Carter W J, Benjamin W S, Faas F H
Biochem J. 1982 Apr 15;204(1):69-74. doi: 10.1042/bj2040069.
The effect of T3 (3,3',5-tri-iodothyronine) on protein turnover in skeletal and cardiac muscle was measured in intact rats by means of a 6 h [14C]tyrosine-infusion technique. Treatment with 25-30 micrograms of T3/100 g body wt. daily for 4-7 days increased the fractional rate of protein synthesis in skeletal muscle. Since the fractional growth rate of the muscle was decreased or unchanged, T3 treatment increased the rate of muscle protein breakdown. These findings suggest that increased protein degradation is an important factor in decreasing skeletal-muscle mass in hyperthyroidism. In contrast with skeletal muscle, T3 treatment for 7 days caused an equivalent increase in the rate of cardiac muscle growth and protein synthesis. This suggests that hyperthyroidism does not increase protein breakdown in heart muscle as it does in skeletal muscle. The failure of T3 to increase proteolysis in heart muscle may be due to a different action on the cardiac myocyte or to systemic effects of T3 which increase cardiac work.
通过6小时的[14C]酪氨酸输注技术，在完整大鼠中测量了三碘甲状腺原氨酸（T3）对骨骼肌和心肌蛋白质周转的影响。以每天25 - 30微克T3/100克体重的剂量处理4 - 7天，可提高骨骼肌中蛋白质合成的分数率。由于肌肉的分数生长率降低或未改变，T3处理增加了肌肉蛋白质分解的速率。这些发现表明，蛋白质降解增加是甲状腺功能亢进症中骨骼肌质量下降的一个重要因素。与骨骼肌相反，T3处理7天导致心肌生长速率和蛋白质合成速率同等增加。这表明甲状腺功能亢进症不会像在骨骼肌中那样增加心肌中的蛋白质分解。T3未能增加心肌中的蛋白水解作用，可能是由于其对心肌细胞的不同作用，或者是由于T3的全身效应增加了心脏做功。
