Study for regulatory mechanism for atrophy of tongue and masticatory muscles by the system of model mouse

在本研究中获得了以下新发现1。结论：1.舌肌发生的调控程序与四肢肌发生的调控程序相似，但头部肌发生的调控程序不同。与其他肌肉相比，咀嚼肌的肌肉发生和突触发生延迟，甚至在出生时也没有完成，而舌肌的发育速度比其他肌肉快，在出生前后结束。胰岛素样生长因子及其受体和结合蛋白参与了硬性饮食向软性饮食转变所致的小鼠咬肌萎缩。咬肌卫星细胞池大小大于其他肌肉如腓肠肌、比目鱼肌和横隔肌，池大小是决定肌纤维变性程度的因素之一。转化生长因子β_8和肌肉生长抑制素对β_2肾上腺素能激动剂克伦特罗诱导的肥大起负调节作用，而胰岛素样生长因子则起正调节作用。

The following new findings were obtained in the present study.1. The regulatory program for myogenesis of tongue is similar to that for limb myogenesis other than head myogenesis.2. Myogenesis and synaptogenesis in the masticatory muscles are delayed in comparison with other muscles and are not completed even at birth, whereas the development of tongue muscles proceeds faster than those of other muscles and ends at around birth.3. Insulin-like growth factors, their receptors and binding proteins are involved in the atrophy of mouse masseter muscle induced by the transition from hard to soft diets.4. The pool size of satellite cells in the masseter muscle is greater than those in other muscles such as gastrocnemius, soleus and diaphragm muscles of mdx mouse and the pool size is one factor for determining the extent of myofiber degeneration.5. Transforming growth factor β_8 and myostatin function as negative regulators for the hypertrophy induced by clenbuterol, a β_2 adrenergic agonist, whereas Insulin-like growth factors work as positive regulators.