogenous beta-cell lipolysis in the coupling mechanism of glucose-stimulated insulin secretion. |
| 205 | 11522661 | A role for hormone-sensitive lipase in glucose-stimulated insulin secretion: a study in hormone-sensitive lipase-deficient mice. |
| 206 | 11522661 | In addition, hormone-sensitive lipase (HSL) is expressed in beta-cells and may provide fatty acids necessary for the generation of coupling factors linking glucose metabolism to insulin release. |
| 207 | 11522661 | We have recently created HSL-deficient mice that were used to directly assess the role of HSL in insulin secretion and action. |
| 208 | 11522661 | Freshly isolated islets from HSL-deficient mice displayed elevated secretion at low (3 mmol/l) glucose, failed to release insulin in response to high (20 mmol/l) glucose, but had a normal secretion when challenged with elevated KCl. |
| 209 | 11522661 | The results demonstrate an important role of HSL and endogenous beta-cell lipolysis in the coupling mechanism of glucose-stimulated insulin secretion. |
| 210 | 11522661 | A role for hormone-sensitive lipase in glucose-stimulated insulin secretion: a study in hormone-sensitive lipase-deficient mice. |
| 211 | 11522661 | In addition, hormone-sensitive lipase (HSL) is expressed in beta-cells and may provide fatty acids necessary for the generation of coupling factors linking glucose metabolism to insulin release. |
| 212 | 11522661 | We have recently created HSL-deficient mice that were used to directly assess the role of HSL in insulin secretion and action. |
| 213 | 11522661 | Freshly isolated islets from HSL-deficient mice displayed elevated secretion at low (3 mmol/l) glucose, failed to release insulin in response to high (20 mmol/l) glucose, but had a normal secretion when challenged with elevated KCl. |
| 214 | 11522661 | The results demonstrate an important role of HSL and endogenous beta-cell lipolysis in the coupling mechanism of glucose-stimulated insulin secretion. |
| 215 | 11522661 | A role for hormone-sensitive lipase in glucose-stimulated insulin secretion: a study in hormone-sensitive lipase-deficient mice. |
| 216 | 11522661 | In addition, hormone-sensitive lipase (HSL) is expressed in beta-cells and may provide fatty acids necessary for the generation of coupling factors linking glucose metabolism to insulin release. |
| 217 | 11522661 | We have recently created HSL-deficient mice that were used to directly assess the role of HSL in insulin secretion and action. |
| 218 | 11522661 | Freshly isolated islets from HSL-deficient mice displayed elevated secretion at low (3 mmol/l) glucose, failed to release insulin in response to high (20 mmol/l) glucose, but had a normal secretion when challenged with elevated KCl. |
| 219 | 11522661 | The results demonstrate an important role of HSL and endogenous beta-cell lipolysis in the coupling mechanism of glucose-stimulated insulin secretion. |
| 220 | 11522674 | Because changes in the extracellular matrix (ECM) components are often associated with such cellular remodeling, we studied the adipocyte expression of the matrix metalloproteinases (MMPs) 2 and 9, two key enzymes involved in the modulation of ECM. |
| 221 | 11522674 | The present study provides the first evidence that human adipose tissue produces and secretes MMP-2 and -9 as shown by gelatin zymography analysis performed on media conditioned by human subcutaneous adipose tissue and human preadipocytes in primary cultures and by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis on transcripts from mature human adipocytes. |
| 222 | 11522674 | Finally, preadipocyte treatment with MMP inhibitors such as batimastat and captopril, as well as neutralizing antibodies, markedly decreased adipocyte differentiation as demonstrated by the inhibition in the appearance of lipogenic (triglycerides) and lipolytic (glycerol release and hormone-sensitive lipase expression) markers. |
| 223 | 11522674 | These data suggest that MMP-2 and -9 could be important key regulators of adipocyte differentiation. |
| 224 | 11574402 | Hormone-sensitive lipase (HSL) is expressed and enzymatically active in beta-cells and has been proposed to be involved in the generation of the lipid-derived signal that seems to be necessary for glucose-stimulated insulin secretion. |
| 225 | 11574402 | In this study, we investigated whether the expression of HSL in INS-1 cells and in rat islets is affected by exposure to high glucose concentrations. |
| 226 | 11574402 | Hormone-sensitive lipase (HSL) is expressed and enzymatically active in beta-cells and has been proposed to be involved in the generation of the lipid-derived signal that seems to be necessary for glucose-stimulated insulin secretion. |
| 227 | 11574402 | In this study, we investigated whether the expression of HSL in INS-1 cells and in rat islets is affected by exposure to high glucose concentrations. |
| 228 | 11574428 | A common hormone-sensitive lipase i6 gene polymorphism is associated with decreased human adipocyte lipolytic function. |
| 229 | 11574428 | The lipolysis rate induced by norepinephrine isoprenaline (acting on beta-adrenoceptors), forskolin (acting on adenylyl cyclase), and dibutyryl cyclic AMP (acting on HSL) were all decreased by approximately 50% in allele 5 homozygotes, as compared with noncarriers. |
| 230 | 11574428 | A common hormone-sensitive lipase i6 gene polymorphism is associated with decreased human adipocyte lipolytic function. |
| 231 | 11574428 | The lipolysis rate induced by norepinephrine isoprenaline (acting on beta-adrenoceptors), forskolin (acting on adenylyl cyclase), and dibutyryl cyclic AMP (acting on HSL) were all decreased by approximately 50% in allele 5 homozygotes, as compared with noncarriers. |
| 232 | 11731226 | Variation in the promoter of the human hormone sensitive lipase gene shows gender specific effects on insulin and lipid levels: results from the Ely study. |
| 233 | 11731226 | HSL is also expressed in pancreatic beta-cells where its activity therefore may affect insulin secretion. |
| 234 | 11731226 | In the women, carriers of the HSL -60G allele had significantly lower fasting insulin levels (P=0.0005) and a lower total area under the curve for insulin during the oral glucose tolerance test (P=0.005). |
| 235 | 11731226 | This study provides additional evidence for a role for HSL in the development of insulin resistance, from which carriers of the -60G allele, associated here with markers of insulin sensitivity in women, and with lower NEFA levels in men, might be protected. |
| 236 | 11731226 | Variation in the promoter of the human hormone sensitive lipase gene shows gender specific effects on insulin and lipid levels: results from the Ely study. |
| 237 | 11731226 | HSL is also expressed in pancreatic beta-cells where its activity therefore may affect insulin secretion. |
| 238 | 11731226 | In the women, carriers of the HSL -60G allele had significantly lower fasting insulin levels (P=0.0005) and a lower total area under the curve for insulin during the oral glucose tolerance test (P=0.005). |
| 239 | 11731226 | This study provides additional evidence for a role for HSL in the development of insulin resistance, from which carriers of the -60G allele, associated here with markers of insulin sensitivity in women, and with lower NEFA levels in men, might be protected. |
| 240 | 11731226 | Variation in the promoter of the human hormone sensitive lipase gene shows gender specific effects on insulin and lipid levels: results from the Ely study. |
| 241 | 11731226 | HSL is also expressed in pancreatic beta-cells where its activity therefore may affect insulin secretion. |
| 242 | 11731226 | In the women, carriers of the HSL -60G allele had significantly lower fasting insulin levels (P=0.0005) and a lower total area under the curve for insulin during the oral glucose tolerance test (P=0.005). |
| 243 | 11731226 | This study provides additional evidence for a role for HSL in the development of insulin resistance, from which carriers of the -60G allele, associated here with markers of insulin sensitivity in women, and with lower NEFA levels in men, might be protected. |
| 244 | 11731226 | Variation in the promoter of the human hormone sensitive lipase gene shows gender specific effects on insulin and lipid levels: results from the Ely study. |
| 245 | 11731226 | HSL is also expressed in pancreatic beta-cells where its activity therefore may affect insulin secretion. |
| 246 | 11731226 | In the women, carriers of the HSL -60G allele had significantly lower fasting insulin levels (P=0.0005) and a lower total area under the curve for insulin during the oral glucose tolerance test (P=0.005). |
| 247 | 11731226 | This study provides additional evidence for a role for HSL in the development of insulin resistance, from which carriers of the -60G allele, associated here with markers of insulin sensitivity in women, and with lower NEFA levels in men, might be protected. |
| 248 | 11812735 | Transcriptional regulation of adipocyte hormone-sensitive lipase by glucose. |
| 249 | 11812735 | Pools of stably transfected 3T3-F442A adipocytes were generated with human adipocyte HSL promoter fragments from -2,400/+38 to -31/+38 bp linked to the luciferase gene. |
| 250 | 11812735 | Electromobility shift assays showed that upstream stimulatory factor (USF)-1 and USF2 and Sp1 and Sp3 bound to a consensus E-box and two GC-boxes in the -137-bp region. |
| 251 | 11812735 | Cotransfection of the -137/+38 construct with USF1 and USF2 expression vectors produced enhanced luciferase activity. |
| 252 | 11812735 | Moreover, HSL mRNA levels were decreased in USF1- and USF2-deficient mice. |
| 253 | 11812735 | Transcriptional regulation of adipocyte hormone-sensitive lipase by glucose. |
| 254 | 11812735 | Pools of stably transfected 3T3-F442A adipocytes were generated with human adipocyte HSL promoter fragments from -2,400/+38 to -31/+38 bp linked to the luciferase gene. |
| 255 | 11812735 | Electromobility shift assays showed that upstream stimulatory factor (USF)-1 and USF2 and Sp1 and Sp3 bound to a consensus E-box and two GC-boxes in the -137-bp region. |
| 256 | 11812735 | Cotransfection of the -137/+38 construct with USF1 and USF2 expression vectors produced enhanced luciferase activity. |
| 257 | 11812735 | Moreover, HSL mRNA levels were decreased in USF1- and USF2-deficient mice. |
| 258 | 11812735 | Transcriptional regulation of adipocyte hormone-sensitive lipase by glucose. |
| 259 | 11812735 | Pools of stably transfected 3T3-F442A adipocytes were generated with human adipocyte HSL promoter fragments from -2,400/+38 to -31/+38 bp linked to the luciferase gene. |
| 260 | 11812735 | Electromobility shift assays showed that upstream stimulatory factor (USF)-1 and USF2 and Sp1 and Sp3 bound to a consensus E-box and two GC-boxes in the -137-bp region. |
| 261 | 11812735 | Cotransfection of the -137/+38 construct with USF1 and USF2 expression vectors produced enhanced luciferase activity. |
| 262 | 11812735 | Moreover, HSL mRNA levels were decreased in USF1- and USF2-deficient mice. |
| 263 | 11812759 | In vitro lipolysis regulation and stoichiometric properties of the final step in lipolysis activation, namely the protein kinase A (PKA)-hormone sensitive lipase (HSL) complex, were investigated in isolated visceral (i.e., omental) fat cells. |
| 264 | 11934676 | These results indicate that, under euglycemic conditions in the presence of low insulin levels, the reduction in FA disposal to oxidation and the decrease in HSL content may contribute to the accumulation of TG in muscle of old animals. |
| 265 | 11965829 | Candidate genes for the metabolic syndrome include those for the beta 3-adrenergic receptor, lipoprotein lipase, hormone sensitive lipase, peroxisome proliferator-activated receptor-gamma, insulin receptor substrate-1 and glycogen synthase. |
