| First Author | Arias-Loza PA | Year | 2012 |
| Journal | Hypertension | Volume | 60 |
| Issue | 4 | Pages | 1070-7 |
| PubMed ID | 22892812 | Mgi Jnum | J:281387 |
| Mgi Id | MGI:6378702 | Doi | 10.1161/HYPERTENSIONAHA.111.190389 |
| Citation | Arias-Loza PA, et al. (2012) The estrogen receptor-alpha is required and sufficient to maintain physiological glucose uptake in the mouse heart. Hypertension 60(4):1070-7 |
| abstractText | Estrogens attenuate cardiac hypertrophy and increase cardiac contractility via their cognate estrogen receptors (ERs) ERalpha and ERbeta. Because female sex hormones enhance global glucose use and because myocardial function and mass are tightly linked to cardiac glucose metabolism, we tested the hypothesis that expression and activation of the ERalpha might be required and sufficient to maintain physiological cardiac glucose uptake in the murine heart. Cardiac glucose uptake quantified in vivo by 18F-fluorodeoxyglucose positron emission tomography was strongly impaired in ovariectomized compared with gonadal intact female C57BL/6JO mice. The selective ERalpha agonist 16alpha-LE2 and the nonselective ERalpha and ERbeta agonist 17beta-estradiol completely restored cardiac glucose uptake in ovariectomized mice. Cardiac 18F-fluorodeoxyglucose uptake was strongly decreased in female ERalpha knockout mice compared with wild-type littermates. Analysis of cardiac mRNA accumulation by quantitative RT-PCR revealed an upregulation of genes involved in glycolisis and tricarboxylic acid cycle by ERalpha treatment. In conclusion, systemic activation of ERalpha is sufficient, and its expression is required to maintain physiological glucose uptake in the murine heart, which is likely to contribute to known cardioprotective estrogen effects. |
