Key result
Insulin therapy in diabetic rats produced progressive normalization of myocardial function and contractile protein biochemistry as blood glucose returned to normal.
Why the study?
Does insulin therapy improve myocardial function and contractile protein biochemistry in diabetic rats?
Does insulin therapy improve myocardial function and contractile protein biochemistry in diabetic rats?
Insulin therapy in diabetic rats produces continuous, dose-dependent improvement in cardiac function and biochemistry as euglycemia is approached.
May support glycemic control for diabetic cardiomyopathy in models; leaves open human translation pending clinical trials.
Diabetes mellitus causes congestive heart failure in humans, independent of atherosclerosis. The present study extends previous work on the reversibility, with insulin, of the alterations in myocardial function and contractile protein biochemistry observed in diabetic rats. The response of these alterations to different fixed doses of insulin was explored. Diabetic rats were given 0, 0.5, 1, 1.5, 2, or 2.5 U of insulin daily for 6 wk. Papillary muscle function, actomyosin ATPase, and myosin isoenzyme distribution showed progressive normalization with increasing insulin dose as blood glucose concentration returned to normal. Thus insulin therapy in diabetic rats on a normal diet produces continuous improvement in cardiac function and biochemistry as euglycemia is approached. This study also suggests that mild diabetes results in qualitatively identical, although quantitatively less pronounced, myocardial changes compared with those observed in severely diabetic rats.
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Fein et al. (1984) studied Diabetic cardiomyopathy. Insulin vs. 0 U insulin (untreated diabetic rats) was evaluated on Papillary muscle function, actomyosin ATPase, and myosin isoenzyme distribution. Insulin therapy in diabetic rats produced progressive normalization of myocardial function and contractile protein biochemistry as blood glucose returned to normal.
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