| 266 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 267 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 268 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 269 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 270 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 271 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 272 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 273 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 274 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 275 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 276 | 11978647 | Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. |
| 277 | 11978647 | In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 +/- 0.0 [mean +/- SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 +/- 0.13; 100 nmol/l insulin, 1.68 +/- 0.19; P < 0.001). |
| 278 | 11978647 | In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 +/- 0.05; P < 0.05), while no significant reduction was observed at other doses. |
| 279 | 11978647 | Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 +/- 0.07; P < 0.01) and LPL (control 1.00 +/- 0.0; 1,000 nmol/l insulin, 2.66 +/- 0.27; P < 0.01) protein expression. |
| 280 | 11978647 | Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). |
| 281 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 282 | 11978647 | In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. |
| 283 | 11978647 | Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. |
| 284 | 11978647 | In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 +/- 0.0 [mean +/- SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 +/- 0.13; 100 nmol/l insulin, 1.68 +/- 0.19; P < 0.001). |
| 285 | 11978647 | In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 +/- 0.05; P < 0.05), while no significant reduction was observed at other doses. |
| 286 | 11978647 | Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 +/- 0.07; P < 0.01) and LPL (control 1.00 +/- 0.0; 1,000 nmol/l insulin, 2.66 +/- 0.27; P < 0.01) protein expression. |
| 287 | 11978647 | Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). |
| 288 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 289 | 11978647 | In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. |
| 290 | 11978647 | Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. |
| 291 | 11978647 | In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 +/- 0.0 [mean +/- SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 +/- 0.13; 100 nmol/l insulin, 1.68 +/- 0.19; P < 0.001). |
| 292 | 11978647 | In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 +/- 0.05; P < 0.05), while no significant reduction was observed at other doses. |
| 293 | 11978647 | Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 +/- 0.07; P < 0.01) and LPL (control 1.00 +/- 0.0; 1,000 nmol/l insulin, 2.66 +/- 0.27; P < 0.01) protein expression. |
| 294 | 11978647 | Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). |
| 295 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 296 | 11978647 | In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. |
| 297 | 11978647 | Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. |
| 298 | 11978647 | In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 +/- 0.0 [mean +/- SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 +/- 0.13; 100 nmol/l insulin, 1.68 +/- 0.19; P < 0.001). |
| 299 | 11978647 | In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 +/- 0.05; P < 0.05), while no significant reduction was observed at other doses. |
| 300 | 11978647 | Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 +/- 0.07; P < 0.01) and LPL (control 1.00 +/- 0.0; 1,000 nmol/l insulin, 2.66 +/- 0.27; P < 0.01) protein expression. |
| 301 | 11978647 | Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). |
| 302 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 303 | 11978647 | In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. |
| 304 | 12047400 | The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue. |
| 305 | 12047400 | This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. |
| 306 | 12047400 | Relative protein expression of HSL, LPL and AR was determined. |
| 307 | 12047400 | In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). |
| 308 | 12047400 | These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. |
| 309 | 12047400 | The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue. |
| 310 | 12047400 | This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. |
| 311 | 12047400 | Relative protein expression of HSL, LPL and AR was determined. |
| 312 | 12047400 | In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). |
| 313 | 12047400 | These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. |
| 314 | 12047400 | The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue. |
| 315 | 12047400 | This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. |
| 316 | 12047400 | Relative protein expression of HSL, LPL and AR was determined. |
| 317 | 12047400 | In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). |
| 318 | 12047400 | These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. |
| 319 | 12047400 | The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue. |
| 320 | 12047400 | This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. |
| 321 | 12047400 | Relative protein expression of HSL, LPL and AR was determined. |
| 322 | 12047400 | In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). |
| 323 | 12047400 | These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. |
| 324 | 12047400 | The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue. |
| 325 | 12047400 | This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. |
| 326 | 12047400 | Relative protein expression of HSL, LPL and AR was determined. |
| 327 | 12047400 | In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). |
| 328 | 12047400 | These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. |
| 329 | 12097653 | Furthermore, SRHW inhibited porcine pancreatic lipase (PL), rat adipose tissue-derived lipoprotein lipase (LPL) and glycerophosphate dehydrogenase (GPDH) activities with 50% inhibitory concentrations (IC(50)) of 264 (95% confidence limits: 203-393) mg/L, 15 (12-18) mg/L and 54 (35-85) mg/L, respectively, but did not inhibit hormone-sensitive lipase activity in rat adipose tissue. |
| 330 | 12200416 | In the presence of high glucose, both insulin and leptin increased the rate of cholesterol ester synthesis, although they did not further increase uptake of acetylated low density lipoprotein. |
| 331 | 12200416 | However, in the presence of high glucose both insulin and leptin caused a significant increase in the activity of acyl-CoA: cholesterol O-acyltransferase (ACAT) combined with a significant reduction in the level of hormone-sensitive lipase (HSL). |
| 332 | 12200416 | Because ACAT is the main enzyme responsible for cholesterol ester synthesis and HSL contributes significantly to neutral cholesterol ester hydrolase activity, this suggests that glucose primes the J774.2 cells so that in the presence of high insulin or leptin they will store cholesterol esters. |
| 333 | 12200416 | This contrasts with 3T3-L1 adipocytes, where HSL activity and expression are increased by insulin in high glucose conditions. |
| 334 | 12200416 | In the presence of high glucose, both insulin and leptin increased the rate of cholesterol ester synthesis, although they did not further increase uptake of acetylated low density lipoprotein. |
| 335 | 12200416 | However, in the presence of high glucose both insulin and leptin caused a significant increase in the activity of acyl-CoA: cholesterol O-acyltransferase (ACAT) combined with a significant reduction in the level of hormone-sensitive lipase (HSL). |
| 336 | 12200416 | Because ACAT is the main enzyme responsible for cholesterol ester synthesis and HSL contributes significantly to neutral cholesterol ester hydrolase activity, this suggests that glucose primes the J774.2 cells so that in the presence of high insulin or leptin they will store cholesterol esters. |
| 337 | 12200416 | This contrasts with 3T3-L1 adipocytes, where HSL activity and expression are increased by insulin in high glucose conditions. |
| 338 | 12200416 | In the presence of high glucose, both insulin and leptin increased the rate of cholesterol ester synthesis, although they did not further increase uptake of acetylated low density lipoprotein. |
| 339 | 12200416 | However, in the presence of high glucose both insulin and leptin caused a significant increase in the activity of acyl-CoA: cholesterol O-acyltransferase (ACAT) combined with a significant reduction in the level of hormone-sensitive lipase (HSL). |
| 340 | 12200416 | Because ACAT is the main enzyme responsible for cholesterol ester synthesis and HSL contributes significantly to neutral cholesterol ester hydrolase activity, this suggests that glucose primes the J774.2 cells so that in the presence of high insulin or leptin they will store cholesterol esters. |
| 341 | 12200416 | This contrasts with 3T3-L1 adipocytes, where HSL activity and expression are increased by insulin in high glucose conditions. |
| 342 | 12204806 | In FCHL and DM2 in vivo insulin mediated muscle glucose uptake and inhibition of lipolysis were studied by euglycemic hyperinsulinemic clamp. |
| 343 | 12204806 | Insulin mediated glucose uptake was impaired to the same extent in both FCHL and DM2. |
| 344 | 12204806 | To analyze these possibilities in more detail, control, FCHL, and DM2 adipocytes were studied in vitro. |
| 345 | 12204806 | Genetic linkage analysis in 18 Dutch families with FCHL revealed no evidence for involvement of LIPE, the hormone sensitive lipase gene, indicating that genetic variation in adipocyte lipolysis by LIPE is not the key defect in FCHL. |
| 346 | 12364542 | This has led to important insights into its function, including the interaction of HSL with other intracellular proteins, such as adipocyte lipid binding protein. |
| 347 | 12364542 | Accumulating evidence has defined important functions for HSL in normal physiology, affecting adipocyte lipolysis, steroidogenesis, spermatogenesis, and perhaps insulin secretion and insulin action; however, direct links between abnormal expression or genetic variations of HSL and human disorders, such as obesity, insulin resistance, type 2 diabetes, and hyperlipidemia, await further clarification. |
| 348 | 12364542 | This has led to important insights into its function, including the interaction of HSL with other intracellular proteins, such as adipocyte lipid binding protein. |
| 349 | 12364542 | Accumulating evidence has defined important functions for HSL in normal physiology, affecting adipocyte lipolysis, steroidogenesis, spermatogenesis, and perhaps insulin secretion and insulin action; however, direct links between abnormal expression or genetic variations of HSL and human disorders, such as obesity, insulin resistance, type 2 diabetes, and hyperlipidemia, await further clarification. |
| 350 | 12453888 | Both isoproterenol (ISO) and tumor necrosis factor (TNF)-alpha stimulated the rate of lipolysis in HSL-/- MEF adipocytes, although to a lesser extent than in wild-type cells, and these lipolytic activities were inhibited by H-89, a cAMP-dependent protein kinase inhibitor, and troglitazone, respectively. |
| 351 | 12453888 | Thus, the responses of the residual lipolytic activity to lipolytic hormones and TNF-alpha were well conserved in the absence of HSL. |
| 352 | 12453888 | Both isoproterenol (ISO) and tumor necrosis factor (TNF)-alpha stimulated the rate of lipolysis in HSL-/- MEF adipocytes, although to a lesser extent than in wild-type cells, and these lipolytic activities were inhibited by H-89, a cAMP-dependent protein kinase inhibitor, and troglitazone, respectively. |
