| First Author | Johnson JA | Year | 2012 |
| Journal | J Steroid Biochem Mol Biol | Volume | 132 |
| Issue | 3-5 | Pages | 212-9 |
| PubMed ID | 22750459 | Mgi Jnum | J:190163 |
| Mgi Id | MGI:5448331 | Doi | 10.1016/j.jsbmb.2012.06.002 |
| Citation | Johnson JA, et al. (2012) Testosterone interacts with the feedback mechanisms engaged by Tyr985 of the leptin receptor and diet-induced obesity. J Steroid Biochem Mol Biol 132(3-5):212-9 |
| abstractText | Inhibitory signaling through Tyr985 of the leptin receptor contributes to the attenuation of anorectic leptin action in obese animals. Leptin receptor (LEPR-B) Tyr985Leu homozygote mutant mice (termed l/l) were previously generated to study Tyr985's contributions to inhibition of LEPR-B signaling; young female l/l mice display a lean, leptin-sensitive phenotype, while young male l/l are not significantly different from wild-type. We report here that testosterone (but not estrogen) determines the sex-specificity of the l/l phenotype. This provides additional insight into the cellular mechanism by which gonadal hormones determine central sensitivity to leptin, and may help elucidate the long-noted sex differences in leptin sensitivity. Additionally, we observed that Tyr985 signaling protects against a diet-dependent switch that exacerbates obesity with high fat feeding, such that the enhanced leptin sensitivity of l/l mice on a normal diet leads to increased adiposity in the face of chronic high-fat diet. |
