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Physiol. Genomics 33: 333-340, 2008. First published March 18, 2008; doi:10.1152/physiolgenomics.00226.2007
1094-8341/08 $8.00
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Received 28 September 2007; accepted in final form 12 March 2008.
Physiological Genomics 33:333-340 (2008)
1094-8341/08 $8.00 © 2008 American Physiological Society

Uncoupling protein 1 expression in murine skeletal muscle increases AMPK activation, glucose turnover, and insulin sensitivity in vivo

Susanne Neschen *, Yvonne Katterle *, Julia Richter , Robert Augustin , Stephan Scherneck , Farshad Mirhashemi , Annette Schürmann , Hans-Georg Joost and Susanne Klaus

Department of Pharmacology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany

Uncoupling of oxidative phosphorylation represents a potential target for the treatment of hyperglycemia and insulin resistance in obesity and type 2 diabetes. The present study investigated whether the expression of uncoupling protein 1 in skeletal muscles of transgenic (mUCP1 TG) mice modulates insulin action in major insulin target tissues in vivo. Euglycemic-hyperinsulinemic clamps (17 pM·kg lean body mass–1·min–1) were performed in 9-mo-old hemizygous male mUCP1 TG mice and wild-type (WT) littermates matched for body composition. mUCP1 TG mice exhibited fasting hypoglycemia and hypoinsulinemia compared with WT mice, whereas fasting hepatic glucose production rates were comparable in both genotypes. mUCP1 TG mice were markedly more sensitive to insulin action compared with WT mice and displayed threefold higher glucose infusion rates, enhanced skeletal muscle and white adipose tissue glucose uptake, and whole body glycolysis rates. In the absence of alterations in plasma adiponectin concentrations, acceleration of insulin-stimulated glucose turnover in skeletal muscle of mUCP1 TG mice was accompanied by increased phosphorylated Akt-to-Akt and phosphorylated AMP-activated protein kinase (AMPK)-to-AMPK ratios compared with WT mice. UCP1-mediated uncoupling of oxidative phosphorylation in skeletal muscle was paralleled by AMPK activation and thereby stimulated insulin-mediated glucose uptake in skeletal muscle.

euglycemic-hyperinsulinemic clamp; glycolysis; lactate; white adipose tissue; triacylglycerol; adiponectin




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