| 353 | 12453888 | Thus, the responses of the residual lipolytic activity to lipolytic hormones and TNF-alpha were well conserved in the absence of HSL. |
| 354 | 12514936 | Association of the hormone sensitive lipase -60C > G variant with fasting insulin levels in healthy young men. |
| 355 | 12765952 | These results suggest that the presence of the truncated HSL protein is associated with an impaired adipocyte lipolysis. |
| 356 | 12810697 | Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. |
| 357 | 12810697 | Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. |
| 358 | 12810697 | We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. |
| 359 | 12810697 | On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. |
| 360 | 12810697 | Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. |
| 361 | 12810697 | Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. |
| 362 | 12810697 | Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. |
| 363 | 12810697 | We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. |
| 364 | 12810697 | On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. |
| 365 | 12810697 | Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. |
| 366 | 12810697 | Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. |
| 367 | 12810697 | Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. |
| 368 | 12810697 | We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. |
| 369 | 12810697 | On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. |
| 370 | 12810697 | Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. |
| 371 | 12810697 | Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. |
| 372 | 12810697 | Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. |
| 373 | 12810697 | We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. |
| 374 | 12810697 | On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. |
| 375 | 12810697 | Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. |
| 376 | 12810697 | Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. |
| 377 | 12810697 | Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. |
| 378 | 12810697 | We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. |
| 379 | 12810697 | On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. |
| 380 | 12810697 | Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. |
| 381 | 13680127 | We present arguments in support of the following: (i) A source of fatty acid either exogenous or endogenous (derived by lipolysis of triglyceride) is necessary to support normal insulin secretion; (ii) a rapid increase of fatty acids potentiates glucose-stimulated secretion by increasing fatty acyl-CoA or complex lipid concentrations that act distally by modulating key enzymes such as protein kinase C or the exocytotic machinery; (iii) a chronic increase of fatty acids enhances basal secretion by the same mechanism, but promotes obesity and a diminished response to stimulatory glucose; (iv) agents which raise cAMP act as incretins, at least in part, by stimulating lipolysis via beta-cell hormone-sensitive lipase activation. |
| 382 | 14711311 | The central role of the intracellular enzyme hormone-sensitive lipase (HSL) in regulating fatty acid metabolism makes it an interesting pharmacological target for the treatment of insulin resistant and dyslipidemic disorders where a decrease in delivery of fatty acids to the circulation is desirable, e.g., in individuals with type 2 diabetes, metabolic syndrome, or impaired glucose tolerance. |
| 383 | 14711311 | These compounds do not inhibit other hydrolases such as hepatic lipase, lipoprotein lipase, pancreatic lipase, and butyrylcholine esterase. |
| 384 | 14725507 | Although described initially as an intracellular adipocyte-specific triacylglycerol lipase, it is now clear that HSL (hormone-sensitive lipase) is expressed in multiple tissues and plays a number of roles in lipid metabolism, including that of a neutral cholesteryl ester hydrolase. |
| 385 | 14984467 | Hormone-sensitive lipase (HSL) catalyzes the intracellular hydrolysis of triacylglycerols and cholesteryl esters, and it is involved in regulating body fat, steroidogenesis, and insulin secretion. |
| 386 | 14984467 | Conversely, female carriers of the LIPE 14672G allele had significantly higher TC (p = 0.047), LDLc (p = 0.041), and apoE (p = 0.041) levels. |
| 387 | 14984467 | Hormone-sensitive lipase (HSL) catalyzes the intracellular hydrolysis of triacylglycerols and cholesteryl esters, and it is involved in regulating body fat, steroidogenesis, and insulin secretion. |
| 388 | 14984467 | Conversely, female carriers of the LIPE 14672G allele had significantly higher TC (p = 0.047), LDLc (p = 0.041), and apoE (p = 0.041) levels. |
| 389 | 15220197 | Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. |
| 390 | 15220197 | We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro. |
| 391 | 15220197 | The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. |
| 392 | 15220197 | Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice. |
| 393 | 15220197 | GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. |
| 394 | 15220197 | Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. |
| 395 | 15220197 | We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro. |
| 396 | 15220197 | The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. |
| 397 | 15220197 | Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice. |
| 398 | 15220197 | GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. |
| 399 | 15220197 | Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. |
| 400 | 15220197 | We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro. |
| 401 | 15220197 | The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. |
| 402 | 15220197 | Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice. |
| 403 | 15220197 | GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. |
| 404 | 15220197 | Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. |
| 405 | 15220197 | We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro. |
| 406 | 15220197 | The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. |
| 407 | 15220197 | Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice. |
| 408 | 15220197 | GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. |
| 409 | 15220197 | Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. |
| 410 | 15220197 | We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro. |
| 411 | 15220197 | The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. |
| 412 | 15220197 | Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice. |
| 413 | 15220197 | GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. |
| 414 | 15331200 | Function of hormone-sensitive lipase in diacylglycerol-protein kinase C pathway. |
| 415 | 15331200 | To explore the functional effects of hormone-sensitive lipase (HSL) in diacylglycerol (DAG) metabolism, Chinese hamster ovary cells were stably transfected with rat HSL cDNA (wt-HSL), inactive mutant S423A-HSL cDNA (S423A) and pcDNA3 vector alone (Ct). [(14)C]Glucose-incorporation into triglyceride (TG) was 75% lower in the presence or absence of insulin in cells expressing wt-HSL compared to Ct or S423A. [(14)C]Glucose-incorporation into DAG was 33% lower without insulin and 51% lower with insulin in cells expressing wt-HSL compared to Ct or S423A. |
| 416 | 15331200 | These data show that HSL potentially hydrolyzes cellular DAG generated either by de novo synthesis from glucose or release from membrane phospholipids by phospholipase C, resulting in a reduction in the translocation of DAG-sensitive PKCs. |
| 417 | 15331200 | Function of hormone-sensitive lipase in diacylglycerol-protein kinase C pathway. |
| 418 | 15331200 | To explore the functional effects of hormone-sensitive lipase (HSL) in diacylglycerol (DAG) metabolism, Chinese hamster ovary cells were stably transfected with rat HSL cDNA (wt-HSL), inactive mutant S423A-HSL cDNA (S423A) and pcDNA3 vector alone (Ct). [(14)C]Glucose-incorporation into triglyceride (TG) was 75% lower in the presence or absence of insulin in cells expressing wt-HSL compared to Ct or S423A. [(14)C]Glucose-incorporation into DAG was 33% lower without insulin and 51% lower with insulin in cells expressing wt-HSL compared to Ct or S423A. |
| 419 | 15331200 | These data show that HSL potentially hydrolyzes cellular DAG generated either by de novo synthesis from glucose or release from membrane phospholipids by phospholipase C, resulting in a reduction in the translocation of DAG-sensitive PKCs. |
| 420 | 15331200 | Function of hormone-sensitive lipase in diacylglycerol-protein kinase C pathway. |
| 421 | 15331200 | To explore the functional effects of hormone-sensitive lipase (HSL) in diacylglycerol (DAG) metabolism, Chinese hamster ovary cells were stably transfected with rat HSL cDNA (wt-HSL), inactive mutant S423A-HSL cDNA (S423A) and pcDNA3 vector alone (Ct). [(14)C]Glucose-incorporation into triglyceride (TG) was 75% lower in the presence or absence of insulin in cells expressing wt-HSL compared to Ct or S423A. [(14)C]Glucose-incorporation into DAG was 33% lower without insulin and 51% lower with insulin in cells expressing wt-HSL compared to Ct or S423A. |
| 422 | 15331200 | These data show that HSL potentially hydrolyzes cellular DAG generated either by de novo synthesis from glucose or release from membrane phospholipids by phospholipase C, resulting in a reduction in the translocation of DAG-sensitive PKCs. |
| 423 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 424 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 425 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 426 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 427 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 428 | 15525599 | Transcripts involved in energy metabolism, such as glyceraldehyde-3-phosphate dehydrogenase, malic enzyme supernatant, fatty acid synthase, lipoprotein lipase, hormone-sensitive lipase and monoglyceride lipase, were upregulated by DHT. |
| 429 | 15525599 | Transcripts involved in adipogenesis, and cell cycle and cell shape organization, such as DDX5, C/EBPalpha, cyclin I, procollagen types I, III, IV, V and VI, SPARC and matrix metalloproteinase 2, were upregulated by DHT. |
| 430 | 15525872 | The release of glycerol and free fatty acids from human adipose tissue is mainly dependent on hormone-sensitive lipase which is intensively regulated by hormones and agents, such as insulin (inhibition of lipolysis) and catecholamines (stimulation of lipolysis). |
| 431 | 15525872 | Released into circulation as non-esterified fatty acids by lipoprotein lipase, those are taken up by adipose tissue via specific plasma fatty acid transporters (CD36, FATP, FABPpm) and used for triacylglycerol synthesis. |
| 432 | 15545214 | The central role of perilipin a in lipid metabolism and adipocyte lipolysis. |
| 433 | 15545214 | Work in recent years has revealed that both hormone-sensitive lipase (HSL), generally thought to be the rate-limiting enzyme, and perilipin, a lipid droplet surface protein, are required for optimal lipid storage and fatty acid release. |
| 434 | 15545214 | The perilipin proteins are polyphosphorylated by protein kinase A and phosphorylation is necessary for translocation of HSL to the lipid droplet and enhanced lipolysis. |
| 435 | 15545214 | The central role of perilipin a in lipid metabolism and adipocyte lipolysis. |
| 436 | 15545214 | Work in recent years has revealed that both hormone-sensitive lipase (HSL), generally thought to be the rate-limiting enzyme, and perilipin, a lipid droplet surface protein, are required for optimal lipid storage and fatty acid release. |
