Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of gastric inhibitory polypeptide (GIP), glucagon-like peptide-1(7-36) amide, (GLP-1(7-36) amide), glucagon-like peptide-2 (GLP-2), glucagon and insulin on fatty acid synthesis in explants of rat adipose tissue from various sites was investigated. GIP, GLP-1(7-36) amide and insulin stimulated fatty acid synthesis, as determined by measuring the incorporation of [14C]acetate into saponifiable fat, in a dose-dependent manner, over the concentration range 5-15 ng/ml (0.87-2.61 nmol/l) for insulin and 0.5-7.5 ng/ml for GIP (0.10-1.50 nmol/l) and GLP-1(7-36) amide (0.15-2.27 nmol/l). Insulin and GIP caused a significantly greater stimulation of [14C]acetate incorporation into fatty acids in omental adipose tissue than in either epididymal or subcutaneous adipose tissue. Both GIP and GLP-1(7-36) amide had the ability to stimulate fatty acid synthesis within the physiological range of the circulating hormones. At lower concentrations of the hormones, GLP-1(7-36) amide was a more potent stimulator of fatty acid synthesis than GIP in omental adipose tissue culture; the basal rate of fatty acid synthesis was 0.41 +/- 0.03 pmol acetate incorporated/mg wet weight tissue per 2 h; at 0.10 nmol hormone/1 1.15 +/- 0.10 and 3.40 +/- 0.12 pmol acetate incorporated/mg wet weight tissue per 2 h for GIP and GLP-1(7-36) amide respectively (P less than 0.01). GLP-2 and glucagon were without effect on fatty acid synthesis in omental adipose tissue. The study indicates that GIP and GLP-1(7-36)amide, in addition to stimulating insulin secretion, may play a direct physiological role in vivo, in common with insulin, in promoting fatty acid synthesis in adipose tissue.
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PMID:Effect of the entero-pancreatic hormones, gastric inhibitory polypeptide and glucagon-like polypeptide-1(7-36) amide, on fatty acid synthesis in explants of rat adipose tissue. 191 97

To determine the mechanism by which gastric inhibitory polypeptide (GIP) and insulin stimulate the in vitro fatty acid incorporation into adipose tissue (FIAT), we measured the cyclic AMP variations and FIAT in epididymal fat pads of lean Fa/-- and obese fa/fa Zucker rats. GIP was used at 1, 2 and 4 ng/ml and insulin at a concentration of 100 microU/ml. There was no significant variation of cAMP when FIAT was stimulated either by GIP, either by insulin or by both hormones. There was no correlation at all between FIAT increases and cAMP levels. We conclude that GIP and insulin act through cAMP independent mechanisms in adipose tissue. The modification by GIP of insulin binding to adipocytes or an easier passage of fatty acids through the membrane could constitute alternative solutions for such mechanisms.
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PMID:The effects of gastric inhibitory polypeptide and insulin on fatty acid uptake in adipose tissue are not mediated through cyclic AMP in lean and obese Zucker rats. 283 84

Relations exist between insulin, somatostatin (S) and gastric inhibitory polypeptide (GIP) for the reciprocal control of their secretion but also for their role in lipid metabolism. In the present experiment, we studied the effects of somatostatin on fatty acid incorporation into epididymal adipose tissue (FIAT) of Wistar rats when it was stimulated by insulin and GIP. Cyclic somatostatin-14 was used at physiological (S1 : 50 pg/ml, S2 : 200 pg/ml) and supraphysiological (S3 : 666 pg/ml) concentrations whereas insulin and GIP were used at postprandial levels (100 microU/ml and 2 ng/ml respectively). Results were expressed as percent of basal incorporation (without any hormones). Somatostatin inhibited basal FIAT at all concentrations and totally abolished the insulin-stimulated FIAT (from 106.4 +/- 2.3 per cent with insulin alone to 92.6 +/- 2.5 per cent with S3, P less than 0.001). GIP enhanced the insulin-stimulated FIAT from 106.4 +/- 2.3 per cent to 113 +/- 3.0 per cent (P less than 0.01). On the contrary, when somatostatin was added with GIP and insulin, FIAT decreased to 102.3 +/- 2.5 per cent for S1 (P less than 0.01) and to 98.2 +/- 2.6 per cent for S3 (P less than 0.001). These results indicate that somatostatin totally inhibits the fatty acid esterification induced by insulin and in the same proportions that induced by insulin associated with GIP. Somatostatin is not only an inhibitor of the secretion of these hormones but also a regulator of their biological action in adipose tissue.
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PMID:Effects of somatostatin on the insulin- and gastric inhibitory polypeptide-stimulated fatty acid esterification in rat adipose tissue. 289 78

