Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2014, Article ID 618652, 12 pages
Review Article

Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes

1Lille 2 University, European Genomic Institute for Diabetes (EGID), FR 3508, UMR-8199 Lille, France
2Service of Internal Medicine, Hospital-University of Lausanne (CHUV), 1011 Lausanne, Switzerland
3Department of Fundamental Neurosciences, University of Lausanne, 1005 Lausanne, Switzerland

Received 24 October 2013; Accepted 24 January 2014; Published 5 March 2014

Academic Editor: Stephane Dalle

Copyright © 2014 Valérie Plaisance 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.


Pancreatic beta-cell function and mass are markedly adaptive to compensate for the changes in insulin requirement observed during several situations such as pregnancy, obesity, glucocorticoids excess, or administration. This requires a beta-cell compensation which is achieved through a gain of beta-cell mass and function. Elucidating the physiological mechanisms that promote functional beta-cell mass expansion and that protect cells against death, is a key therapeutic target for diabetes. In this respect, several recent studies have emphasized the instrumental role of microRNAs in the control of beta-cell function. MicroRNAs are negative regulators of gene expression, and are pivotal for the control of beta-cell proliferation, function, and survival. On the one hand, changes in specific microRNA levels have been associated with beta-cell compensation and are triggered by hormones or bioactive peptides that promote beta-cell survival and function. Conversely, modifications in the expression of other specific microRNAs contribute to beta-cell dysfunction and death elicited by diabetogenic factors including, cytokines, chronic hyperlipidemia, hyperglycemia, and oxidized LDL. This review underlines the importance of targeting the microRNA network for future innovative therapies aiming at preventing the beta-cell decline in diabetes.