Communication between skeletal muscle and adipose tissues by myostatin

肌肉生长抑素是转化生长因子-β超家族成员之一，调节骨骼肌量。它还调节脂肪组织质量和动态平衡。我们设计了阻断肌肉抑制素功能的方法，并研制出了高肌肉型转基因小鼠。通过使用该模型，我们已经表明，肌肉生长抑素抑制的小鼠的脂肪组织并没有因为线粒体数量的增加而表现出肥大。高脂饮食诱导的脂肪肝可以通过抑制肌肉抑制素来预防，这主要是通过阻断骨骼肌中的肌肉生长抑素信号来实现的。高脂饮食小鼠肝脏脂肪酸组成与野生型和肌肉生长抑素抑制小鼠不同。我们还发现，几种miRNAs的表达被肌肉抑制素刺激和/或抑制而改变，这可能与肌肉抑制素调节肌肉的动态平衡和脂肪细胞的生长和周转有关。

Myostatin, one of the TGF-β superfamily member, regulates skeletal muscle mass. It also regulates adipose tissue mass and homeostasis. We have devised the method to block myostatin function, and developed hypermuscular transgenic mice. By using the model, we have shown that adipose tissue in myostatin inhibited mice did not show hypertrophy due to increased numbers of mitochondria. Fatty liver induced by high fat diet feeding was prevented by myostatin inhibition, primarily due to blockade of myostatin signaling in skeletal muscle. Fatty acid composition in liver by high fat diet was different between wildtype and myostatin inhibited mice. We also discovered that expression of several miRNAs is altered by myostatin stimulaton and/or inhibition, which could be responsible for actions of myostatin in regulating muscle homeostasis and dynamics of adipocyte growth and turnover.