In obesity-related diabetes, cardiac mitochondrial uncoupling is driven by UCP activation rather than increased expression, leading to elevated oxidative stress.
Supports UCP activation as driver of cardiac oxidative stress in obesity-diabetes models; leaves open therapeutic targeting in patients.
These data demonstrate that mitochondrial uncoupling in the heart in obesity and diabetes is mediated by activation of UCPs independently of changes in expression levels. This likely occurs on the basis of increased delivery of reducing equivalents from beta-oxidation to the electron transport chain, which coupled with decreased oxidative phosphorylation capacity increases ROS production and lipid peroxidation.
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Boudina et al. (2007) studied this question.
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