Inhibition of myostatin signaling increases glucose in insulin-deficient diabetic mice

Background Myostatin (MSTN), a TGF-b superfamily member, is a negative regulator of muscle mass that plays an important role in metabolism. Mstn KO mice have increased muscle mass, reduced adipose mass and improved insulin sensitivity. We have recently shown that MSTN inhibition in muscle prevents the development of diabetes in a mouse model of lipodystrophy. Whether inhibition of MSTN in a type I diabetes model would improve hyperglycemia is unknown.