The effect of T3 and reverse T3 administration on muscle protein catabolism during fasting as measured by 3-methylhistidine excretion

Since recent studies have indicated that measurement in urine of the amino acid, 3-methylhistidine, accurately reflects the extent of muscle catabolism, and because it has been suggested that thyroid hormones may influence muscle breakdown, especially during fasting, the effect of T3 and reverse T3 (rT3) administration on the excretion of 3-methylhistidine was examined in obese subjects during fasting. The mean (± SE) 3-methylhistidine excretion in patients fed an egg protein diet (devoid of meat protein) was 256 ± 35 μmoles/day and decreased to 190 ± 14 μmoles/day during fasting. T3 administration (100 μg/day × 5 days) increased 3-methylhistidine excretion to 304 ± 37 μmoles/day during its ingestion and to 485 ± 46 μmoles/day in the T3 posttreatment interval. T3 doses of 10 μg every 4 hr (q4h) for the first 6 days of fasting also appeared capable of increasing 3-mehis excretion whereas 5 μg T3 q4h administered during the first 6 days of fasting did not increase 3-mehis excretion. Reverse T3 administration (80 μg q6h) during fasting was associated with a mean 3-methylhistidine of 130 ± 13 μmoles/day, a value no higher than in patients fasted alone. These observations suggest that: (1) skeletal muscle catabolism decreases during fasting; and (2) pathophysiologic doses of T3 (60 μg/day or more), but not reverse T3, enhance muscle catabolism during fasting.