4.2 Article

Increasing muscle mass to improve metabolism

期刊

ADIPOCYTE
卷 2, 期 2, 页码 92-98

出版社

TAYLOR & FRANCIS INC
DOI: 10.4161/adip.22500

关键词

myostatin; lipodystrophy; muscle hypertrophy; hyperphagia; diabetes; insulin resistance; leptin; adipose tissue; skeletal muscle; food intake

资金

  1. Intramural Research Program of the NIH
  2. NIDDK
  3. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [ZICDK070002, ZIADK075048] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Skeletal muscle insulin resistance is a predictor of the development of type 2 diabetes and maintenance of adequate muscle glucose disposal in muscle may help to prevent diabetes. Lipodystrophy is a type of diabetes caused by a reduction of white adipose tissue and the adipokine leptin. Lipidemia, insulin resistance and hyperphagia develop as a consequence. In a recent study, we showed that increasing skeletal muscle mass by inhibiting signaling of myostatin, a transforming growth factor beta (TGF beta) family member that negatively regulates muscle growth, prevents the development of diabetes in a mouse model of lipodystrophy. Muscle-specific myostatin inhibition also prevented hyperphagia suggesting muscle may regulate food intake. Here we discuss these results in the context of strategies to increase muscle insulin sensitivity as well as new findings about the effects of myostatin and other TGF beta family members on similar metabolic processes.

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