Porcine mesenchymal stem cells in postnatal muscle have been demonstrated to differentiate into adipocytes. This increases adipocyte number and lipid accumulation, and is thought to be the origin of intramuscular fat....Porcine mesenchymal stem cells in postnatal muscle have been demonstrated to differentiate into adipocytes. This increases adipocyte number and lipid accumulation, and is thought to be the origin of intramuscular fat. In this study, the effects of myostatin and arginine on adipogenic differentiation in mesenchymal stem cells derived from porcine muscle （pMDSCs） were investigated in vitro. Intracellular triglyceride levels were reduced by exogenous myostatin and increased by arginine supplementation or myostatin antibody （P〈0.01）. The inhibition of lipid accumulation by rnyostatin in pMDSCs was alleviated by arginine supplementation （P〈0.01）. Expression patterns of adipogenic transcription factors showed that exogenous myostatin suppressed PPAR72 and aP2 expression （P〈0.01）, while supplemental arginine or myostatin antibody promoted ADD1 expression （P〈0.01）. Furthermore, compared with the addition of either myostatin protein or antibody alone, ADD1 and PPARδ expression were promoted by the combination of arginine and myostatin （P〈0.01）, and arginine combined with myostatin antibody promoted the expression of ADD1, PPARδ, C/EBPα, PPARγ2 and LPL in pMDSCs （P〈0.05）. These results suggest that myostatin inhibits adipogenesis in pMDSCs, and that this can be alleviated by arginine supplementation, at least in part, through promoting ADD1 and PPARδ expression.展开更多
基金supported by the National Natural Science Foundation of China (Grant No.30972119)
文摘Porcine mesenchymal stem cells in postnatal muscle have been demonstrated to differentiate into adipocytes. This increases adipocyte number and lipid accumulation, and is thought to be the origin of intramuscular fat. In this study, the effects of myostatin and arginine on adipogenic differentiation in mesenchymal stem cells derived from porcine muscle （pMDSCs） were investigated in vitro. Intracellular triglyceride levels were reduced by exogenous myostatin and increased by arginine supplementation or myostatin antibody （P〈0.01）. The inhibition of lipid accumulation by rnyostatin in pMDSCs was alleviated by arginine supplementation （P〈0.01）. Expression patterns of adipogenic transcription factors showed that exogenous myostatin suppressed PPAR72 and aP2 expression （P〈0.01）, while supplemental arginine or myostatin antibody promoted ADD1 expression （P〈0.01）. Furthermore, compared with the addition of either myostatin protein or antibody alone, ADD1 and PPARδ expression were promoted by the combination of arginine and myostatin （P〈0.01）, and arginine combined with myostatin antibody promoted the expression of ADD1, PPARδ, C/EBPα, PPARγ2 and LPL in pMDSCs （P〈0.05）. These results suggest that myostatin inhibits adipogenesis in pMDSCs, and that this can be alleviated by arginine supplementation, at least in part, through promoting ADD1 and PPARδ expression.
