Journal article
Reactive Oxygen Species Enhance Insulin Sensitivity
K Loh, H Deng, A Fukushima, X Cai, B Boivin, S Galic, C Bruce, BJ Shields, B Skiba, LM Ooms, N Stepto, B Wu, CA Mitchell, NK Tonks, MJ Watt, MA Febbraio, PJ Crack, S Andrikopoulos, T Tiganis
Cell Metabolism | CELL PRESS | Published : 2009
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 si..
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Awarded by National Institutes of Health
Funding Acknowledgements
We thank Christine Yang, Moses Zhang, Teresa Tiganis, Debbie Lane, Amy Blair, Ray Spark, Robert Southgate, and Ian Harper for technical support. This work was supported by the National Health and Medical Research Council (NH&MRC) of Australia (to T.T., M.A.F., P.J.C., S.A., M.J.W., and C.A.M.), Diabetes Australia Research Trust (to T.T.), and the National Institutes of Health (NIH) (to N.K.T.; CA53840, GM55989). C.B., M.J.W., M.A.F., and T.T. are NH&MRC research fellows.