Myosin isoenzyme expression in rat ventricle: effects of thyroid hormone analogs, catecholamines, glucocorticoids and high carbohydrate diet.

The effects on ventricular myosin isoenzyme expression of naturally occurring and synthetic thyroid analogs (3,5,3'-L-triiodothyronine, 3,5,3'-D-triiodothyronine, 3,3',5'-L- triiodothyronine , 3,5,3'-L-triiodothyroacetic acid and 3,5-L-diiodothyronine), catecholamines and high carbohydrate diets have been studied in thyroidectomized and hypophysectomized rats. Also, the effects on myosin isoenzyme expression of adrenalectomy and hydrocortisone replacement have been studied in euthyroid animals. Myocardial CO2 production and hepatic alpha-glycerolphosphate dehydrogenase activity were measured to monitor the effects of these interventions on tissue respiration. The results indicate that there was no significant separation between the actions of thyroid analogs on metabolic parameters and myosin isoenzyme patterns. However, high carbohydrate feeding in hypophysectomized rats increased the isoenzyme V1 from 12% to about 36% of total myosin; partial replacement with 3,5,3'-L-triiodothyronine and fructose feeding had synergistic actions. In thyroidectomized rats, feeding a high carbohydrate diet increased the V1 form from undetectable levels to about 28% of total myosin; partial 3,5,3'-L-triiodothyronine replacement had an additive effect. Beta adrenergic stimulation with isoproterenol and blockade with propranolol did not affect myosin isoenzyme expression. Adrenalectomy in euthyroid rats caused a 33% decrease in the V1 form and a corresponding increase in the V3 isoenzyme, which could be reversed by treatment with hydrocortisone. Thus, thyroid analogs do not selectively stimulate myosin isoenzyme expression as compared with their effects on energy production. Furthermore, the results suggest that the mechanism for regulation of cardiac myosin isoenzymes may involve a primary signal related to dietary carbohydrate, which is modulated by thyroid hormone, and possibly glucocorticoids.