Morris G S, Surdyka D G, Haddad F, Baldwin K M
Department of Physiology and Biophysics, University of California, Irvine 92717.
Am J Physiol. 1990 Feb;258(2 Pt 2):R346-51. doi: 10.1152/ajpregu.1990.258.2.R346.
In addition to thyroid hormone, carbohydrate oxidation appears to influence the relative distribution of rodent cardiac isomyosin (V1, V2, V3), especially in diabetic, thyroid-deficient, and food-restricted animals. To determine whether metabolic variations within the myocardium itself contribute to cardiac isomyosin distribution, food-restricted rats (predominantly V3) were treated with oxfenicine, a cardiospecific inhibitor of fatty acid metabolism. Animals received a mixed diet (50% carbohydrates) ad libitum (FE-M) or in restricted quantities (45% of FE-M; FR-M). Additional food-restricted animals received oxfenicine (75 mg/kg, twice daily) and either a mixed diet (FR-M-OXF) or a high-carbohydrate diet (75% carbohydrates, FR-HC-OXF). After 3 wk, hemodynamic and metabolic measurements were taken, serum 3,5,3'-triiodothyronine (T3) levels were measured, and cardiac citrate synthase (CS) activity and isomyosin distribution (percent V1, V2, V3) was determined. Relative to the FE-M group, thyroid status (CS, T3) was reduced only in the FR-M-OXF and the FR-HC-OXF groups (P less than 0.05). Oxfenicine treatment of food-restricted animals partially preserved the isomyosin profile of the FE-M group (P less than 0.05), suggesting that, within the context of food restriction, cardiac metabolism can influence cardiac isomyosin distribution independently of thyroid status.
