Deficiency of liver-X-receptor-α reduces glucose uptake and worsens post-myocardial infarction remodeling

MI was induced in mice by permanent ligation of the left anterior descending coronary artery (LCA). Genetic LXRα deletion significantly worsened cardiac remodeling and impaired cardiac function at 4 weeks after MI. Cardiac 18F-fluorodeoxyglucose (FDG) uptake by positron emission tomography (PET) demonstrated that the FDG standardized uptake value (SUV) was significantly lower in LXRα−/− mice as compared to WT mice. Mechanistically, GLUT1/4 and AMPK phosphorylation were significantly downregulated while CD36 expression was markedly upregulated in LXRα−/− mice. This study demonstrated that deficiency of LXRα decreased glucose uptake after MI, resulting in a metabolic shift that suppressed glucose metabolism, which was in association with adverse cardiac remodeling.