Bioenergetic functions in subpopulations of heart mitochondria are preserved in a non-obese type 2 diabetes rat model (Goto-Kakizaki)

• Published in: Scientific reports Vol. 10; no. 1; p. 5444
• Main Authors: Lai, N., Kummitha, C. M., Loy, F., Isola, R., Hoppel, C. L.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 25.03.2020; Nature Publishing Group
• Subjects: 101/58; 14/10; 631/45; 692/699/75; Aconitate Hydratase - metabolism; Animals; Bioenergetics; Cardiomyopathy; Cardiovascular diseases; Diabetes; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - metabolism; Diabetic Cardiomyopathies - metabolism; Disease Models, Animal; Electron transport chain; Electron Transport Chain Complex Proteins - metabolism; Energy Metabolism; Enzymatic activity; Health risks; Heart; Humanities and Social Sciences; Mitochondria; Mitochondria, Heart - metabolism; multidisciplinary; Obesity; Oxidative Phosphorylation; Oxidative stress; Oxidative Stress - genetics; Phosphorylation; Preservation; Rats; Science; Science (multidisciplinary); Subpopulations
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-020-62370-8

A distinct bioenergetic impairment of heart mitochondrial subpopulations in diabetic cardiomyopathy is associated with obesity; however, many type 2 diabetic (T2DM) patients with high-risk for cardiovascular disease are not obese. In the absence of obesity, it is unclear whether bioenergetic function in the subpopulations of mitochondria is affected in heart with T2DM. To address this issue, a rat model of non-obese T2DM was used to study heart mitochondrial energy metabolism, measuring bioenergetics and enzyme activities of the electron transport chain (ETC). Oxidative phosphorylation in the presence of substrates for ETC and ETC activities in both populations of heart mitochondria in T2DM rats were unchanged. Despite the preservation of mitochondrial function, aconitase activity in T2DM heart was reduced, suggesting oxidative stress in mitochondria. Our study indicate that metabolic function of heart mitochondria is unchanged in the face of oxidative stress and point to a critical role of obesity in T2DM cardiomyopathy.