Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2013 (2013), Article ID 750540, 14 pages
Review Article

Update on the Protective Molecular Pathways Improving Pancreatic Beta-Cell Dysfunction

1Department of Internal Medicine, University of Genoa, Viale Benedetto XV 6, 16132 Genova, Italy
2Division of Cardiology, Geneva University Hospitals, Faculty of Medicine, Foundation for Medical Researches, Avenue de la Roseraie 64, 1211 Geneva 4, Switzerland
3First Medical Clinic, Laboratory of Phagocyte Physiopathology and Inflammation, Department of Internal Medicine, University of Genoa, Viale Benedetto XV 6, 16132 Genova, Italy

Received 5 February 2013; Accepted 10 April 2013

Academic Editor: Oreste Gualillo

Copyright © 2013 Alessandra Puddu 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.


The primary function of pancreatic beta-cells is to produce and release insulin in response to increment in extracellular glucose concentrations, thus maintaining glucose homeostasis. Deficient beta-cell function can have profound metabolic consequences, leading to the development of hyperglycemia and, ultimately, diabetes mellitus. Therefore, strategies targeting the maintenance of the normal function and protecting pancreatic beta-cells from injury or death might be crucial in the treatment of diabetes. This narrative review will update evidence from the recently identified molecular regulators preserving beta-cell mass and function recovery in order to suggest potential therapeutic targets against diabetes. This review will also highlight the relevance for novel molecular pathways potentially improving beta-cell dysfunction.