Key result
Insulin restores depressed cardiac CK-M and CK-B mRNA levels to normal in diabetic rats.
Why the study?
The molecular mechanisms responsible for decreased cardiac performance in diabetes mellitus are incompletely explored, and insulin-responsive cardiac gene products have not been described.
Does insulin administration restore CK-M and CK-B mRNA levels in the hearts of rats with experimental diabetes mellitus?
Population
Rats with experimental diabetes mellitus
Comparison
Diabetic rats with and without insulin administration versus control rats
Design
Preclinical molecular biology study
Follow-up
Up to 1 month
Authors
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Does not support changes in clinical insulin use; leaves open whether CK mRNA effects translate to human diabetic cardiomyopathy.
Does insulin administration restore CK-M and CK-B mRNA levels in the hearts of rats with experimental diabetes mellitus?
Effect estimate: 1.6-fold increase (CK-M) and 2.2-fold increase (CK-B) at 5h
Insulin therapy restores the markedly depressed CK-M and CK-B mRNA levels in the diabetic rat heart, suggesting a molecular mechanism for insulin's effect on cardiac performance in diabetes.
Popovich et al. (1991) studied Experimental diabetes mellitus. Insulin vs. Untreated diabetic control was evaluated on CK-M and CK-B mRNA levels (1.6-fold increase (CK-M) and 2.2-fold increase (CK-B) at 5h). Insulin administration in diabetic rats significantly increased depressed cardiac CK-M and CK-B mRNA levels, restoring them to normal or above-normal values.
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