| 437 | 15545214 | The perilipin proteins are polyphosphorylated by protein kinase A and phosphorylation is necessary for translocation of HSL to the lipid droplet and enhanced lipolysis. |
| 438 | 15609025 | Hormone-sensitive lipase is reduced in the adipose tissue of patients with type 2 diabetes mellitus: influence of IL-6 infusion. |
| 439 | 15655711 | A role for glucagon-like peptide 1 (GLP-1) has been suggested in stimulating beta-cell lipolysis via elevation of cAMP and activation of protein kinase A, which in turn may activate hormone-sensitive lipase (HSL), thereby contributing to fatty acid generation (FFA) from intracellular triglyceride stores. |
| 440 | 15655711 | Since HSL is expressed in islet beta-cells, this effect could contribute to the stimulation of insulin secretion by GLP-1, provided that a lipid signal of importance for insulin secretion is generated. |
| 441 | 15655711 | To examine this hypothesis, we have studied the acute effect of GLP-1 on isolated mouse islets from normal mice and from mice with high-fat diet induced insulin resistance. |
| 442 | 15655711 | We found, however, that although GLP-1 (100 nM) markedly potentiated glucose-stimulated insulin secretion from islets of both feeding groups, the peptide was not able to stimulate islet palmitate oxidation or increase lipolysis measured as glycerol release. |
| 443 | 15655711 | This indicates that a lipid signal does not contribute to the acute stimulation of insulin secretion by GLP-1. |
| 444 | 15655711 | To test whether lipolysis might be involved in the islet effects of long-term GLP-1 action, mice from the two feeding groups were chronically treated with exendin-4, a peptide that lowers blood glucose by interacting with GLP-1 receptors, in order to stimulate insulin secretion, for 16 days before isolation of the islets. |
| 445 | 15655711 | A role for glucagon-like peptide 1 (GLP-1) has been suggested in stimulating beta-cell lipolysis via elevation of cAMP and activation of protein kinase A, which in turn may activate hormone-sensitive lipase (HSL), thereby contributing to fatty acid generation (FFA) from intracellular triglyceride stores. |
| 446 | 15655711 | Since HSL is expressed in islet beta-cells, this effect could contribute to the stimulation of insulin secretion by GLP-1, provided that a lipid signal of importance for insulin secretion is generated. |
| 447 | 15655711 | To examine this hypothesis, we have studied the acute effect of GLP-1 on isolated mouse islets from normal mice and from mice with high-fat diet induced insulin resistance. |
| 448 | 15655711 | We found, however, that although GLP-1 (100 nM) markedly potentiated glucose-stimulated insulin secretion from islets of both feeding groups, the peptide was not able to stimulate islet palmitate oxidation or increase lipolysis measured as glycerol release. |
| 449 | 15655711 | This indicates that a lipid signal does not contribute to the acute stimulation of insulin secretion by GLP-1. |
| 450 | 15655711 | To test whether lipolysis might be involved in the islet effects of long-term GLP-1 action, mice from the two feeding groups were chronically treated with exendin-4, a peptide that lowers blood glucose by interacting with GLP-1 receptors, in order to stimulate insulin secretion, for 16 days before isolation of the islets. |
| 451 | 15701680 | Hormone-sensitive lipase knockout mice have increased hepatic insulin sensitivity and are protected from short-term diet-induced insulin resistance in skeletal muscle and heart. |
| 452 | 15701680 | To determine the metabolic role of HSL, we examined the changes in tissue-specific insulin action and glucose metabolism in vivo during hyperinsulinemic euglycemic clamps after 3 wk of high-fat or normal chow diet in awake, HSL-deficient (HSL-KO) mice. |
| 453 | 15701680 | Hormone-sensitive lipase knockout mice have increased hepatic insulin sensitivity and are protected from short-term diet-induced insulin resistance in skeletal muscle and heart. |
| 454 | 15701680 | To determine the metabolic role of HSL, we examined the changes in tissue-specific insulin action and glucose metabolism in vivo during hyperinsulinemic euglycemic clamps after 3 wk of high-fat or normal chow diet in awake, HSL-deficient (HSL-KO) mice. |
| 455 | 15713705 | Colectomized subjects exhibited lower insulin sensitivity (homeostatic model assessment model, 33% reduction, P = 0.03; minimal model, 29% reduction, P = 0.05), elevated aldosterone (9-fold, P = 0.003), leptin (2.2-fold, P = 0.03), and an increased rate of nonesterified fatty acid and glycerol release from adipose tissue (P = 0.02) especially in the late postprandial period. |
| 456 | 15713705 | The uptake of fatty acids into muscle was also significantly increased (P = 0.007), as were muscle CD36 and LPL mRNA expression compared with controls. |
| 457 | 15713705 | In adipose tissue, hormone-sensitive lipase mRNA expression was increased (P = 0.015), whereas peroxisome proliferator-activated receptor-gamma expression was decreased (P = 0.02), as was that of CD36 (P = 0.001). |
| 458 | 15887043 | Rosiglitazone up-regulates lipoprotein lipase, hormone-sensitive lipase and uncoupling protein-1, and down-regulates insulin-induced fatty acid synthase gene expression in brown adipocytes of Wistar rats. |
| 459 | 15961788 | Gene-targeted HSL-deficient (HSL-/-) mice with no detectable HSL peptide or activity (measured as cholesteryl esterase) have WAT abnormalities, including low mass, marked heterogeneity of cell diameter, increased diacylglycerol content, and low beta-adrenergic stimulation of adipocyte lipolysis. |
| 460 | 16123323 | Atrial natriuretic peptide increases the intracellular 3', 5'-cyclic guanosine monophosphate (cGMP) concentration which activates cGMP-dependent protein kinase leading to perilipin and hormone-sensitive lipase phosphorylation and lipolysis. |
| 461 | 16162821 | Hormone-sensitive lipase (HSL) is a critical enzyme involved in the hormonally regulated release of fatty acids and glycerol from adipocyte lipid stores, and its inhibition may thus improve insulin sensitivity and blood glucose handling in type 2 diabetes. |
| 462 | 16177793 | Insulin disrupts beta-adrenergic signalling to protein kinase A in adipocytes. |
| 463 | 16177793 | In adipocytes, stimulation of beta-adrenergic receptors increases cyclic AMP levels and activates protein kinase A (PKA), which stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin. |
| 464 | 16177793 | Acute insulin treatment activates phosphodiesterase 3B, reduces cAMP levels and quenches beta-adrenergic receptor signalling. |
| 465 | 16249444 | The mobilization of fat stored in adipose tissue is mediated by hormone-sensitive lipase (HSL) and the recently characterized adipose triglyceride lipase (ATGL), yet their relative importance in lipolysis is unknown. |
| 466 | 16249444 | HSL and ATGL mRNA levels increased concomitantly during adipocyte differentiation. |
| 467 | 16249444 | In conclusion, HSL is the major lipase for catecholamine- and natriuretic peptide-stimulated lipolysis, whereas ATGL mediates the hydrolysis of triglycerides during basal lipolysis. |
| 468 | 16249444 | The mobilization of fat stored in adipose tissue is mediated by hormone-sensitive lipase (HSL) and the recently characterized adipose triglyceride lipase (ATGL), yet their relative importance in lipolysis is unknown. |
| 469 | 16249444 | HSL and ATGL mRNA levels increased concomitantly during adipocyte differentiation. |
| 470 | 16249444 | In conclusion, HSL is the major lipase for catecholamine- and natriuretic peptide-stimulated lipolysis, whereas ATGL mediates the hydrolysis of triglycerides during basal lipolysis. |
| 471 | 16249444 | The mobilization of fat stored in adipose tissue is mediated by hormone-sensitive lipase (HSL) and the recently characterized adipose triglyceride lipase (ATGL), yet their relative importance in lipolysis is unknown. |
| 472 | 16249444 | HSL and ATGL mRNA levels increased concomitantly during adipocyte differentiation. |
| 473 | 16249444 | In conclusion, HSL is the major lipase for catecholamine- and natriuretic peptide-stimulated lipolysis, whereas ATGL mediates the hydrolysis of triglycerides during basal lipolysis. |
| 474 | 16269451 | Peroxisome proliferator-activated receptor-gamma transcriptionally up-regulates hormone-sensitive lipase via the involvement of specificity protein-1. |
| 475 | 16269451 | Both peroxisome proliferator-activated receptor (PPAR)-gamma and hormone-sensitive lipase (HSL) play important roles in lipid metabolism and insulin sensitivity. |
| 476 | 16269451 | We demonstrate that expression of the HSL gene is up-regulated by PPARgamma and PPARgamma agonists (rosiglitazone and pioglitazone) in the cultured hepatic cells and differentiating preadipocytes. |
| 477 | 16269451 | This important promoter region contains two GC-boxes and binds the transcription factor specificity protein-1 (Sp1) but not PPARgamma. |
| 478 | 16269451 | The Sp1-promoter binding activity can be endogenously enhanced by PPARgamma and rosiglitazone, as demonstrated by analysis of EMSA and chromatin immunoprecipitation assay. |
| 479 | 16269451 | Mutations in the GC-box sequences reduce the promoter binding activity of Sp1 and the transactivating activity of PPARgamma. |
| 480 | 16269451 | These results indicate that PPARgamma positively regulates the HSL gene expression, and up-regulation of HSL by PPARgamma requires the involvement of Sp1. |
| 481 | 16269451 | Taken together, this study suggests that HSL may be a newly identified PPARgamma target gene, and up-regulation of HSL may be an important mechanism involved in action of PPARgamma agonists in type 2 diabetes. |
| 482 | 16269451 | Peroxisome proliferator-activated receptor-gamma transcriptionally up-regulates hormone-sensitive lipase via the involvement of specificity protein-1. |
| 483 | 16269451 | Both peroxisome proliferator-activated receptor (PPAR)-gamma and hormone-sensitive lipase (HSL) play important roles in lipid metabolism and insulin sensitivity. |
| 484 | 16269451 | We demonstrate that expression of the HSL gene is up-regulated by PPARgamma and PPARgamma agonists (rosiglitazone and pioglitazone) in the cultured hepatic cells and differentiating preadipocytes. |
| 485 | 16269451 | This important promoter region contains two GC-boxes and binds the transcription factor specificity protein-1 (Sp1) but not PPARgamma. |
| 486 | 16269451 | The Sp1-promoter binding activity can be endogenously enhanced by PPARgamma and rosiglitazone, as demonstrated by analysis of EMSA and chromatin immunoprecipitation assay. |
| 487 | 16269451 | Mutations in the GC-box sequences reduce the promoter binding activity of Sp1 and the transactivating activity of PPARgamma. |
| 488 | 16269451 | These results indicate that PPARgamma positively regulates the HSL gene expression, and up-regulation of HSL by PPARgamma requires the involvement of Sp1. |
| 489 | 16269451 | Taken together, this study suggests that HSL may be a newly identified PPARgamma target gene, and up-regulation of HSL may be an important mechanism involved in action of PPARgamma agonists in type 2 diabetes. |
| 490 | 16269451 | Peroxisome proliferator-activated receptor-gamma transcriptionally up-regulates hormone-sensitive lipase via the involvement of specificity protein-1. |
| 491 | 16269451 | Both peroxisome proliferator-activated receptor (PPAR)-gamma and hormone-sensitive lipase (HSL) play important roles in lipid metabolism and insulin sensitivity. |
| 492 | 16269451 | We demonstrate that expression of the HSL gene is up-regulated by PPARgamma and PPARgamma agonists (rosiglitazone and pioglitazone) in the cultured hepatic cells and differentiating preadipocytes. |
