雌激素通过瘦素信号通路途径调节脂肪细胞代谢生成

雌激素通过瘦素信号通路途径调节脂肪细胞代谢生成

雌激素通过瘦素信号通路途径调节脂肪细

胞代谢生成#

李文娟，许良智，陈焱，牟丽，许文明，程萌，庄静，李婷婷，詹晶**

10 15 20 25 30 35 40

（四川大学华西第二医院，成都 610041）

摘要：目的：探讨雌激素是否是通过瘦素相关信号通路对女性形体改变产生影响。方法：二

月龄雌性 SD 大鼠随机为去势组及假手术组，术后 14 周收集生殖器周围脂肪、内脏脂肪和

皮下脂肪，并分别检测瘦素受体表达，同时通过 17-β雌二醇及瘦素对脂肪细胞前体细胞

MSCs 进行干预，检验瘦素受体亚型、瘦素表达及成脂分化的指标 PPARγ的变化。结果：

通过对造模期间大鼠体重的每周监测，发现去势组体重增长及术后 14 周Lee’s 指数均明显

高于假手术组 P 0.001 。瘦素受体在去势组的脂肪组织中表达显著增加，内脏脂肪中尤为明

显。体外实验显示，随着瘦素和雌激素浓度的增加，MSCs 上瘦素长形受体和短受体的表达

均随之下降；随雌激素浓度的增加，MSCs 中瘦素表达呈下降趋势，同时，MSCs 中 PPAR

γ表达也受到抑制。结论：在低雌激素的影响下，去势后大鼠发生类似绝经后女性样的形体

改变，高浓度雌激素可抑制大鼠间充质干细胞向脂肪细胞分化，雌激素对瘦素及瘦素受体的

影响可能是绝经后女性体型变化发生变化的原因。

关键词：妇产科学；雌激素；瘦素；瘦素受；脂肪；间充质干细胞

中图分类号：R339.6

Estrogen regulate adipocyte metabolism through leptin

signaling pathway

LI Wenjuan, XU Liangzhi, CHEN Yan, MU Li, XU Wenming, CHENG Meng, ZHUANG Jing, LI Tingting, ZHAN Jing

West China Second University Hospital, Sichuan University, Chengdu 610041

Abstract: Postmenopausal women often present obvious body composition changes under the

absence of estrogen, including overweight, obesity and android-like body fat distribution,

therefore poses serious threaten for women’s health. Although the intimate relationship between

estrogen and body appearance have been noticed, mechanism remains unclear. We assumed that

estrogen may regulate fat distribution through affecting leptin signal pathway, which has been

shown playing major role in energy homeostasis. To test this hypothesis, we randomized female

SD rat into ovariectomy OVX and sham group, and then collected adipose tissue around genital,

retroperitoneal and subcutaneous after 14 week. Leptin receptor expression in adipose tissue was

measured by western blot. Results indicated that leptin receptor were significantly down-regulated

in ovariectomy group, especially in fat around genital. Weight changes were observed every week,

repeated measures analysis of variance showed that OVX group has higher weight gain compared

with sham group during the 3 month P 0.001 , and so does the Lee’s index P 0.001 , which

were calculated at the end of the study. We further used mesenchymal stem cells MSCs , the

progenitor of Adipocytes as an in vitro model to figure out the effect of estrogen on leptin receptor

expression. After MSCs were treated by increasingconcentration of 17-βestradiol and letpin

respectively, QPCR were used to test the mRNA expression of leptin receptor subtype, OBRb

long form and OBRa short form . Negative correlation was noticed between estrogen

concentration and leptin receptor subtype expression. Similar tendency were also observed in