Interaction of thyroid status and diet on muscle protein breakdown in the rat, as measured by N tau-methylhistidine excretion
- PMID: 7242372
- DOI: 10.1016/0026-0495(81)90083-4
Interaction of thyroid status and diet on muscle protein breakdown in the rat, as measured by N tau-methylhistidine excretion
Abstract
The effects of thyroid status and of dietary protein and energy content on muscle protein breakdown have been compared in young rats, using urinary N tau-methylhistidine (3-methylhistidine; 3-Mehis) output as a measure of myofibrillar protein breakdown. Recently, thyroidectomized young rats receiving an adequate diet grew slowly and showed a reduction in 3-Mehis output, relative to the weight of their leg muscles. When the thyroidectomized rats were given 2-5 microgram thyroxine (T4) per 100 g body weight, output of 3-Mehis increased, even when growth was prevented by feeding a diet low in protein. This demonstrates that thyroid-status affects muscle protein breakdown through a mechanism other than via a change in growth rate. In confirmation of previous studies, administration of a diet low in protein to young rats prevented growth and reduced output of 3-Mehis relative to leg muscle weight. The reduction in protein breakdown is not likely to be due to reduced thyroid function, since the diet low in protein increased plasma total triiodothyronine (T3) levels. Furthermore, thyroidectomized rats fed the low-protein diet also underwent a decrease in output of 3-Mehis. In contrast to protein deficiency, a moderate dietary energy deficiency allowed some growth to occur, and output of 3-Mehis, relative to muscle mass, was not depressed. Nevertheless, total T3 concentration in the plasma of these animals was considerably reduced, indicating once more that total circulating thyroid hormone levels are not the only determinants of muscle protein breakdown. Finally, reduced plasma total T3 levels occurred in energy-deficient diets even in thyroidectomized rats receiving exogenous T4. This suggests that diet affects metabolism of the hormone independently of changes in secretory output from the thyroid gland.
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