Effect of myo-inositol and T3 on myocardial lipids and cardiac function in streptozocin-induced diabetic rats
- 1 November 1988
- journal article
- research article
- Published by American Diabetes Association in Diabetes
- Vol. 37 (11) , 1542-1548
- https://doi.org/10.2337/diabetes.37.11.1542
Abstract
Numerous experimental studies have implied a link between diabetes-induced abnormal lipid buildup in the myocardium and the development of cardiomyopathy. Because the diabetic state in rats is associated with lowered T3 (triiodothyronine) and T4 levels and because diabetic patients excrete large amounts of myo -inositol, a lipotropic agent, we investigated the effects of myo -inositol and T3 on the elevated myocardial lipid levels and depressed cardiac performance of streptozocin (55 mg/kg i.v.)-induced diabetic (STZ-D) rats, myo -inositol (2.5 g kg−1 day−1 in the drinking water) and T3 (30 μg · kg−1 · day−1 s.c.) were given for an 8-wk period 3 days after diabetes induction. Untreated diabetic rats were characterized by a decreased rate of body weight gain, hyperglycemia, and hypoinsulinemia, which were not altered after myo -inositol and/or T3 treatment. Thyroid status of diabetic animals was normalized by T3 alone or in combination with myo -inositol but not by myo -inositol alone. The elevations in plasma and myocardial lipids associated with the diabetic state were prevented by myo -inositol treatment. However, the plasma lipid and myocardial cholesterol levels in diabetic rats remained elevated or were further increased with treatment with T3 or myo -inositol plus T3. myo -inositol treatment partially improved cardiac performance in STZ-D rats. T3 treatment alone did not prevent cardiac dysfunction in diabetic rats. There was, however, some improvement in heart function in the groups treated with both myo -inositol and T3, coinciding with a significant decrease in the myocardial triacylglycerol level. The data indicate that a possible correlation may exist between elevated myocardial triacylglycerol levels and cardiac dysfunction in diabetic rats.Keywords
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