| First Author | Ji Q | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 488 |
| Issue | 3 | Pages | 489-495 |
| PubMed ID | 28511797 | Mgi Jnum | J:250747 |
| Mgi Id | MGI:6102770 | Doi | 10.1016/j.bbrc.2017.05.072 |
| Citation | Ji Q, et al. (2017) Deficiency of liver-X-receptor-alpha reduces glucose uptake and worsens post-myocardial infarction remodeling. Biochem Biophys Res Commun 488(3):489-495 |
| abstractText | Liver X receptor alpha (LXRalpha) is an endogenous protective receptor against ischemic heart diseases. However, whether LXRalpha regulated glucose metabolism in ischemic heart diseases has not been investigated. In this study we investigated the involvement of LXRalpha on glucose metabolism in cardiac remodeling after myocardial infarction (MI). MI was induced in mice by permanent ligation of the left anterior descending coronary artery (LCA). Genetic LXRalpha 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 LXRalpha(-/-) mice as compared to WT mice. Mechanistically, GLUT1/4 and AMPK phosphorylation were significantly downregulated while CD36 expression was markedly upregulated in LXRalpha(-/-) mice. This study demonstrated that deficiency of LXRalpha decreased glucose uptake after MI, resulting in a metabolic shift that suppressed glucose metabolism, which was in association with adverse cardiac remodeling. |
