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Comparison of the Effect of a Protein-Free and Restricted High Protein—Low Carbohydrate Diet on Ventricular Myosin ATPase Activity and Isomyosin Profile in Young Rats: Evidence That Protein-Depleted Animals Are Euthyroid1

William J. Carter, Fred H. Faas, Carol A. Perry and Mary E. Lynch

Veterans Administration Medical Center and Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205

Young rats fed a protein-deficient diet have elevated total triiodothyronine (T3) levels in spite of decreased skeletal muscle protein turnover. Interpretation of the thyroid status of these animals is complicated by increased T3 binding by serum proteins. Free T3 levels ranging from normal to low and decreased resting oxygen consumption have been reported. To investigate the thyroid status of animals fed a protein-free diet, ventricular myosin ATPase activity and isomyosin profile have been used as an index of thyroid hormone activity. The effect of the protein-free diet has been compared to a restricted high protein-low carbohydrate diet, which causes clear evidence of decreased thyroid hormone effect. After 28 d, calcium-activated myosin ATPase activity was 1.50 ± 0.05 µmol P1/(mg protein · min) in animals fed the basal diet, 1.16 ± 0.03 µmol P1/ (mg protein · min) in animals fed the restricted high protein-low carbohydrate diet and 1.48 ± 0.04 µmol P1/(mg protein · min) in animals fed the protein-free diet. In addition, a shift in isomyosin content with the appearance of V2 and V3 isomyosins occurred with the restricted high protein-low carbohydrate diet but not the protein-free diet. The failure of the protein-depleted rats to decrease myosin ATPase activity and alter isomyosin content suggests that they are euthyroid.


KEY WORDS: • protein deficiency • thyroid status • ventricular isomyosin • ventricular myosin ATPase activity

1 This work was supported by Veterans Administration Research funds, Project No. 430-66-8721-0002, and by the National Institutes of Health, Grant No. 2-R01-AM20718-08.

Manuscript received 3 April 1987. Revision accepted 31 August 1987.







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