Mitochondrial uncoupling attenuates sarcopenic obesity by enhancing skeletal muscle mitophagy and quality control

Authors
WS Dantas, ERM Zunica, EC Heintz et al

Lab
Pennington Biomedical Research Center, Baton Rouge, LA, USA

Journal
Journal of Cachexia, Sarcopenia and Muscle

Abstract
Sarcopenic obesity is a highly prevalent disease with poor survival and ineffective medical interventions. Mitochondrial dysfunction is purported to be central in the pathogenesis of sarcopenic obesity by impairing both organelle biogenesis and quality control. We have previously identified that a mitochondrial-targeted furazano[3,4-b]pyrazine named BAM15 is orally available and selectively lowers respiratory coupling efficiency and protects against diet-induced obesity in mice. Here, we tested the hypothesis that mitochondrial uncoupling simultaneously attenuates loss of muscle function and weight gain in a mouse model of sarcopenic obesity.

BIOSEB Instruments Used:
Grip strength test (BIO-GS3)