Uncoupling protein 3 deficiency impairs myocardial fatty acid oxidation and contractile recovery following ischemia/reperfusion.

ABSTRACT: Patients with insulin resistance and type 2 diabetes have poor cardiac outcomes following myocardial infarction (MI). The mitochondrial uncoupling protein 3 (UCP3) is down-regulated in the heart with insulin resistance. We hypothesized that decreased UCP3 levels contribute to poor cardiac recovery following ischemia/reperfusion (I/R). After confirming that myocardial UCP3 levels were systematically decreased by 20-49% in animal models of insulin resistance and type 2 diabetes, we genetically engineered Sprague-Dawley rats with partial loss of UCP3 (ucp3^+/-). Wild-type littermates (ucp3^+/+) were used as controls. Isolated working hearts from ucp3^+/- rats were characterized by impaired recovery of cardiac power and decreased long-chain fatty acid (LCFA) oxida

SUBMITTER: Edwards KS 

PROVIDER: S-EPMC6208686 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature