Inhibition of GPR40 protects MIN6 β cells from palmitate-induced ER stress and apoptosis

✍ Scribed by Jinwei Wu; Peng Sun; Xiaodong Zhang; Hong Liu; Hualiang Jiang; Weiliang Zhu; Heyao Wang

• Book ID: 102301853
• Publisher: John Wiley and Sons
• Year: 2012
• Tongue: English
• Weight: 425 KB
• Volume: 113
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.23450

✦ Synopsis

Abstract

Chronic exposure to elevated concentration of free fatty acids (FFA) has been verified to induce endoplasmic reticulum (ER) stress, which leads to pancreatic β‐cell apoptosis. As one of the medium and long chain FFA receptors, GPR40 is highly expressed in pancreatic β cells, mediates both acute and chronic effects of FFA on β‐cell function, but the role of GPR40 in FFA‐induced β‐cell apoptosis remains unclear. In this study, we investigated the possible effects of GPR40 in palmitate‐induced MIN6 β‐cell apoptosis, and found that DC260126, a novel small molecular antagonist of GPR40, could protect MIN6 β cells from palmitate‐induced ER stress and apoptosis. Similar results were observed in GPR40‐deficient MIN6 cells, indicating that palmitate‐induced β‐cell apoptosis is at least partially dependent on ER stress pathway via GRP40. J. Cell. Biochem. 113: 1152–1158, 2012. © 2011 Wiley Periodicals, Inc.