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Journal of Diabetes Research
Volume 2014 (2014), Article ID 768024, 7 pages
Review Article

Decompensation of β-Cells in Diabetes: When Pancreatic β-Cells Are on ICE(R)

1European Genomic Institute for Diabetes (EGID), Lille 2 University, UMR 8199, 3508 Lille, France
2Faculty of Medicine West, 1 Place de Verdun, 59045 Lille, France

Received 24 October 2013; Accepted 3 January 2014; Published 10 February 2014

Academic Editor: Stephane Dalle

Copyright © 2014 Roberto Salvi and Amar Abderrahmani. 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 production and secretion are temporally regulated. Keeping insulin secretion at rest after a rise of glucose prevents exhaustion and ultimately failure of β-cells. Among the mechanisms that reduce β-cell activity is the inducible cAMP early repressor (ICER). ICER is an immediate early gene, which is rapidly induced by the cyclic AMP (cAMP) signaling cascade. The seminal function of ICER is to negatively regulate the production and secretion of insulin by repressing the genes expression. This is part of adaptive response required for proper β-cells function in response to environmental factors. Inappropriate induction of ICER accounts for pancreatic β-cells dysfunction and ultimately death elicited by chronic hyperglycemia, fatty acids, and oxidized LDL. This review underlines the importance of balancing the negative regulation achieved by ICER for preserving β-cell function and survival in diabetes.