title: Effect of estrodiol on leptin receptors expression in regulating fat distribution and adipocyte genesis.
abstract: OBJECTIVE
  To examine how estradiol influence fat distribution and adipocyte genesis through regulating leptin function.
  
  
  METHODS
  We randomized female SD rats into ovariectomy and sham group. After 14 weeks, we examined leptin receptor expression in perigenital, mesenteric and subcutaneous adipose tissues and leptin in serum. We further introduced mesenchymal stem cells (MSCs) to figure out the effect of 17-β estradiol on expression of leptin receptors (OBRb and OBRa), leptin and PPARγ2.
  
  
  RESULTS
  Weight and Lee's index was both significantly higher in ovariectomized group than sham group (p < 0.001). The interaction of serum E2 and leptin was negatively correlated with body weight. Expression of leptin receptor protein was extremely upregulated in ovariectomized group in perigenital and mesenteric fat. Both estradiol and leptin upregulated mRNA expression of OBRb, and created a dose-dependent decreasing manner in MSCs. Higher doses of estradiol (10(-7)-10(-5) M) inhibited adipogenic markers mRNA expression of leptin and PPARγ2, but low doses promoted leptin expression.
  
  
  CONCLUSIONS
  In ovariectomized rats, low level of serum estradiol may change body composition and promote adipocyte genesis through affecting leptin function.
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Li
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Liangzhi
authors.initials: L
authors.lastname: Xu
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Li
authors.initials: L
authors.lastname: Mu
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Meng
authors.initials: M
authors.lastname: Cheng
authors.affiliation: b The Joint Laboratory for Reproductive Medicine of Sichuan University, The Chinese University of Hong Kong , Hong Kong.
authors.forename: Wenming
authors.initials: W
authors.lastname: Xu
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhuang
authors.affiliation: a Department of Obstetrics and Gynecology , West China Second University Hospital, Sichuan University , Chengdu , China and.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
mesh_terms: D017667:Adipocytes / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D020738:Leptin / Q000097:blood*; D010052:Ovariectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D054411:Receptors, Leptin / Q000378:metabolism*
chemical_list: D020738:Leptin; D054411:Receptors, Leptin; D004958:Estradiol
keywords: Body mass index; estrogens; leptin; menopause