Open Access

ARTICLE

Heart mitochondrial dysfunction in diabetic rats

S.S. Bombicino^*, D.E. Iglesias, I.A. Rukavina Mikusic, A. Boveris, L.B. Valdez

* Address correspondence to: Silvina S. Bombicino sbombicino@ffyb.uba.ar

BIOCELL 2016, 40(1), 7-10. https://doi.org/10.32604/biocell.2016.40.007

Abstract

Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. Alterations in the contractile response and lusitropic reserve were observed in streptozotocin diabetic rats after β-adrenergic stimuli. Additionally, tissue O₂ consumption was declined. A condition of mitochondrial dysfunction with decreased mitochondrial state 3 O₂ consumption, respiratory control ratio, mitochondrial respiratory complexes activities and ATP production were present in hearts of diabetic animals. We observed an increase in NO production by heart mitochondria and in cytochrome oxidase activity in heart homogenates. The latter suggests an increase of newly formed mitochondria. Thus, the impairment of mitochondrial function with increased mitochondrial biogenesis may precede the onset of diabetic cardiomyopathy. However, mitochondrial biogenesis does not necessarily imply that the resultant mitochondria are functional, which might explain the changes in cardiac energy metabolism occurring in hearts of diabetic rats.

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