Triiodothyronine decreases the accumulation of 1,2-diacylglycerol in rat hearts.

1,2-Diacylglycerol (DAG) is an intracellular signal mediator that may initiate protein synthesis and cardiac hypertrophy via activation of protein kinase C. The amounts of 1,2-DAG and its fatty acid components in the myocardium was assessed and compared with the concentrations of RNA and DNA in cardiac hypertrophy induced by administering triiodothyronine (T3) with and without cycloheximide, an inhibitor of protein synthesis. After the first injection of T3 no cardiac hypertrophy was observed, and there were no differences in myocardial 1,2-DAG content or in RNA and DNA concentrations. Cardiac hypertrophy was present on days 3 and 7 after a daily injection of T3. Myocardial RNA concentration was increased by 26% on day 3 and by 34% on day 7, whereas the myocardial 1,2-DAG content was decreased by 8% on day 3 and by 24% on day 7. Pretreatment with cycloheximide of T3-treated rats prevented the development of cardiac hypertrophy, but elevated the RNA concentration and lowered the 1,2-DAG content compared with the findings in T3-treated rats. Analysis of the fatty acid components of 1,2-DAG revealed that the amounts of 16:0, 18:1 and 18:2 were decreased, accompanied by an elevation of RNA concentration and a decrease in 1,2-DAG content. It seems that RNA synthesis preceded the alteration in 1,2-DAG. These findings suggest that 1,2-DAG is not involved in the initiation of cardiac hypertrophy induced by T3, but is affected by the enhanced concentration of RNA resulting from the introduction of thyroid hormones into the myocardium.