Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance

Jae Man Lee

doi:10.4093/dmj.2017.41.1.10

Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance

Diabetes Metab J. 2017 Feb;41(1):10-19. doi: 10.4093/dmj.2017.41.1.10.

Author

Jae Man Lee^{1

2}

Affiliations

¹ Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Kyungpook National University School of Medicine, Daegu, Korea.
² BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, Kyungpook National University School of Medicine, Daegu, Korea. jaemanlee@knu.ac.kr.

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.

Keywords: Diabetes mellitus, type 2; Endoplasmic reticulum stress; Hepatic steatosis; Insulin resistance; Receptors, cytoplasmic and nuclear; Unfolded protein response.

Publication types

Review