Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance.

Author: Jae Man LEE ¹
Author Information

1. Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Kyungpook National University School of Medicine, Daegu, Korea. jaemanlee@knu.ac.kr
Publication Type:Review
Keywords: Diabetes mellitus, type 2; Endoplasmic reticulum stress; Hepatic steatosis; Insulin resistance; Receptors, cytoplasmic and nuclear; Unfolded protein response
MeSH: Diabetes Mellitus, Type 2; Endoplasmic Reticulum Stress*; Endoplasmic Reticulum*; Insulin Resistance*; Insulin*; Liver; Receptors, Cytoplasmic and Nuclear*; Unfolded Protein Response
From:Diabetes & Metabolism Journal 2017;41(1):10-19
CountryRepublic of Korea
Language:English
Abstract: Chronic endoplasmic reticulum (ER) stress culminating in proteotoxicity contributes to the development of insulin resistance and progression to type 2 diabetes mellitus. Pharmacologic interventions targeting several different nuclear receptors have emerged as potential treatments for insulin resistance. The mechanistic basis for these antidiabetic effects has primarily been attributed to multiple metabolic and inflammatory functions. Here we review recent advances in our understanding of the association of ER stress with insulin resistance and the role of nuclear receptors in promoting ER stress resolution and improving insulin resistance in the liver.