Abstract
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
Current Pharmaceutical Design
Title: Oxidative Stress and Mitochondrial Dysfunction in Type 2 Diabetes
Volume: 17 Issue: 36
Author(s): Victor M. Victor, Milagros Rocha, Raul Herance and Antonio Hernandez-Mijares
Affiliation:
Keywords: Diabetes, mitochondria, oxidative stress, reactive oxygen species, insulin signaling pathway, vitamin C, vitamin E, autophagy, redox potential, transition metal ions
Abstract: 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.
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Cite this article as:
M. Victor Victor, Rocha Milagros, Herance Raul and Hernandez-Mijares Antonio, Oxidative Stress and Mitochondrial Dysfunction in Type 2 Diabetes, Current Pharmaceutical Design 2011; 17 (36) . https://dx.doi.org/10.2174/138161211798764915
DOI https://dx.doi.org/10.2174/138161211798764915 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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