Journal
GYNECOLOGICAL ENDOCRINOLOGY
Volume 32, Issue 6, Pages 464-468Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/09513590.2015.1130810
Keywords
Body mass index; estrogens; leptin; menopause
Funding
- National Natural Science Foundation of China [81070464]
- Research Fund for the Doctoral Program of Higher Education, China [20100181110007]
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Objective: To examine how estradiol influence fat distribution and adipocyte genesis through regulating leptin function. Design and 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-beta estradiol on expression of leptin receptors (OBRb and OBRa), leptin and PPAR gamma 2. Results: Weight and Lee's index was both significantly higher in ovariectomized group than sham group (p<0.001). The interaction of serum E-2 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 PPAR gamma 2, 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.
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