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Biochemistry Research International
Volume 2012, Article ID 247275, 5 pages
http://dx.doi.org/10.1155/2012/247275
Review Article

Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes

1Center for Molecular Medicine and Genetics, The Wayne State University School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USA
2Department of Immunology and Microbiology, The Wayne State University School of Medicine, Detroit, MI 48201, USA
3Karmanos Cancer Institute, The Wayne State University School of Medicine, Detroit, MI 48201, USA

Received 2 September 2011; Revised 14 November 2011; Accepted 15 November 2011

Academic Editor: Huiping Zhou

Copyright © 2012 Xuebao Zhang and Kezhong Zhang. 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.

Abstract

Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is caused by insufficient insulin production due to excessive loss of pancreatic β cells (type I diabetes) or impaired insulin signaling due to peripheral insulin resistance (type II diabetes). Pancreatic β cell is the only insulin-secreting cell type that has highly developed endoplasmic reticulum (ER) to cope with high demands of insulin synthesis and secretion. Therefore, ER homeostasis is crucial to the proper function of insulin signaling. Accumulating evidence suggests that deleterious ER stress and excessive intracellular lipids in nonadipose tissues, such as myocyte, cardiomyocyte, and hepatocyte, cause pancreatic β-cell dysfunction and peripheral insulin resistance, leading to type II diabetes. The excessive deposition of lipid droplets (LDs) in specialized cell types, such as adipocytes, hepatocytes, and macrophages, has been found as a hallmark in ER stress-associated metabolic diseases, including obesity, diabetes, fatty liver disease, and atherosclerosis. However, much work remains to be done in understanding the mechanism by which ER stress response regulates LD formation and the pathophysiologic role of ER stress-associated LD in metabolic disease. This paper briefly summarizes the recent advances in ER stress-associated LD formation and its involvement in type II diabetes.