The influence of gastric inhibitory polypeptide (GIP) on fatty acid incorporation into adipose tissue (FIAT) was studied in the rat on epididymal fat pads at concentrations amounting to 1, 2 and 4 ng/ml. Without insulin in the incubation medium, GIP induced a slight though significant FIAT decrease with a maximum of 9% for 2 ng/ml concentration. In the presence of rat insulin (100 microU/ml), it significantly enhanced the insulin-induced FIAT increase, that progressed from 106.4% of the basal value to 110.5% for 1 ng/ml concentration (P less than 0.025) and to 118.2% for 4 ng/ml concentration (P less than 0.0025). The existence of such a phenomenon as well as that of an hyperactive enteroinsular axis in obese subjects could represent two important factors in the development of obesity.
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PMID:Gastric inhibitory polypeptide enhancement of the insulin effect on fatty acid incorporation into adipose tissue in the rat. 635 87

This study evaluated whether long-term supplementation with dietary yerba mate has beneficial effects on adiposity and its related metabolic dysfunctions in diet-induced obese mice. C57BL/6J mice were randomly divided into two groups and fed their respective experimental diets for 16 weeks as follows: (1) control group fed with high-fat diet (HFD) and (2) mate group fed with HFD plus yerba mate. Dietary yerba mate increased energy expenditure and thermogenic gene mRNA expression in white adipose tissue (WAT) and decreased fatty acid synthase (FAS) mRNA expression in WAT, which may be linked to observed decreases in body weight, WAT weight, epididymal adipocyte size, and plasma leptin level. Yerba mate also decreased levels of plasma lipids (free fatty acids, triglycerides, and total cholesterol) and liver aminotransferase enzymes, as well as the accumulation of hepatic lipid droplets and lipid content by inhibiting the activities of hepatic lipogenic enzymes, such as FAS and phosphatidate phosphohydrolase, and increasing fecal lipid excretion. Moreover, yerba mate decreased the levels of plasma insulin as well as the homeostasis model assessment of insulin resistance, and improved glucose tolerance. Circulating levels of gastric inhibitory polypeptide and resistin were also decreased in the mate group. These findings suggest that long-term supplementation of dietary yerba mate may be beneficial for improving diet-induced adiposity, insulin resistance, dyslipidemia, and hepatic steatosis.
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PMID:Long-Term Dietary Supplementation with Yerba Mate Ameliorates Diet-Induced Obesity and Metabolic Disorders in Mice by Regulating Energy Expenditure and Lipid Metabolism. 2887 27

This study was to investigate the protective role of luteolin on inflammation-mediated metabolic diseases, focusing on the role of luteolin in the modulation of the Toll-like receptor (TLR) signaling pathway. C57BL/6J mice were fed a normal, high-fat, or high-fat + 0.005% (w/w) luteolin diet for 16 weeks. Luteolin improved chronic low-grade inflammation by modulating the TLR signaling pathway, resulting in reduced pro-inflammatory cytokines and macrophage accumulation. A positive relationship was detected between gene expressions of Tlr5, Map2k7, Mapk12, Mapk13, and Mapk9 and lipogenesis in epididymal white adipose tissue (eWAT) of luteolin-treated mice, which was linked to attenuation of hepatic lipotoxicity by increasing free fatty acid (FFA) flux to the WAT. Luteolin prevented fibrosis by decreasing extracellular matrix accumulation and cathepsin gene expressions, while enhancing the hepatic antioxidant system. Emr1 and Ccl7, important markers inducing low-grade inflammation, were affected by advanced age and greater body weight, which were normalized by luteolin treatment. Luteolin improved insulin resistance by normalizing pancreatic islet dysfunction and differentially modulating the plasma glucagon-like peptide-1 and gastric inhibitory polypeptide levels. Our results suggest that luteolin ameliorates diet-induced obesity and its comorbidities. Overall, this study provides novel insights into the effect of luteolin on the links among adiposopathy, insulin resistance, hepatic steatosis, and fibrosis.
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PMID:Luteolin Targets the Toll-Like Receptor Signaling Pathway in Prevention of Hepatic and Adipocyte Fibrosis and Insulin Resistance in Diet-Induced Obese Mice. 3028 2