Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/64530
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Type: Journal article
Title: Does skeletal muscle oxidative stress initiate insulin resistance in genetically predisposed individuals?
Author: Samocha-Bonet, D.
Heilbronn, L.
Lichtenberg, D.
Campbell, L.
Citation: Trends in Endocrinology and Metabolism, 2010; 21(2):83-88
Publisher: Elsevier Science London
Issue Date: 2010
ISSN: 1043-2760
1879-3061
Statement of
Responsibility: 
Dorit Samocha-Bonet, Leonie K. Heilbronn, Dov Lichtenberg and Lesley V. Campbell
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.
Keywords: Muscle, Skeletal; Animals; Humans; Diabetes Mellitus, Type 2; Prediabetic State; Insulin Resistance; Disease Models, Animal; Genetic Predisposition to Disease; Family; Oxidative Stress; Models, Biological; Lipid Metabolism
Rights: © 2009 Elsevier Ltd. All rights reserved.
RMID: 0020106400
DOI: 10.1016/j.tem.2009.09.008
Appears in Collections:Medicine publications

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