Endocrine Abstracts

Brown adipose tissue (BAT) and skeletal muscle are play vital roles in the regulation of thermogenesis. In addition to thermogenesis through muscle activity, heat can be produced by non-shivering thermogenesis of BAT to produce heat. The heat production of BAT is dependent on the activity of uncoupling protein 1 (UCP1), which generates heat by dissipating the mitochondrial proton gradient. Recent studies suggested that UCP1 deficiency might cause the compensatory thermogenesis in the skeletal muscle. However, the changes of development and function of skeletal muscle in UCP-1 knockout mice in vivo is not clear. Furthermore, whether the BAT UCP1 expression can affect development of skeletal muscle in vitro is need to be elucidated. Results of our study showed that the gastrocnemius weight in skeletal muscle and cross-sectional area of muscle fiber from UCP1 knockout mice was significantly decreased compared with that from wild-type mice. Compared control conditioned-medium derived from control WT-1 brown adipocytes, decreased expression of myosin heavy chain (MHC) and increased expressions of atrophy markers, such as atrogin-1, MuRF-1 and myostatin, were found in C2C12 myotubes treated with conditioned-medium derived from UCP1-knockdown WT-1 brown adipocytes. In conclusion, UCP1 deficiency in BAT might cause skeletal muscle atrophy via upregulating atrogin-1, MuRF-1 and myostatin.