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International Journal of Endocrinology
Volume 2010, Article ID 515136, 10 pages
http://dx.doi.org/10.1155/2010/515136
Review Article

Cytokines in the Progression of Pancreatic β-Cell Dysfunction

Department of Physiology and Pathophysiology, Peking University Diabetes Center, Peking University Health Science Center, Beijing 100191, China

Received 28 April 2010; Revised 5 August 2010; Accepted 7 October 2010

Academic Editor: Robert R. Henry

Copyright © 2010 Chunjiong Wang 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.

Abstract

The dysfunction of pancreatic β-cell and the reduction in β-cell mass are the decisive events in the progression of type 2 diabetes. There is increasing evidence that cytokines play important roles in the procedure of β-cell failure. Cytokines, such as IL-1β, IFN-γ, TNF-α, leptin, resistin, adiponectin, and visfatin, have been shown to diversely regulate pancreatic β-cell function. Recently, islet-derived cytokine PANcreatic DERived factor (PANDER or FAM3B) has also been demonstrated to be a regulator of islet β-cell function. The change in cytokine profile in islet and plasma is associated with pancreatic β-cell dysfunction and apoptosis. In this paper, we summarize and discuss the recent studies on the effects of certain important cytokines on pancreatic β-cell function. The imbalance in deleterious and protective cytokines plays pivotal roles in the development and progression of pancreatic β-cell dysfunction under insulin-resistant conditions.