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Experimental Diabetes Research
Volume 2012, Article ID 618396, 11 pages
Review Article

Endoplasmic Reticulum Stress in the β-Cell Pathogenesis of Type 2 Diabetes

1School of Biological Sciences, University of Ulsan, Daehak-ro, Nam-gu, Ulsan 680-749, Republic of Korea
2Department of Medicine, Graduate School, University of Ulsan, Seoul, 138-736, Republic of Korea
3Department of Biological Chemistry, University of Michigan Medical Center, Ann Arbor, MI 48109, USA

Received 16 May 2011; Accepted 6 July 2011

Academic Editor: In-Kyu Lee

Copyright © 2012 Sung Hoon Back 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.


Type 2 diabetes is a complex metabolic disorder characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency by β-cell failure. Even if the mechanisms underlying the pathogenesis of β-cell failure are still under investigation, recent increasing genetic, experimental, and clinical evidence indicate that hyperactivation of the unfolded protein response (UPR) to counteract metabolic stresses is closely related to β-cell dysfunction and apoptosis. Signaling pathways of the UPR are “a double-edged sword” that can promote adaptation or apoptosis depending on the nature of the ER stress condition. In this paper, we summarized our current understanding of the mechanisms and components related to ER stress in the β-cell pathogenesis of type 2 diabetes.