Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control

• Published in: Scientific reports Vol. 11; no. 1; pp. 19116 - 12
• Main Authors: Zhang, Wenliang, You, Baiyang, Qi, Dake, Qiu, Ling, Ripley-Gonzalez, Jeffrey W., Zheng, Fan, Fu, Siqian, Li, Cui, Dun, Yaoshan, Liu, Suixin
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 27.09.2021; Nature Publishing Group; Nature Portfolio
• Subjects: 692/163; 692/308/153; 692/308/2778; Animal models; Animals; Atrophy; Cell culture; Cell Line; Combined Modality Therapy; Diet; Diet, High-Fat - adverse effects; Disease Models, Animal; High fat diet; Humanities and Social Sciences; Humans; Lipid Metabolism - drug effects; Lipid peroxidation; Male; Metabolism; Mice; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; multidisciplinary; Muscle, Skeletal - drug effects; Muscle, Skeletal - metabolism; Muscle, Skeletal - physiopathology; Muscular Atrophy - etiology; Muscular Atrophy - metabolism; Muscular Atrophy - physiopathology; Muscular Atrophy - therapy; Musculoskeletal system; Myoblasts; Obesity; Obesity - etiology; Obesity - metabolism; Obesity - therapy; Oxidation; Oxidation-Reduction; Palmitic acid; Palmitic Acid - toxicity; Physical Conditioning, Animal; Quality control; Science; Science (multidisciplinary); Skeletal muscle; Trimetazidine; Trimetazidine - pharmacology; Trimetazidine - therapeutic use

Obesity induces skeletal muscle dysfunction. The pathogenesis of which appears to substantially involve mitochondrial dysfunction, arising from impaired quality control. Exercise is a major therapeutic strategy against muscle dysfunction. Trimetazidine, a partial inhibitor of lipid oxidation, has be...