| First Author | Xu Y | Year | 2011 |
| Journal | Cell Metab | Volume | 14 |
| Issue | 4 | Pages | 453-65 |
| PubMed ID | 21982706 | Mgi Jnum | J:177649 |
| Mgi Id | MGI:5295789 | Doi | 10.1016/j.cmet.2011.08.009 |
| Citation | Xu Y, et al. (2011) Distinct hypothalamic neurons mediate estrogenic effects on energy homeostasis and reproduction. Cell Metab 14(4):453-65 |
| abstractText | Estrogens regulate body weight and reproduction primarily through actions on estrogen receptor-alpha (ERalpha). However, ERalpha-expressing cells mediating these effects are not identified. We demonstrate that brain-specific deletion of ERalpha in female mice causes abdominal obesity stemming from both hyperphagia and hypometabolism. Hypometabolism and abdominal obesity, but not hyperphagia, are recapitulated in female mice lacking ERalpha in hypothalamic steroidogenic factor-1 (SF1) neurons. In contrast, deletion of ERalpha in hypothalamic pro-opiomelanocortin (POMC) neurons leads to hyperphagia, without directly influencing energy expenditure or fat distribution. Further, simultaneous deletion of ERalpha from both SF1 and POMC neurons causes hypometabolism, hyperphagia, and increased visceral adiposity. Additionally, female mice lacking ERalpha in SF1 neurons develop anovulation and infertility, while POMC-specific deletion of ERalpha inhibits negative feedback regulation of estrogens and impairs fertility in females. These results indicate that estrogens act on distinct hypothalamic ERalpha neurons to regulate different aspects of energy homeostasis and reproduction. |
