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Experimental Diabetes Research
Volume 2012, Article ID 509437, 7 pages
Review Article

Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review

1Department of Internal Medicine, Keimyung University School of Medicine, Daegu 700-712, Republic of Korea
2World Class University Program, Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu 700-721, Republic of Korea

Received 14 April 2011; Accepted 6 December 2011

Academic Editor: Muthuswamy Balasubramanyam

Copyright © 2012 Mi-Kyung Kim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis.