Subject    :    [2017 Feb;41(1)] Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance
Writer KDA
Date 2017-03-23 10:31:29 Hit 7,328
Diabetes Metab J. 2017 Feb;41(1):10-19. English. Published online Feb 16, 2017.  https://doi.org/10.4093/dmj.2017.41.1.10 
Copyright © 2017 Korean Diabetes Association
   
Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance
Jae Man Lee1,2
1Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Kyungpook National University School of Medicine, Daegu, Korea.
2BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, Kyungpook National University School of Medicine, Daegu, Korea.
Corresponding author: Jae Man Lee. Department of Biochemistry and Cell Biology, Kyungpook National University School of Medicine, 680 Gukchaebosang-ro, Jung-gu, Daegu 41944, Korea. Email: jaemanlee@knu.ac.kr 
 
Received November 05, 2016; Accepted December 02, 2016.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

 
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

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