| First Author | Patterson CM | Year | 2012 |
| Journal | Mol Metab | Volume | 1 |
| Issue | 1-2 | Pages | 61-9 |
| PubMed ID | 24024119 | Mgi Jnum | J:221245 |
| Mgi Id | MGI:5638531 | Doi | 10.1016/j.molmet.2012.05.001 |
| Citation | Patterson CM, et al. (2012) Leptin action via LepR-b Tyr1077 contributes to the control of energy balance and female reproduction. Mol Metab 1(1-2):61-9 |
| abstractText | Leptin action in the brain signals the repletion of adipose energy stores, suppressing feeding and permitting energy expenditure on a variety of processes, including reproduction. Leptin binding to its receptor (LepR-b) promotes the tyrosine phosphorylation of three sites on LepR-b, each of which mediates distinct downstream signals. While the signals mediated by LepR-b Tyr1138 and Tyr985 control important aspects of energy homeostasis and LepR-b signal attenuation, respectively, the role of the remaining LepR-b phosphorylation site (Tyr1077) in leptin action has not been studied. To examine the function of Tyr1077, we generated a "knock-in" mouse model expressing LepR-b (F1077), which is mutant for LepR-b Tyr1077. Mice expressing LepR-b (F1077) demonstrate modestly increased body weight and adiposity. Furthermore, females display impairments in estrous cycling. Our results suggest that signaling by LepR-b Tyr1077 plays a modest role in the control of metabolism by leptin, and is an important link between body adiposity and the reproductive axis. |
