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J Cell Physiol. 2019 Apr;234(4):5143-5152. doi: 10.1002/jcp.27318. Epub 2018 Oct 26.

Taurine improves low-level inorganic arsenic-induced insulin resistance by activating PPARγ-mTORC2 signalling and inhibiting hepatic autophagy.

Author information

1
Department of Occupational and Environmental Health, Dalian Medical University, Dalian, China.
2
Liaoning Anti-Degenerative Diseases Natural Products Engineering Research Center, Dalian Medical University, Dalian, China.
3
Department of Nutrition & Food Safety, School of Public Health, Dalian Medical University, Dalian, China.

Abstract

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 γ (PPARγ), 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 PPARγ 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 PPARγ 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 PPARγ-mTORC2 signalling and subsequently inhibiting hepatic autophagy.

KEYWORDS:

PPARγ; inorganic arsenic; insulin resistance; mTORC2; taurine

PMID:
30362509
DOI:
10.1002/jcp.27318

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