| 493 | 16269451 | This important promoter region contains two GC-boxes and binds the transcription factor specificity protein-1 (Sp1) but not PPARgamma. |
| 494 | 16269451 | The Sp1-promoter binding activity can be endogenously enhanced by PPARgamma and rosiglitazone, as demonstrated by analysis of EMSA and chromatin immunoprecipitation assay. |
| 495 | 16269451 | Mutations in the GC-box sequences reduce the promoter binding activity of Sp1 and the transactivating activity of PPARgamma. |
| 496 | 16269451 | These results indicate that PPARgamma positively regulates the HSL gene expression, and up-regulation of HSL by PPARgamma requires the involvement of Sp1. |
| 497 | 16269451 | Taken together, this study suggests that HSL may be a newly identified PPARgamma target gene, and up-regulation of HSL may be an important mechanism involved in action of PPARgamma agonists in type 2 diabetes. |
| 498 | 16269451 | Peroxisome proliferator-activated receptor-gamma transcriptionally up-regulates hormone-sensitive lipase via the involvement of specificity protein-1. |
| 499 | 16269451 | Both peroxisome proliferator-activated receptor (PPAR)-gamma and hormone-sensitive lipase (HSL) play important roles in lipid metabolism and insulin sensitivity. |
| 500 | 16269451 | We demonstrate that expression of the HSL gene is up-regulated by PPARgamma and PPARgamma agonists (rosiglitazone and pioglitazone) in the cultured hepatic cells and differentiating preadipocytes. |
| 501 | 16269451 | This important promoter region contains two GC-boxes and binds the transcription factor specificity protein-1 (Sp1) but not PPARgamma. |
| 502 | 16269451 | The Sp1-promoter binding activity can be endogenously enhanced by PPARgamma and rosiglitazone, as demonstrated by analysis of EMSA and chromatin immunoprecipitation assay. |
| 503 | 16269451 | Mutations in the GC-box sequences reduce the promoter binding activity of Sp1 and the transactivating activity of PPARgamma. |
| 504 | 16269451 | These results indicate that PPARgamma positively regulates the HSL gene expression, and up-regulation of HSL by PPARgamma requires the involvement of Sp1. |
| 505 | 16269451 | Taken together, this study suggests that HSL may be a newly identified PPARgamma target gene, and up-regulation of HSL may be an important mechanism involved in action of PPARgamma agonists in type 2 diabetes. |
| 506 | 16269451 | Peroxisome proliferator-activated receptor-gamma transcriptionally up-regulates hormone-sensitive lipase via the involvement of specificity protein-1. |
| 507 | 16269451 | Both peroxisome proliferator-activated receptor (PPAR)-gamma and hormone-sensitive lipase (HSL) play important roles in lipid metabolism and insulin sensitivity. |
| 508 | 16269451 | We demonstrate that expression of the HSL gene is up-regulated by PPARgamma and PPARgamma agonists (rosiglitazone and pioglitazone) in the cultured hepatic cells and differentiating preadipocytes. |
| 509 | 16269451 | This important promoter region contains two GC-boxes and binds the transcription factor specificity protein-1 (Sp1) but not PPARgamma. |
| 510 | 16269451 | The Sp1-promoter binding activity can be endogenously enhanced by PPARgamma and rosiglitazone, as demonstrated by analysis of EMSA and chromatin immunoprecipitation assay. |
| 511 | 16269451 | Mutations in the GC-box sequences reduce the promoter binding activity of Sp1 and the transactivating activity of PPARgamma. |
| 512 | 16269451 | These results indicate that PPARgamma positively regulates the HSL gene expression, and up-regulation of HSL by PPARgamma requires the involvement of Sp1. |
| 513 | 16269451 | Taken together, this study suggests that HSL may be a newly identified PPARgamma target gene, and up-regulation of HSL may be an important mechanism involved in action of PPARgamma agonists in type 2 diabetes. |
| 514 | 16534522 | The hormone-sensitive lipase C-60G promoter polymorphism is associated with increased waist circumference in normal-weight subjects. |
| 515 | 16704309 | When in complex with fatty acids, FABP4 interacts with and modulates the activity of two important regulators of metabolism: hormone-sensitive lipase and peroxisome proliferator-activated receptor gamma. |
| 516 | 16704309 | Recombinant glutathione S-transferase (GST)-FABP4 or His-FABP4 was expressed in bacteria, affinity purified, and used for immunization of mice, enzyme-linked immunosorbent assay (ELISA) screening, and characterization of selected clones. |
| 517 | 16765472 | Recent findings suggest that HSL could be involved in the regulation of glucose stimulated insulin secretion (GSIS), however, these findings are controversial. |
| 518 | 16765472 | To test the hypothesis that HSL is involved in control of normal GSIS via changes in its expression and/or activity in response to stimuli, we examined the effects of free fatty acid (FFA) loading and glucagon like peptide-1 (GLP-1) stimulation on the regulation of HSL expression and activity. |
| 519 | 16765472 | Short-term treatment with GLP-1 increased HSL activity without changing the expression of the beta-cell isoform of HSL. |
| 520 | 16765472 | Basal insulin secretion was increased, whereas GLP-1 potentiation of GSIS was decreased in islets isolated from HSL-/- mice, as compared to islets from wild type mice. |
| 521 | 16765472 | Quantitative PCR for selected genes also revealed changes in genes that are related to insulin secretion, such as UCP-2. |
| 522 | 16765472 | Recent findings suggest that HSL could be involved in the regulation of glucose stimulated insulin secretion (GSIS), however, these findings are controversial. |
| 523 | 16765472 | To test the hypothesis that HSL is involved in control of normal GSIS via changes in its expression and/or activity in response to stimuli, we examined the effects of free fatty acid (FFA) loading and glucagon like peptide-1 (GLP-1) stimulation on the regulation of HSL expression and activity. |
| 524 | 16765472 | Short-term treatment with GLP-1 increased HSL activity without changing the expression of the beta-cell isoform of HSL. |
| 525 | 16765472 | Basal insulin secretion was increased, whereas GLP-1 potentiation of GSIS was decreased in islets isolated from HSL-/- mice, as compared to islets from wild type mice. |
| 526 | 16765472 | Quantitative PCR for selected genes also revealed changes in genes that are related to insulin secretion, such as UCP-2. |
| 527 | 16765472 | Recent findings suggest that HSL could be involved in the regulation of glucose stimulated insulin secretion (GSIS), however, these findings are controversial. |
| 528 | 16765472 | To test the hypothesis that HSL is involved in control of normal GSIS via changes in its expression and/or activity in response to stimuli, we examined the effects of free fatty acid (FFA) loading and glucagon like peptide-1 (GLP-1) stimulation on the regulation of HSL expression and activity. |
| 529 | 16765472 | Short-term treatment with GLP-1 increased HSL activity without changing the expression of the beta-cell isoform of HSL. |
| 530 | 16765472 | Basal insulin secretion was increased, whereas GLP-1 potentiation of GSIS was decreased in islets isolated from HSL-/- mice, as compared to islets from wild type mice. |
| 531 | 16765472 | Quantitative PCR for selected genes also revealed changes in genes that are related to insulin secretion, such as UCP-2. |
| 532 | 16765472 | Recent findings suggest that HSL could be involved in the regulation of glucose stimulated insulin secretion (GSIS), however, these findings are controversial. |
| 533 | 16765472 | To test the hypothesis that HSL is involved in control of normal GSIS via changes in its expression and/or activity in response to stimuli, we examined the effects of free fatty acid (FFA) loading and glucagon like peptide-1 (GLP-1) stimulation on the regulation of HSL expression and activity. |
| 534 | 16765472 | Short-term treatment with GLP-1 increased HSL activity without changing the expression of the beta-cell isoform of HSL. |
| 535 | 16765472 | Basal insulin secretion was increased, whereas GLP-1 potentiation of GSIS was decreased in islets isolated from HSL-/- mice, as compared to islets from wild type mice. |
| 536 | 16765472 | Quantitative PCR for selected genes also revealed changes in genes that are related to insulin secretion, such as UCP-2. |
| 537 | 16803459 | These caveolae contained caveolin-1 and caveolin-2. |
| 538 | 16803459 | Another class of high-density caveolae contained caveolin-1, caveolin-2 and specifically fatty acid transport protein-1, fatty acid transport protein-4, fatty acyl-CoA synthetase, hormone-sensitive lipase, perilipin, and insulin-regulated glucose transporter-4. |
| 539 | 16803459 | A third class of low-density caveolae contained the insulin receptor, class B scavenger receptor-1, and insulin-regulated glucose transporter-4. |
| 540 | 16803459 | In response to insulin, the insulin receptor autophosphorylation and the amount of insulin-regulated glucose transporter-4 increased in these caveolae. |
| 541 | 16940551 | The placental triglyceride (TG) concentration and mRNA expression of endothelial lipase (EL) and hormone-sensitive lipase (HSL) were increased in placentas from women with diabetes. |
| 542 | 17009729 | Upon activation of protein kinase A (PKA), two proteins, hormone-sensitive lipase (HSL) and perilipins, are phosphorylated. |
| 543 | 17009729 | The phosphorylated perilipin is required for inducing the translocation of HSL from the cytosol to the lipid droplets of adipocytes and is essential for the initiation of lipolytic reaction. |
| 544 | 17009729 | It is proposed that phosphorylation of perilipin is a key step for the activation of lipolytic cascade via PKA and ERK signaling pathways. |
| 545 | 17009729 | Upon activation of protein kinase A (PKA), two proteins, hormone-sensitive lipase (HSL) and perilipins, are phosphorylated. |
| 546 | 17009729 | The phosphorylated perilipin is required for inducing the translocation of HSL from the cytosol to the lipid droplets of adipocytes and is essential for the initiation of lipolytic reaction. |
| 547 | 17009729 | It is proposed that phosphorylation of perilipin is a key step for the activation of lipolytic cascade via PKA and ERK signaling pathways. |
| 548 | 17026959 | Association and insulin regulated translocation of hormone-sensitive lipase with PTRF. |
| 549 | 17026959 | This localization was under control of insulin, which translocated PTRF to the cytosol and nucleus, indicating a novel role for PTRF in insulin transcriptional control. |
| 550 | 17026959 | In the plasma membrane PTRF was specifically bound to a triacylglycerol-metabolizing subclass of caveolae containing hormone-sensitive lipase (HSL). |
| 551 | 17026959 | In response to insulin PTRF was translocated to the cytosol in parallel with HSL. |
| 552 | 17026959 | PTRF and HSL were quantitatively immunoprecipitated from the cytosol by antibodies against either PTRF or HSL. |
| 553 | 17026959 | Association and insulin regulated translocation of hormone-sensitive lipase with PTRF. |
| 554 | 17026959 | This localization was under control of insulin, which translocated PTRF to the cytosol and nucleus, indicating a novel role for PTRF in insulin transcriptional control. |
| 555 | 17026959 | In the plasma membrane PTRF was specifically bound to a triacylglycerol-metabolizing subclass of caveolae containing hormone-sensitive lipase (HSL). |
| 556 | 17026959 | In response to insulin PTRF was translocated to the cytosol in parallel with HSL. |
| 557 | 17026959 | PTRF and HSL were quantitatively immunoprecipitated from the cytosol by antibodies against either PTRF or HSL. |
| 558 | 17026959 | Association and insulin regulated translocation of hormone-sensitive lipase with PTRF. |
