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Abstract
The purpose was to investigate an effect of hypoestrogenia and exogenous 17β-estradiol on mitochondrial heart function in female rats with type 2 diabetes. Materials and methods. Glucose homeostasis, intensity of reactive oxygen species production, aconitase and succinate dehydrogenase activities, and concentration of cytochrome respiratory chain in the heart mitochondria were assessed. Results. It was established that estrogen deficiency enhances the development of mitochondrial dysfunction in cardiomyocytes
of type 2 diabetic rats, increasing the reactive oxygen species production, and decreasing the aconitase activity. At the same time oral administration of 17β-estradiol preventes mitochondrial dysfunction in heart of ovariectomized diabetic rats, by reducing intensity of oxidative stress and increasing aconitase activity and component content of III and IV complexes in electron transport chain. Conclusions. The observed protective effect of exogenous 17β-estradiol on mitochondrial dysfunction of cardiomyocytes in diabetic rats with hypoestrogenia indicates a promising future researchs towards the development of gender-specific prevention and treatment of diabetic cardiovascular complications in women
after menopause.
References
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