期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 234, 期 4, 页码 5143-5152出版社
WILEY
DOI: 10.1002/jcp.27318
关键词
inorganic arsenic; insulin resistance; mTORC2; PPAR; taurine
资金
- National Natural Science Foundation of China [81872566]
- Natural Science Foundation of Liaoning Province [2014023050]
Inorganic arsenic (iAs) is reportedly associated with the increased incidence of type 2 diabetes in the population. Here, we found that iAs exposure significantly decreased the expression of glycolytic genes and glycogen content and increased gluconeogenesis gene levels in C57/BL6J mice. The expression of peroxisome proliferator-activated receptor (PPAR), and mechanistic target of rapamycin complex 2 (mTORC2) were decreased in the livers of iAs-treated mice. Furthermore, in iAs-treated HepG2 cells, we found that PPAR agonist rosiglitazone (RGS) increased the expression of mTORC2, inhibited autophagy, and improved glucose metabolism. mTORC2 agonist palmitic acid inhibited autophagy and improved glucose metabolism as well as the autophagosome formation inhibitor 3-methyladenine. Taurine, a natural compound, reversed impaired glucose metabolism and decreased expression of PPAR and mTORC2 induced by iAs in mice liver and HepG2 cells. These data indicated that taurine administration could ameliorate iAs-induced insulin resistance through activating PPAR-mTORC2 signalling and subsequently inhibiting hepatic autophagy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据