| 559 | 17026959 | This localization was under control of insulin, which translocated PTRF to the cytosol and nucleus, indicating a novel role for PTRF in insulin transcriptional control. |
| 560 | 17026959 | In the plasma membrane PTRF was specifically bound to a triacylglycerol-metabolizing subclass of caveolae containing hormone-sensitive lipase (HSL). |
| 561 | 17026959 | In response to insulin PTRF was translocated to the cytosol in parallel with HSL. |
| 562 | 17026959 | PTRF and HSL were quantitatively immunoprecipitated from the cytosol by antibodies against either PTRF or HSL. |
| 563 | 17026959 | Association and insulin regulated translocation of hormone-sensitive lipase with PTRF. |
| 564 | 17026959 | This localization was under control of insulin, which translocated PTRF to the cytosol and nucleus, indicating a novel role for PTRF in insulin transcriptional control. |
| 565 | 17026959 | In the plasma membrane PTRF was specifically bound to a triacylglycerol-metabolizing subclass of caveolae containing hormone-sensitive lipase (HSL). |
| 566 | 17026959 | In response to insulin PTRF was translocated to the cytosol in parallel with HSL. |
| 567 | 17026959 | PTRF and HSL were quantitatively immunoprecipitated from the cytosol by antibodies against either PTRF or HSL. |
| 568 | 17823267 | Central leptin administration down-regulates delta-6-desaturase expression in liver and adipose tissue, in parallel with the decrease of the expression of sterol regulatory element binding protein-1c in liver and peroxisome proliferator activated receptor alpha in adipose tissue. |
| 569 | 17823267 | Finally, leptin treatment, by regulating adipose triglyceride lipase/hormone sensitive lipase/diacylglycerol transferase 1 expression, also established a new partitioning in the FA-triacylglyceride cycling in adipose tissue, increasing lipolysis and probably the FA efflux from this tissue, and favoring in parallel the FA uptake and oxidation in the liver. |
| 570 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 571 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 572 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 573 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 574 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 575 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 576 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 577 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 578 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 579 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 580 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 581 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 582 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 583 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 584 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 585 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 586 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 587 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 588 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 589 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 590 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 591 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 592 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 593 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 594 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 595 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 596 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 597 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 598 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 599 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 600 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 601 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 602 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 603 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 604 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 605 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 606 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 607 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 608 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 609 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 610 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 611 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 612 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 613 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 614 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 615 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 616 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 617 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 618 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 619 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 620 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 621 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 622 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 623 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 624 | 18072017 | Variation in the expression of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been reported. |
| 625 | 18072017 | We therefore hypothesized that expression of adipose triglyceride lipase (ATGL) is different in visceral and SC depot and investigated whether ATGL mRNA expression is related to obesity, fat distribution and insulin sensitivity. |
| 626 | 18072017 | ATGL, LPL, and HSL mRNA expression was measured in 85 paired samples of omental and subcutaneous adipose tissue in normal glucose tolerant lean and obese individuals. |
| 627 | 18072017 | ATGL mRNA levels are significantly decreased in insulin resistant obese subjects. |
| 628 | 18072017 | Independently of body fat mass, omental ATGL mRNA correlates with fasting insulin concentration, glucose uptake during the steady state of the clamp and HSL mRNA expression. |
| 629 | 18072017 | In obese, but not in lean subjects, LPL and HSL mRNA expression was significantly higher in omental compared to SC fat. |
| 630 | 18072017 | Visceral HSL mRNA expression is closely related to adipocyte size and fasting plasma insulin concentrations, whereas visceral fat area significantly predicts visceral LPL mRNA expression. |
| 631 | 18072017 | HSL, but not ATGL mRNA expression is closely related to individual and regional differences in adipocyte size. |
| 632 | 18072017 | Impaired insulin sensitivity was associated with decreased ATGL and HSL mRNA expression, independently of body fat mass and fat distribution. |
| 633 | 18262211 | There is evidence of both HSL and ATGL activity and/or expression in skeletal muscle. |
| 634 | 18262211 | It is tempting to speculate that an imbalance between ATGL and HSL expression results in incomplete lipolysis and increased accumulation of lipid intermediates in skeletal muscle of obese insulin resistant subjects. |
| 635 | 18262211 | There is evidence of both HSL and ATGL activity and/or expression in skeletal muscle. |
| 636 | 18262211 | It is tempting to speculate that an imbalance between ATGL and HSL expression results in incomplete lipolysis and increased accumulation of lipid intermediates in skeletal muscle of obese insulin resistant subjects. |
| 637 | 18357681 | [Adipose triglyceride lipase regulates adipocyte lipolysis]. |
| 638 | 18357681 | Hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) are two major enzymes in the control of triacylglycerol hydrolysis in adipose tissue. |
| 639 | 18357681 | ATGL expressed predominantly in white adipose tissue specifically initiates triacylglycerol hydrolysis to generate diacylglycerols and FFA, a role distinguished from HSL that mainly hydrolyzes diacylglycerols. |
| 640 | 18357681 | ATGL activity is regulated by CGI-58. |
| 641 | 18357681 | Under basal conditions, interaction of CGI-58 with a lipid droplet associating protein, perilipin, results in an inactivation of ATGL activity. |
| 642 | 18357681 | During PKA-stimulated lipolysis, CGI-58 is released from phosphorylated perilipin and in turn, binds to ATGL. |
| 643 | 18357681 | [Adipose triglyceride lipase regulates adipocyte lipolysis]. |
| 644 | 18357681 | Hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) are two major enzymes in the control of triacylglycerol hydrolysis in adipose tissue. |
| 645 | 18357681 | ATGL expressed predominantly in white adipose tissue specifically initiates triacylglycerol hydrolysis to generate diacylglycerols and FFA, a role distinguished from HSL that mainly hydrolyzes diacylglycerols. |
| 646 | 18357681 | ATGL activity is regulated by CGI-58. |
| 647 | 18357681 | Under basal conditions, interaction of CGI-58 with a lipid droplet associating protein, perilipin, results in an inactivation of ATGL activity. |
| 648 | 18357681 | During PKA-stimulated lipolysis, CGI-58 is released from phosphorylated perilipin and in turn, binds to ATGL. |
| 649 | 18511057 | To determine if adiponectin can modulate lipid metabolism in macrophages, we expressed the adiponectin gene in human THP-1 macrophage foam cells using a lentiviral vector expression system and demonstrated that macrophages transduced with the adiponectin gene had decreased lipid accumulation compared with control macrophages transduced with the LacZ gene. |
| 650 | 18511057 | The second mechanism involves decreased lipid uptake and increased lipid hydrolysis which may result from decreased SR-AI and increased SR-BI and HSL gene activities in the transformed macrophage foam cells. |
| 651 | 18511057 | We also demonstrated that the expression of two proatherogenic cytokines, MCP-1 and TNFalpha, were decreased in the adiponectin-transduced macrophage foam cells. |
| 652 | 18804448 | Lack of cholesterol mobilization in islets of hormone-sensitive lipase deficient mice impairs insulin secretion. |
| 653 | 18804448 | The observations that hormone-sensitive lipase (HSL) is located in close association to insulin granules in beta-cells and that cholesterol ester hydrolase activity is completely blunted in islets of HSL null mice made us hypothesize that the role of HSL in beta-cells is to provide cholesterol for the exocytosis of insulin. |
| 654 | 18804448 | A significant reduction in insulin secretion from HSL null islets was observed whereas wt islets were unaffected. |
| 655 | 18804448 | Using synaptosomal protein of 25 kDa (SNAP-25) as indicator of cholesterol-rich microdomains, confocal microscopy was used to show that HSL null beta-cells treated with mbetacd contained fewer clusters than wt beta-cells. |
| 656 | 18804448 | These results indicate that HSL plays an important role in insulin secretion by providing free cholesterol for the formation and maintenance of cholesterol-rich patches for docking of SNARE-proteins to the plasma membrane. |
| 657 | 18804448 | Lack of cholesterol mobilization in islets of hormone-sensitive lipase deficient mice impairs insulin secretion. |
| 658 | 18804448 | The observations that hormone-sensitive lipase (HSL) is located in close association to insulin granules in beta-cells and that cholesterol ester hydrolase activity is completely blunted in islets of HSL null mice made us hypothesize that the role of HSL in beta-cells is to provide cholesterol for the exocytosis of insulin. |
| 659 | 18804448 | A significant reduction in insulin secretion from HSL null islets was observed whereas wt islets were unaffected. |
| 660 | 18804448 | Using synaptosomal protein of 25 kDa (SNAP-25) as indicator of cholesterol-rich microdomains, confocal microscopy was used to show that HSL null beta-cells treated with mbetacd contained fewer clusters than wt beta-cells. |
| 661 | 18804448 | These results indicate that HSL plays an important role in insulin secretion by providing free cholesterol for the formation and maintenance of cholesterol-rich patches for docking of SNARE-proteins to the plasma membrane. |
