Feb 16, 2016

Loss of Muscle MTCH2 Increases Whole-Body Energy Utilization and Protects from Diet-Induced Obesity

Cell Reports
Liat Buzaglo-AzrielAtan Gross

Abstract

Mitochondrial carrier homolog 2 (MTCH2) is a repressor of mitochondrial oxidative phosphorylation (OXPHOS), and its locus is associated with increased BMI in humans. Here, we demonstrate that mice deficient in muscle MTCH2 are protected from diet-induced obesity and hyperinsulinemia and that they demonstrate increased energy expenditure. Deletion of muscle MTCH2 also increases mitochondrial OXPHOS and mass, triggers conversion from glycolytic to oxidative fibers, increases capacity for endurance exercise, and increases heart function. Moreover, metabolic profiling of mice deficient in muscle MTCH2 reveals a preference for carbohydrate utilization and an increase in mitochondria and glycolytic flux in muscles. Thus, MTCH2 is a critical player in muscle biology, modulating metabolism and mitochondria mass as well as impacting whole-body energy homeostasis.

Mentioned in this Paper

Mitochondrial Membrane Transport Proteins
Metabolic Process, Cellular
MTCH2 gene
Diet
Transcription Repressor/Corepressor
Whole Body Imaging
Energy Metabolism
Gene Deletion Abnormality
Gene Deletion
Soleus Muscle Structure

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