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Inhibition of GPR40 protects MIN6 β cells from palmitate‐induced ER stress and apoptosis
Author(s) -
Wu Jinwei,
Sun Peng,
Zhang Xiaodong,
Liu Hong,
Jiang Hualiang,
Zhu Weiliang,
Wang Heyao
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23450
Subject(s) - free fatty acid receptor 1 , apoptosis , unfolded protein response , endoplasmic reticulum , cell , receptor , microbiology and biotechnology , chemistry , antagonist , medicine , endocrinology , agonist , biology , biochemistry
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.