ABSTRACT
The direct effects of L-and D-triiodothyronine (T3) on cardiac protein metabolism were investigated using fetal mouse hearts in organ culture. This model allowed the production of "thyrotoxicosis" in isolated hearts in vitro in the absence of the usual systemic metabolic and hemodynamic effects of thyroid hormones. Hearts were studied during the first 24 h of T3 exposure in culture, before changes in beating rate due to T3 occurred. Phenylalanine release was decreased by 26 +/- 2.3% (P less than 0.001) by the optimal concentrations of T3 (10(-7) to 10(-6) M). Changes were similar in the presence or absence of insulin. D-T3 was also anabolic, decreasing phenylalanine release by 24 +/- 2.5% (P less than 0.001) at concentrations of 10(-6) to 10(-5) M. The L-isomer increased protein synthesis by 23 +/- 6.8% (P less than 0.05) and decreased protein degradation, as measured by phenylalanine release in the presence of cycloheximide, by 5 +/- 1.6% (P less than 0.01). The D-isomer also increased protein synthesis but had no measurable effect on protein degradation. We conclude that thyroid hormones can exert direct anabolic effects on heart in the absence of systemic hemodynamic and metabolic changes. These effects are mediated primarily through an acceleration of the rate of protein synthesis; in the case of L-T3, a small inhibition of proteolysis may also occur.