| 662 | 18804448 | Lack of cholesterol mobilization in islets of hormone-sensitive lipase deficient mice impairs insulin secretion. |
| 663 | 18804448 | The observations that hormone-sensitive lipase (HSL) is located in close association to insulin granules in beta-cells and that cholesterol ester hydrolase activity is completely blunted in islets of HSL null mice made us hypothesize that the role of HSL in beta-cells is to provide cholesterol for the exocytosis of insulin. |
| 664 | 18804448 | A significant reduction in insulin secretion from HSL null islets was observed whereas wt islets were unaffected. |
| 665 | 18804448 | Using synaptosomal protein of 25 kDa (SNAP-25) as indicator of cholesterol-rich microdomains, confocal microscopy was used to show that HSL null beta-cells treated with mbetacd contained fewer clusters than wt beta-cells. |
| 666 | 18804448 | These results indicate that HSL plays an important role in insulin secretion by providing free cholesterol for the formation and maintenance of cholesterol-rich patches for docking of SNARE-proteins to the plasma membrane. |
| 667 | 18804448 | Lack of cholesterol mobilization in islets of hormone-sensitive lipase deficient mice impairs insulin secretion. |
| 668 | 18804448 | The observations that hormone-sensitive lipase (HSL) is located in close association to insulin granules in beta-cells and that cholesterol ester hydrolase activity is completely blunted in islets of HSL null mice made us hypothesize that the role of HSL in beta-cells is to provide cholesterol for the exocytosis of insulin. |
| 669 | 18804448 | A significant reduction in insulin secretion from HSL null islets was observed whereas wt islets were unaffected. |
| 670 | 18804448 | Using synaptosomal protein of 25 kDa (SNAP-25) as indicator of cholesterol-rich microdomains, confocal microscopy was used to show that HSL null beta-cells treated with mbetacd contained fewer clusters than wt beta-cells. |
| 671 | 18804448 | These results indicate that HSL plays an important role in insulin secretion by providing free cholesterol for the formation and maintenance of cholesterol-rich patches for docking of SNARE-proteins to the plasma membrane. |
| 672 | 18804448 | Lack of cholesterol mobilization in islets of hormone-sensitive lipase deficient mice impairs insulin secretion. |
| 673 | 18804448 | The observations that hormone-sensitive lipase (HSL) is located in close association to insulin granules in beta-cells and that cholesterol ester hydrolase activity is completely blunted in islets of HSL null mice made us hypothesize that the role of HSL in beta-cells is to provide cholesterol for the exocytosis of insulin. |
| 674 | 18804448 | A significant reduction in insulin secretion from HSL null islets was observed whereas wt islets were unaffected. |
| 675 | 18804448 | Using synaptosomal protein of 25 kDa (SNAP-25) as indicator of cholesterol-rich microdomains, confocal microscopy was used to show that HSL null beta-cells treated with mbetacd contained fewer clusters than wt beta-cells. |
| 676 | 18804448 | These results indicate that HSL plays an important role in insulin secretion by providing free cholesterol for the formation and maintenance of cholesterol-rich patches for docking of SNARE-proteins to the plasma membrane. |
| 677 | 19018281 | Ser649 and Ser650 are the major determinants of protein kinase A-mediated activation of human hormone-sensitive lipase against lipid substrates. |
| 678 | 19246492 | Accordingly, genes known to be positively regulated by RA were down-regulated in HSL-null mice, including pRb and RIP140, key factors promoting differentiation into the white over the brown adipocyte lineage. |
| 679 | 19246492 | These findings demonstrate the importance of HSL as an REH of adipose tissue and suggest that HSL via this action provides RA and other retinoids for signaling events that are crucial for adipocyte differentiation and lineage commitment. |
| 680 | 19785415 | Hormone-sensitive lipase (HSL), a key enzyme in fatty acid mobilization from lipid stores, is expressed in the liver and decreased hepatic insulin sensitivity has been reported in our HSL null mouse model. |
| 681 | 19785415 | This study identifies a link between HSL and polyamine metabolism, which deserves further attention in view of the emerging data suggesting that disturbances in polyamine metabolism may affect insulin sensitivity. |
| 682 | 19785415 | Hormone-sensitive lipase (HSL), a key enzyme in fatty acid mobilization from lipid stores, is expressed in the liver and decreased hepatic insulin sensitivity has been reported in our HSL null mouse model. |
| 683 | 19785415 | This study identifies a link between HSL and polyamine metabolism, which deserves further attention in view of the emerging data suggesting that disturbances in polyamine metabolism may affect insulin sensitivity. |
| 684 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 685 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 686 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 687 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 688 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 689 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 690 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 691 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 692 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 693 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 694 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 695 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 696 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 697 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 698 | 19996383 | Nine days of bed rest causes severe peripheral insulin resistance and reduced WBL and skeletal muscle HSL activity, as well as a compensatory increased insulin secretion, with no differences in LBW subjects and controls. |
| 699 | 20158974 | Treatment of asarone significantly inhibited the differentiation of 3T3-L1 preadipocytes through suppression of expression of the transcription factors, CCAAT/enhancer binding protein-alpha and peroxisome proliferator activated receptor-gamma, which activate adipogenesis. |
| 700 | 20158974 | Together, the present findings indicate that asarone inhibits adipogenesis by down-regulation of PPARgamma and C/EBPalpha and reduces lipid accumulation by stimulation of lipolysis through an increase in hormone-sensitive lipase activity. |
| 701 | 20219977 | Because insulin modulates the hypothalamic response to GH secretagogues and acts synergistically with ghrelin on lipogenesis in vitro, we analyzed whether insulin plays a role in the metabolic effects of GHRP-6 in vivo. |
| 702 | 20219977 | Insulin, but not GHRP-6, improved these parameters (P < 0.001 for all), as well as the diabetes-induced increase in hypothalamic mRNA levels of neuropeptide Y and agouti-related peptide and decrease in proopiomelanocortin. |
| 703 | 20219977 | Diabetic rats receiving insulin plus GHRP-6 gained more weight and had increased epididymal fat mass and serum leptin levels compared with all other groups (P < 0.001). |
| 704 | 20219977 | In epididymal adipose tissue, diabetic rats injected with saline had smaller adipocytes (P < 0.001), decreased fatty acid synthase (FAS; P < 0.001), and glucose transporter-4 (P < 0.001) and increased hormone sensitive lipase (P < 0.001) and proliferator-activated receptor-gamma mRNA levels (P < 0.01). |
| 705 | 20219977 | GHRP-6 treatment increased FAS and glucose transporter-4 gene expression and potentiated insulin's effect on epididymal fat mass, adipocyte size (P < 0.001), FAS (P < 0.001), and glucose transporter-4 (P < 0.05). |
| 706 | 20580384 | To elucidate its role in metabolism, we investigated the influence of an overexpression of JAZF1 on 3T3-L1 adipose cells and hepatoma carcinoma Hepa1-6 cells that represent target tissues for diabetes and insulin resistance. |
| 707 | 20580384 | In both cells, JAZF1 overexpression led to a substantial reduction in the expression of acetyl-coenzyme A carboxylase, fatty acid synthetase, and sterol regulatory element-binding protein 1 messenger RNA (mRNA). |
| 708 | 20580384 | The expression of JAZF1 in 3T3-L1 adipocyte exhibited suppressive effects on lipid accumulation and decreased droplet size. |
| 709 | 20580384 | These results showed that JAZF1 in adipocytes and liver cells reduces lipid synthesis and increases lipolysis mainly by down-regulating the levels of sterol regulatory element-binding protein 1, acetyl-coenzyme A carboxylase, and fatty acid synthetase mRNA expression and by increasing hormone-sensitive lipase mRNA expression. |
| 710 | 20682840 | EST overexpression decreased the differentiation of primary adipocytes, and this was associated with reductions in the expression of peroxisome proliferator-activated receptor-γ, fatty acid synthase, hormone-sensitive lipase, lipoprotein lipase, and leptin. |
| 711 | 20682840 | Serum leptin levels were significantly lower in EST transgenic mice, whereas total and high-molecular-weight adiponectin levels were not different in transgenic and wild-type mice. |
| 712 | 20733001 | Insulin regulates adipocyte lipolysis via an Akt-independent signaling pathway. |
| 713 | 20733001 | After a meal, insulin suppresses lipolysis through the activation of its downstream kinase, Akt, resulting in the inhibition of protein kinase A (PKA), the main positive effector of lipolysis. |
| 714 | 20733001 | Here, we describe a noncanonical Akt-independent, phosphoinositide-3 kinase (PI3K)-dependent pathway that regulates adipocyte lipolysis using restricted subcellular signaling. |
| 715 | 20733001 | In contrast, the phosphorylation of another PKA substrate, hormone-sensitive lipase (HSL), remains Akt dependent. |
| 716 | 20739620 | A key enzyme in this process is pyruvate dehydrogenase kinase 4 (PDK4). |
| 717 | 20739620 | We further postulated that the p38 mitogen-activated protein kinase (MAPK) and 5'-AMP-activated protein kinase (AMPK) signaling pathways would control PDK4 mRNA expression in cultured adipose tissue. |
| 718 | 20739620 | In cultured adipose tissue, epinephrine increased p38 and AMPK signaling; however, the direct activation of AMPK by AICAR or metformin led to reductions in PDK4 mRNA levels. |
| 719 | 20739620 | The p38 inhibitor SB202190 reduced epinephrine-mediated increases in p38 MAPK activation without altering hormone-sensitive lipase or AMPK phosphorylation or attenuating epinephrine-induced increases in lipolysis. |
| 720 | 20739620 | Reductions in p38 MAPK signaling were associated with decreases in PDK4 mRNA expression. |
| 721 | 20739620 | Our results are the very first to demonstrate an epinephrine-mediated regulation of PDK4 mRNA levels in white adipose tissue and suggest that p38 MAPK and PPARγ could be involved in this pathway. |
| 722 | 20926921 | Fasting and post-prandial adipose tissue lipoprotein lipase and hormone-sensitive lipase in obesity and type 2 diabetes. |
| 723 | 21042876 | Rapamycin enhanced the isoproterenol-stimulated phosphorylation of hormone sensitive lipase (HSL) on Ser-563 (a PKA site), but had no effect on the phosphorylation of HSL S565 (an AMPK site). |
| 724 | 21216462 | Impairments in leptin-melanocortin signaling are associated with insulin-deficient diabetes and leptin treatment has been shown to be effective in reversing hyperglycemia in animal models of type 1 diabetes. |
| 725 | 21216462 | MTII treatment did not alter expression levels of genes encoding gluconeogenic enzymes including glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK), in the liver of diabetic mice. |
