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, 2012 Nov.
Article
em En
| MEDLINE
| ID: mdl-22750459
ABSTRACT
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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Testosterona
/
Tirosina
/
Receptores para Leptina
/
Obesidade
Tipo de estudo:
Etiology_studies
/
Observational_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article