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Role of Peroxisome Proliferator-Activated Receptor Gamma in Glucose-induced Insulin Secretion

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Peroxisome proliferator-activated receptor (PPAR) isoforms (α and ) are known to be expressed in pancreatic islets as well as in insulin-producing cell lines. Ligands of PPAR have been shown to enhance glucose-induced insulin secretion in rat pancreatic islets. However, their effect on insulin secretion is still unclear. To understand the molecular mechanism by which PPAR exerts its effect on glucose-induced insulin secretion, we examined the endogenous activity of PPAR isoforms, and studied the PPAR function and its target gene expression in INS-1 cells. We found that: (1) endogenous PPAR was activated in a ligand-dependent manner in INS-1 cells; (2) overexpression of PPAR in the absence of PPAR ligands enhanced glucose-induced insulin secretion, which indicates that the increased glucose-induced insulin secretion is a PPAR -mediated event; (3) the addition of both PPAR and retinoid X receptor (RXR) ligands showed a synergistic effect on the augmentation of reporter activity, suggesting that the hetero-dimerization of PPAR and RXR is required for the regulation of the target genes; (4) PPARs upregulated both the glucose transporter 2 (GLUT2) and Cb1-associated protein (CAP) genes in INS-1 cells. Our findings suggest an important mechanistic pathway in which PPAR enhances glucose-induced insulin secretion by activating the expression of GLUT2 and CAP genes in a ligand-dependent manner.

Edited by

Shang-Quan ZHU
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Keywords: Cb1-associated; PPAR; glucose transporter 2; glucose-induced insulin secretion; ligand

Document Type: Research Article

Affiliations: Key Laboratory of Human Functional Genomics of Jiangsu Province, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing 210029, China

Publication date: January 1, 2006

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