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Reactive Oxygen Species Enhance Insulin Sensitivity

Loh, Ki and Deng, Haiyang and Fukushima, Atsushi and Cai, Xiaochu and Boivin, Benoit and Galic, Sandra and Bruce, Clinton and Shields, Benjamin J and Skiba, Beata and Ooms, Lisa M and Stepto, Nigel and Wu, Ben and Mitchell, Christina and Tonks, Nicholas K and Watt, Matthew J and Febbraio, Mark A and Crack, Peter J and Andrikopoulos, Sofianos and Tiganis, Tony (2009) Reactive Oxygen Species Enhance Insulin Sensitivity. Cell Metabolism, 10 (4). pp. 260-272. ISSN 1550-4131

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Abstract

Chronic reactive oxygen species (ROS) production by mitochondria may contribute to the development of insulin resistance, a primary feature of type 2 diabetes. In recent years it has become apparent that ROS generation in response to physiological stimuli such as insulin may also facilitate signaling by reversibly oxidizing and inhibiting protein tyrosine phosphatases (PTPs). Here we report that mice lacking one of the key enzymes involved in the elimination of physiological ROS, glutathione peroxidase 1 (Gpx1), were protected from high-fat-diet-induced insulin resistance. The increased insulin sensitivity in Gpx1−/− mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the antioxidant N-acetylcysteine. Increased insulin signaling correlated with enhanced oxidation of the PTP family member PTEN, which terminates signals generated by phosphatidylinositol-3-kinase. These studies provide causal evidence for the enhancement of insulin signaling by ROS in vivo.

Item Type: Article
Uncontrolled Keywords: ResPubID18211, human disease, reactive oxygen species, insulin sensitivity
Subjects: Faculty/School/Research Centre/Department > Centre for Ageing, Rehabilitation, Exercise & Sport Science (CARES)
FOR Classification > 1101 Medical Biochemistry and Metabolomics
SEO Classification > 970111 Expanding Knowledge in the Medical and Health Sciences
Depositing User: VUIR
Date Deposited: 03 May 2012 05:25
Last Modified: 04 Feb 2015 06:02
URI: http://vuir.vu.edu.au/id/eprint/4434
DOI: 10.1016/j.cmet.2009.08.009
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Citations in Scopus: 177 - View on Scopus

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