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Effect of T₃-induced hyperthyroidism on mitochondrial and cytoplasmic protein synthesis rates in oxidative and glycolytic tissues in rats

Endocrine Research Unit, Mayo Clinic College of Medicine, Rochester, Minnesota

Submitted 7 August 2006 ; accepted in final form 10 October 2006

Hyperthyroidism increases metabolic rate, mitochondrial ATP production, and protein synthesis, but it remains to be determined whether all tissues and synthesis of specific protein pools are equally affected by hyperthyroidism. Previous studies showed that mitochondrial function was less responsive to elevated triiodothyronine (T₃) levels in the low-oxidative plantaris muscle compared with other tissues in rats. We tested the hypothesis that in T₃-treated animals mitochondrial protein synthesis would increase in oxidative but not glycolytic tissues. Male rats received either T₃ (200 µg/day, n = 10) or saline (controls, n = 9) by subcutaneous pump for 14 days, and then in vivo protein synthesis rates were measured using [¹⁵N]phenylalanine in liver, heart, plantaris, and red gastrocnemius (Red Gast). Mitochondrial protein synthesis rate in T₃-treated rats was higher than in controls by 62% in Red Gast and plantaris and 89 and 115% in liver and heart, respectively (P < 0.01). Cytoplasmic protein synthesis rates in the T₃ group were 107–176% higher than control values (P < 0.01). There was also indirect evidence that protein breakdown was increased in all tissues of the T₃-treated rats. Phosphorylation of selected regulators of protein synthesis in plantaris and Red Gast (mTOR, p70 S6 kinase, 4E-BP1), however, were not significantly affected by T₃. We conclude that T₃ infusion stimulates a general increase in mitochondrial and cytoplasmic protein synthesis rate among tissues and that this does not appear to explain the tissue-specific responses in mitochondrial oxidative capacity.

protein metabolism; triiodothyronine; fractional synthesis rate; skeletal muscle