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Current Pharmaceutical Design


ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Oxidative Stress and Mitochondrial Dysfunction in Type 2 Diabetes

Author(s): Victor M. Victor, Milagros Rocha, Raul Herance and Antonio Hernandez-Mijares

Volume 17, Issue 36, 2011

Page: [3947 - 3958] Pages: 12

DOI: 10.2174/138161211798764915

Price: $65


Diabetes is a chronic disease and, as a consequence of the overproduction of reactive oxygen species (ROS), is related with oxidative stress. There are different sources of ROS, of which mitochondria is the main one. Oxidative stress seems to play an important role in mitochondria- mediated disease processes, though the exact molecular mechanisms responsible remain elusive. There are evidences which supports the idea that impaired mitochondrial function is a cause of the insulin insensitivity in different type of cells that arised as a result of an insufficient supply of energy or defects in the insulin signaling pathway. ROS are generally necessary for the proper functioning of the cell, but excessive ROS production can be harmful, which makes antioxidant defenses essential. Moreover, some substances with antioxidant properties, such as vitamin C or vitamin E, erradicate the oxidative stress associated with diabetes. The results of clinical trials employing anti-oxidative stress reagents in patients with diabetes are contradictory, which may be a result of inadequate study design or selected targets. This review considers the process of diabetes from a mitochondrial perspective, and describes the role of autophagy in the development of diabetes. Furthermore, we discuss the possible beneficial effects of selectively targeting antioxidants to mitochondria as a strategy for modulating mitochondrial function in diabetes.

Keywords: Diabetes, mitochondria, oxidative stress, reactive oxygen species, insulin signaling pathway, vitamin C, vitamin E, autophagy, redox potential, transition metal ions

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