Yong Zhang
Tianjin University of Sport, China
Posters-Accepted Abstracts: J Diabetes Metab
Impaired mitochondrial function was relative to Insulin Resistance (IR) and the chronic exercise training can improve insulin sensitivity, but the underlying mechanisms are obscure. Here we report the unbalanced mitochondrial dynamics in fusion and fission in high-fat-diet induced muscular IR and its mediation through chronic exercise training. We used high-fat-diet to create IR mice models and followed the intervention of exercise training. We found that the expression of mitochondrial fusion proteins decreased and fission proteins increased. The number and size of mitochondria decreased, too. The skeletal muscle mitochondria of IR mice showed decreased biogenesis, inclined to fission and dysfunction. Take together with the fact we found that the glucose uptake and mitochondrial respiratory function declined in cultured muscle cells which incubated with Drp1 inhibitor. It suggested that the disturbed balance between fusion and fission of skeletal muscle mitochondrial may involve in the pathogenesis of IR. The skeletal muscle mitochondria in IR mice committed aerobic training showed enhanced respiratory function and ATP synthesis activity. Both of the mitochondrial fusion and fission protein expression increased. The data demonstrated that the chronic aerobic exercise could enhanced muscular insulin sensibility and reversed high-fat-diet induced IR through increasing mitochondrial oxidative phosphorylation. The chronic exercise-induced remodeled balance of mitochondrial dynamics in fusion and fission may contribute to the mechanism against insulin resistance.
Email: yzhangtipe@126.com
