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Journal of Diabetes Research
Volume 2018 (2018), Article ID 9601801, 19 pages
Review Article

Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy

1Pulmonary and Critical Care Medicine Department, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
2Endocrine and Metabolic Research Center, University of Zulia, Maracaibo, Venezuela
3Grupo de Investigación Altos Estudios de Frontera (ALEF), Universidad Simón Bolívar, Cúcuta, Colombia
4Clinical Pharmacology Unit. School of Medicine José María Vargas, Central University of Venezuela, Caracas, Venezuela

Correspondence should be addressed to Juan Salazar

Received 15 August 2017; Revised 15 November 2017; Accepted 6 December 2017; Published 19 February 2018

Academic Editor: Lucy Marzban

Copyright © 2018 Joselyn Rojas 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.


Purpose of Review. Describing the diverse molecular mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus. Recent Findings. Beta cell death is the final event in a series of mechanisms that, up to date, have not been entirely clarified; it represents the pathophysiological mechanism in the natural history of diabetes mellitus. These mechanisms are not limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus. They also include the action of proinflammatory cytokines, the production of reactive oxygen species, DNA fragmentation (typical of necroptosis in type 1 diabetic patients), excessive production of islet amyloid polypeptide with the consequent endoplasmic reticulum stress, disruption in autophagy mechanisms, and protein complex formation, such as the inflammasome, capable of increasing oxidative stress produced by mitochondrial damage. Summary. Necroptosis, autophagy, and pyroptosis are molecular mechanisms that modulate the survival of the pancreatic beta cell, demonstrating the importance of the immune system in glucolipotoxicity processes and the potential role for immunometabolism as another component of what once known as the “ominous octet.”