Why the study?
Does insulin treatment improve mitochondrial function in cardiomyocytes of rats with experimental diabetes?
Population
31 male Sprague-Dawley rats, including 20 with streptozotocin-induced diabetes and 11 non-diabetic controls
Comparison
Subcutaneous ultra lente insulin for 7-15 days vs Untreated diabetic rats and non-diabetic controls
Design
Preclinical
Follow-up
21-35 days after induction of diabetes
Key result
Insulin treatment for 7 days or longer normalized the significant decreases in mitochondrial calcium uptake, transmembrane potential, and cell respiration observed in diabetic rat cardiomyocytes.
Authors
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Should not yet inform clinical care in diabetic cardiomyopathy; leaves open insulin's mitochondrial effects as a preventive mechanism in humans.
Does insulin treatment improve mitochondrial function in cardiomyocytes of rats with experimental diabetes?
Insulin treatment reverses early mitochondrial dysfunction in cardiomyocytes of rats with experimental diabetes, suggesting a potential mechanism for preventing diabetic cardiomyopathy.
TANAKA et al. (1992) studied Experimental diabetes (n=31). Insulin treatment vs. Untreated experimental diabetes and healthy controls was evaluated on Mitochondrial uptake of [45Ca]2+, transmembrane potential gradient, and cell respiration. Insulin treatment for 7 days or longer normalized the significant decreases in mitochondrial calcium uptake, transmembrane potential, and cell respiration observed in diabetic rat cardiomyocytes.