Key result
Increasing myocardial glucose delivery via GLUT4 induction in diabetic mice exacerbated mitochondrial oxidative dysfunction and decreased mitochondrial ATP generation.
Why the study?
Cardiac glucose uptake and oxidation are reduced in diabetes despite hyperglycemia, and it is unclear whether these changes and mitochondrial dysfunction are adaptive or maladaptive.
Does increasing myocardial glucose delivery accelerate mitochondrial dysfunction in a mouse model of diabetic cardiomyopathy?
Does increasing myocardial glucose delivery accelerate mitochondrial dysfunction in a mouse model of diabetic cardiomyopathy?
Restoring glucose delivery to the heart in the context of diabetes may accelerate mitochondrial dysfunction by disrupting protective metabolic adaptations against glucotoxicity.
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May worsen mitochondrial dysfunction in diabetic hearts; hypothesis-generating and leaves open human translation.
Wende et al. (2020) studied Diabetic cardiomyopathy. Inducible cardiomyocyte-specific expression of GLUT4 vs. Uninduced or nondiabetic mice was evaluated on Mitochondrial dysfunction and transcriptomic changes. Increasing myocardial glucose delivery via GLUT4 induction in diabetic mice exacerbated mitochondrial oxidative dysfunction and decreased mitochondrial ATP generation.
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