共查询到20条相似文献,搜索用时 562 毫秒
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Wang H Maechler P Antinozzi PA Hagenfeldt KA Wollheim CB 《The Journal of biological chemistry》2000,275(46):35953-35959
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Neurogenin3 and hepatic nuclear factor 1 cooperate in activating pancreatic expression of Pax4 总被引:3,自引:0,他引:3
Smith SB Gasa R Watada H Wang J Griffen SC German MS 《The Journal of biological chemistry》2003,278(40):38254-38259
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Ramanadham S Song H Hsu FF Zhang S Crankshaw M Grant GA Newgard CB Bao S Ma Z Turk J 《Biochemistry》2003,42(47):13929-13940
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Role of peroxisome proliferator-activated receptor gamma in glucose-induced insulin secretion 总被引:4,自引:0,他引:4
Peroxisome proliferator-activated receptor (PPAR) isoforms (α and γ) are known to beexpressed in pancreatic islets as well as in insulin-producing cell lines.Ligands of PPAR have been shoWn toenhance glucose-induced insulin secretion in rat pancreatic islets.However,their effect on insulin secretionis still unclear.To understand the molecular mechanism by which PPAR7 exerts its effect on glucose-induced insulin secretion,we examined the endogenous activity of PPAR isoforms,and studied the PPARyfunction and its target gene expression in INS-1 cells.We found that:(1)endogenous PPARγ was activatedin a ligand-dependent manner in INS-1 cells;(2)overexpression of PPARy in the absence of PPARγ ligandsenhanced glucose-induced insulin secretion,which indicates that the increased glucose-induced insulin secretionis a PPARγ-mediated event;(3)the addition of both PPARγ and retinoid X receptor (RXR) ligands showed asynergistic effect on the augmentation of reporter activity,suggesting that the hetero-dimerization of PPAR7and RXR is required for the regulation of the target genes;(4)PPARs upregulated both the glucose transporter2 (GLUT2) and Cbl-associated protein (CAP) genes in INS-1 cells.Our findings suggest an importantmechanistic pathway in which PPARγ enhances glucose-induced insulin secretion by activating the expressionof GLUT2 and CAP genes in a ligand-dependent manner. 相似文献
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Human insulin gene is a target gene of hepatocyte nuclear factor-1alpha (HNF-1alpha) and HNF-1beta. 总被引:6,自引:0,他引:6
K Okita Q Yang K Yamagata K A Hangenfeldt J Miyagawa Y Kajimoto H Nakajima M Namba C B Wollheim T Hanafusa Y Matsuzawa 《Biochemical and biophysical research communications》1999,263(2):566-569
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Perilhou A Tourrel-Cuzin C Kharroubi I Henique C Fauveau V Kitamura T Magnan C Postic C Prip-Buus C Vasseur-Cognet M 《Molecular and cellular biology》2008,28(21):6568-6579
COUP-TFII has an important role in regulating metabolism in vivo. We showed this previously by deleting COUP-TFII from pancreatic beta cells in heterozygous mutant mice, which led to abnormal insulin secretion. Here, we report that COUP-TFII expression is reduced in the pancreas and liver of mice refed with a carbohydrate-rich diet and in the pancreas and liver of hyperinsulinemic and hyperglycemic mice. In pancreatic beta cells, COUP-TFII gene expression is repressed by secreted insulin in response to glucose through Foxo1 signaling. Ex vivo COUP-TFII reduces insulin production and secretion. Our results suggest that beta cell insulin secretion is under the control of an autocrine positive feedback loop by alleviating COUP-TFII repression. In hepatocytes, both insulin, through Foxo1, and high glucose concentrations repress COUP-TFII expression. We demonstrate that this negative glucose effect involves ChREBP expression. We propose that COUP-TFII acts in a coordinate fashion to control insulin secretion and glucose metabolism. 相似文献
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