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核受体可缓解内质网应激以改善肝脏胰岛素抵抗。

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

作者信息

Lee Jae Man

机构信息

Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Kyungpook National University School of Medicine, Daegu, Korea.

BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, Kyungpook National University School of Medicine, Daegu, Korea.

出版信息

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

DOI:10.4093/dmj.2017.41.1.10
PMID:28236381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5328691/
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.

摘要

慢性内质网（ER）应激最终导致蛋白毒性，这与胰岛素抵抗的发展以及向2型糖尿病的进展有关。针对几种不同核受体的药物干预已成为胰岛素抵抗的潜在治疗方法。这些抗糖尿病作用的机制基础主要归因于多种代谢和炎症功能。在此，我们综述了我们对ER应激与胰岛素抵抗之间关联的最新认识，以及核受体在促进肝脏中ER应激的缓解和改善胰岛素抵抗方面的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/5328691/477cdf3ff4c5/dmj-41-10-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/5328691/acb09c10af2f/dmj-41-10-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/5328691/477cdf3ff4c5/dmj-41-10-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/5328691/acb09c10af2f/dmj-41-10-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e503/5328691/477cdf3ff4c5/dmj-41-10-g002.jpg

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