| 726 | 21216462 | MTII treatment also significantly reduced expression levels of hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) mRNA in white adipose tissue of diabetic mice without a significant change in serum insulin levels. |
| 727 | 21216462 | Expression levels of lipoprotein lipase (LPL) and fatty acid translocase (FAT/CD36) mRNA in white adipose tissue and skeletal muscle were not changed by MTII treatment. |
| 728 | 21266508 | At the whole-body level, IR reverted after the 10-d treatment; however, tissue-specific indications of IR were observed, such as down-regulation of adipose glucose transporter 4, hepatic peroxisome proliferative activated receptor-γ1 and -2, and muscle insulin receptor substrate-1. |
| 729 | 21266508 | In adipose tissue, increased hormone-sensitive lipase activity led to reduced adipocyte size, concomitant with increased plasma and hepatic triglyceride content and decreased total and high-density lipoprotein cholesterol levels. |
| 730 | 21291723 | Mechanisms explaining this increased risk include adverse cytokine profiles produced by excess adipose tissue, abnormal lipid metabolism by understimulated hormone-sensitive lipase, and abnormal cellular respiration leading to insulin resistance. |
| 731 | 21484150 | The expression of protein kinase B (Akt), glucose transporter 4 (GLUT4), hormone sensitive lipase (HSL), and phosphatidylinositol-3-kinase (PI3 K) genes in SIT-treated adipocytes were assessed by real-time reverse transcription polymerase chain reaction (RT-PCR). |
| 732 | 21484150 | Interestingly, although SIT displayed general insulin-mimetic activity by stimulating glucose uptake and adipogenesis, it also induced lipolysis in adipocytes. |
| 733 | 21484150 | Furthermore, the SIT-induced lipolysis was not attenuated by insulin and co-incubation of SIT with epinephrine improved epinephrine-induced lipolysis. |
| 734 | 21484150 | GLUT4 gene expression was highly down-regulated in SIT-treated adipocytes, compared to insulin-treated adipocytes, which was up-regulated. |
| 735 | 21484150 | Insulin- and SIT-treated adipocytes showed similar levels of Akt, HSL, and PI3 K gene down-regulation. |
| 736 | 21484150 | These observations suggest that the elevation of glucose uptake in SIT-treated adipocytes was unrelated to de novo synthesis of GLUT4 and the SIT-induced lipolysis is associated with the down-regulation of Akt and PI3K genes. |
| 737 | 21484150 | The expression of protein kinase B (Akt), glucose transporter 4 (GLUT4), hormone sensitive lipase (HSL), and phosphatidylinositol-3-kinase (PI3 K) genes in SIT-treated adipocytes were assessed by real-time reverse transcription polymerase chain reaction (RT-PCR). |
| 738 | 21484150 | Interestingly, although SIT displayed general insulin-mimetic activity by stimulating glucose uptake and adipogenesis, it also induced lipolysis in adipocytes. |
| 739 | 21484150 | Furthermore, the SIT-induced lipolysis was not attenuated by insulin and co-incubation of SIT with epinephrine improved epinephrine-induced lipolysis. |
| 740 | 21484150 | GLUT4 gene expression was highly down-regulated in SIT-treated adipocytes, compared to insulin-treated adipocytes, which was up-regulated. |
| 741 | 21484150 | Insulin- and SIT-treated adipocytes showed similar levels of Akt, HSL, and PI3 K gene down-regulation. |
| 742 | 21484150 | These observations suggest that the elevation of glucose uptake in SIT-treated adipocytes was unrelated to de novo synthesis of GLUT4 and the SIT-induced lipolysis is associated with the down-regulation of Akt and PI3K genes. |
| 743 | 21784784 | GPR39, a constitutively active 7TM receptor important for glucose-induced insulin secretion and maturation of pancreatic β-cell function, is up-regulated in adipose tissue on abstinence from food and chemically induced diabetes. |
| 744 | 21784784 | Analysis of the adipose tissue for lipolytic enzymes demonstrated decreased level of phosphorylated hormone-sensitive lipase (HSL) and a decreased level of adipose triglyceride lipase (ATGL) by 35 and 60%, respectively, after food withdrawal in the GPR39-deficient mice. |
| 745 | 22008857 | The inhibition of HSL may offer a pharmacological approach to reduce FFA levels in plasma and diminish peripheral insulin resistance in type 2 diabetes. |
| 746 | 22223650 | Although both ERK1/2 and JNK are activated during ER stress, lipolysis is partially suppressed by inhibiting ERK1/2 but not JNK and p38 MAPK and PKC. |
| 747 | 22223650 | Furthermore, ER stress stimuli did not alter the levels of hormone-sensitive lipase and adipose triglyceride lipase but caused Ser-563 and Ser-660 phosphorylation of hormone-sensitive lipase and moderately elevated its translocation from the cytosol to lipid droplets. |
| 748 | 22942234 | Within knockout WAT, phosphorylation of protein kinase A substrate increased in males and females, phosphorylation of hormone-sensitive lipase (HSL) (ser563) increased in females, and levels of adipose triglyceride lipase, comparative gene identification-58, and phospho-perilipin were higher in male Vgf-/Vgf- WAT compared with wild-type, consistent with increased lipolysis. |
| 749 | 22942234 | The phosphorylation of AMP-activated protein kinase (AMPK) (Thr172) and levels of the AMPK kinase, transforming growth factor β-activated kinase 1, were decreased. |
| 750 | 22942234 | This was associated with a decrease in HSL ser565 phosphorylation, the site phosphorylated by AMPK, in both male and female Vgf-/Vgf- WAT. |
| 751 | 22942234 | No significant differences in phosphorylation of CREB or the p42/44 MAPK were noted. |
| 752 | 22942234 | Within knockout WAT, phosphorylation of protein kinase A substrate increased in males and females, phosphorylation of hormone-sensitive lipase (HSL) (ser563) increased in females, and levels of adipose triglyceride lipase, comparative gene identification-58, and phospho-perilipin were higher in male Vgf-/Vgf- WAT compared with wild-type, consistent with increased lipolysis. |
| 753 | 22942234 | The phosphorylation of AMP-activated protein kinase (AMPK) (Thr172) and levels of the AMPK kinase, transforming growth factor β-activated kinase 1, were decreased. |
| 754 | 22942234 | This was associated with a decrease in HSL ser565 phosphorylation, the site phosphorylated by AMPK, in both male and female Vgf-/Vgf- WAT. |
| 755 | 22942234 | No significant differences in phosphorylation of CREB or the p42/44 MAPK were noted. |
| 756 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 757 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 758 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 759 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 760 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 761 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 762 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 763 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 764 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 765 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 766 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 767 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 768 | 23085101 | In adipocytes, GDS signals through the Htr2b receptor to favor lipolysis by increasing phosphorylation and activity of hormone-sensitive lipase. |
| 769 | 23085101 | In hepatocytes, GDS signaling through Htr2b promotes gluconeogenesis by enhancing activity of two rate-limiting gluconeogenic enzymes, FBPase and G6Pase. |
| 770 | 23291629 | Ablation of TRIP-Br2, a regulator of fat lipolysis, thermogenesis and oxidative metabolism, prevents diet-induced obesity and insulin resistance. |
| 771 | 23291629 | TRIP-Br2-null mice are resistant to obesity and obesity-related insulin resistance. |
| 772 | 23291629 | Adipocytes of these knockout mice showed greater stimulated lipolysis secondary to enhanced expression of hormone sensitive lipase (HSL) and β3-adrenergic (Adrb3) receptors. |
| 773 | 23291629 | These data, together with the observation that TRIP-Br2 expression is selectively elevated in visceral fat in obese humans, suggests that this transcriptional co-regulator is a new therapeutic target for counteracting the development of obesity, insulin resistance and hyperlipidemia. |
| 774 | 23318496 | CART deficient mice exhibit islet dysfunction, impaired insulin secretion and increased body weight. |
| 775 | 23318496 | Stimulating rat primary adipocytes with CART significantly potentiated isoprenaline-induced lipolysis, and hormone sensitive lipase activation (phosphorylation of Ser 563). |
| 776 | 23318496 | On the other hand, CART significantly potentiated the inhibitory effect of insulin on isoprenaline-induced lipolysis. |
| 777 | 23318496 | CART inhibited insulin-induced glucose uptake and lipogenesis, which was associated with inhibition of PKB phosphorylation. |
| 778 | 23318496 | Depending on the surrounding conditions, the effects of CART are insulin-like or insulin-antagonistic. |
| 779 | 23431266 | HSL haploinsufficiency and treatment with a HSL inhibitor resulted in improvement of insulin tolerance without impact on body weight, fat mass, and WAT inflammation in high-fat-diet-fed mice. |
| 780 | 23431266 | In human adipocytes, HSL gene silencing led to improved insulin-stimulated glucose uptake, resulting in increased de novo lipogenesis and activation of cognate gene expression. |
| 781 | 23431266 | HSL haploinsufficiency and treatment with a HSL inhibitor resulted in improvement of insulin tolerance without impact on body weight, fat mass, and WAT inflammation in high-fat-diet-fed mice. |
| 782 | 23431266 | In human adipocytes, HSL gene silencing led to improved insulin-stimulated glucose uptake, resulting in increased de novo lipogenesis and activation of cognate gene expression. |
| 783 | 23434933 | We show diurnal variations in lipolysis rates and release of free fatty acids (FFAs) and glycerol into the blood correlating with rhythmic regulation of two genes encoding the lipolysis pacemaker enzymes, adipose triglyceride (TG) lipase and hormone-sensitive lipase, by self-sustained adipocyte clocks. |
| 784 | 23576171 | Bis(acetylacetonato)-oxovanadium(iv), bis(maltolato)-oxovanadium(iv) and sodium metavanadate induce antilipolytic effects by regulating hormone-sensitive lipase and perilipin via activation of Akt. |
| 785 | 23576171 | The antilipolytic effects of vanadium compounds were further evidenced by a decrease of the levels of phosphorylated HSL at Ser660 and phosphorylated perilipin, which were counteracted by inhibitors of PI3K or Akt but not by an MEK inhibitor. |
| 786 | 23576171 | This indicates that though both Akt and ERK pathways are activated by the vanadium compounds, only Akt activation contributes to the antilipolytic effect of the vanadium compounds, without the involvement of ERK activation. |
| 787 | 23576171 | Bis(acetylacetonato)-oxovanadium(iv), bis(maltolato)-oxovanadium(iv) and sodium metavanadate induce antilipolytic effects by regulating hormone-sensitive lipase and perilipin via activation of Akt. |
| 788 | 23576171 | The antilipolytic effects of vanadium compounds were further evidenced by a decrease of the levels of phosphorylated HSL at Ser660 and phosphorylated perilipin, which were counteracted by inhibitors of PI3K or Akt but not by an MEK inhibitor. |
| 789 | 23576171 | This indicates that though both Akt and ERK pathways are activated by the vanadium compounds, only Akt activation contributes to the antilipolytic effect of the vanadium compounds, without the involvement of ERK activation. |
| 790 | 23688034 | Risk interaction of obesity, insulin resistance and hormone-sensitive lipase promoter polymorphisms (LIPE-60 C > G) in the development of fatty liver. |
| 791 | 23880330 | The increased lipolysis was accompanied by an increase in the expression of hormone sensitive lipase (1.6-fold, p<0.05) and perilipin (1.6-fold, p<0.05). |