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Does skeletal muscle oxidative stress initiate insulin resistance in genetically predisposed individuals?
- Source :
-
Trends in endocrinology and metabolism: TEM [Trends Endocrinol Metab] 2010 Feb; Vol. 21 (2), pp. 83-8. Date of Electronic Publication: 2009 Oct 23. - Publication Year :
- 2010
-
Abstract
- Reactive oxygen species (ROS) are postulated to be a common trigger of insulin resistance. For example, treatment of adipocytes with either tumor-necrosis factor-alpha or dexamethasone increases ROS before impairing glucose uptake. Similarly, treatment with mitochondria-specific antioxidants preserves insulin sensitivity in animal models of insulin resistance. However, it remains unclear whether ROS contribute to insulin resistance in humans. First-degree relatives (FDRs) of type 2 diabetes subjects are at increased risk of developing insulin resistance and type 2 diabetes. Here we review the documented metabolic impairments in FDRs that could contribute to insulin resistance via increased oxidative stress. We propose that lipotoxic intermediates and lipid peroxides in skeletal muscle interfere with insulin signaling and might cause insulin resistance in these 'at risk' individuals.<br /> (Copyright (c) 2009 Elsevier Ltd. All rights reserved.)
- Subjects :
- Animals
Diabetes Mellitus, Type 2 genetics
Disease Models, Animal
Family
Humans
Lipid Metabolism genetics
Lipid Metabolism physiology
Models, Biological
Muscle, Skeletal physiology
Oxidative Stress genetics
Prediabetic State genetics
Prediabetic State metabolism
Genetic Predisposition to Disease
Insulin Resistance genetics
Muscle, Skeletal metabolism
Oxidative Stress physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1879-3061
- Volume :
- 21
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Trends in endocrinology and metabolism: TEM
- Publication Type :
- Academic Journal
- Accession number :
- 19854062
- Full Text :
- https://doi.org/10.1016/j.tem.2009.09.008