Diabetes results in myocardial functional alterations which are accompanied by a 
depression of biochemical parameters such as myosin ATPase and calcium uptake in 
the sarcoplasmic reticulum. Methyl palmoxirate, a fatty acid analog, is reported 
to decrease circulating glucose levels by inhibiting fatty acid metabolism, thus 
forcing carbohydrate utilization. In the present study, we attempted to prevent 
streptozotocin diabetes-induced myocardial alterations in the rat. Using the 
isolated working heart preparation, we observed a depression of myocardial 
function in rats 6 weeks after the induction of diabetes, which was 
characterized by the inability of these hearts to develop left ventricular 
pressures and rates of ventricular contraction and relaxation as well as control 
hearts at higher left atrial filling pressures. Methyl palmoxirate treatment (25 
mg kg-1 day-1 po daily) was unable to control diabetes-induced changes in plasma 
glucose, triglycerides, insulin, and total lipids. Also, the functional 
depression seen in diabetic rat hearts was present despite the treatment. 
However, depression of calcium uptake and elevation of long chain acyl 
carnitines seen in sarcoplasmic reticulum (SR) prepared from diabetic rat hearts 
could be prevented by the treatment. As triiodothyronine (T3) treatment has been 
shown to normalize depression of cardiac myosin ATPase in diabetic rats, we 
repeated the study using a combination of T3 (30 micrograms kg-1 day-1 sc daily) 
and methyl palmoxirate. While diabetic rats treated with T3 alone did not show 
significant improvement of myocardial function when compared with untreated 
diabetics, the function of those treated with both T3 and methyl palmoxirate was 
not significantly different from that in control rat hearts.(ABSTRACT TRUNCATED 
AT 250 WORDS)