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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.
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