Metabolic effects of mitochondrial uncoupling in murine skeletal muscle: Essential role of AMP-activated protein kinase in metabolic improvements of UCP1-transgenic mice?

Abstract

Background and aim: Altering the efficiency of mitochondrial respiration may represent an attractive target for the treatment of obesity as well as related disorders. Transgenic (UCP1-TG) mice with ectopic expression of UCP1 in skeletal muscle (SM) show a phenotype of increased energy expenditure and improved glucose tolerance counteracting most of the detrimental effects of high fat diet. We could show an increased AMPK phosphorylation in SM of UCP1-TG mice, likely due to the energy depletion through uncoupling by UCP1. However, the full molecular mechanisms leading to the ameliorated metabolic phenotype of UCP1-TG mice are still not known. The aim of this study was to investigate the potential role of skeletal muscle AMPK activation in the healthy metabolic phenotype of UCP1-TG mice.