4.7 Article

Adiponectin and leptin systems in human endometrium during window of implantation

期刊

FERTILITY AND STERILITY
卷 97, 期 3, 页码 771-U281

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.fertnstert.2011.12.042

关键词

Adiponectin; leptin; uterine receptivity; implantation failure; infertility

资金

  1. Universite de Versailles Saint Quentin en Yvelines

向作者/读者索取更多资源

Objective: To measure the expression of adiponectin, leptin, and their respective receptors in the human endometria of fertile women compared with women with unexplained recurrent implantation failure (IF) during the window of implantation. Design: Controlled, prospective, clinical study. Setting: Teaching hospital and university research laboratory. Patient(s): Thirty-one endometrial biopsies from women with IF and 19 fertile controls. Intervention(s): Human endometrial biopsies. Main Outcome Measure(s): Gene and protein expression of endometrial biopsies. Result(s): Endometrial leptin expression was significantly lower in the IF group compared with fertile women. In contrast, leptin receptor (Ob-R) expression was higher in endometria of women with IF. Concerning the adiponectin system, adiponectin was expressed to the same extent in both groups. Conversely, the expression of its two receptors, AdipoR1 and AdipoR2, was reduced in endometria of women with IF compared with fertile women. Conclusion(s): Although progesterone resistance seems to be a common state of the endometrium in some human reproductive disorders, such as endometriosis or polycystic ovary syndrome, modification in leptin endometrial expression seems to be specific to IF. These results strongly suggest that changes in Ob-R and AdipoR expression profiles [ 1] should be implicated in the development of uterine receptivity, and [ 2] may therefore be potential new targets for prediction of IF. (Fertil Steril (R) 2012; 97: 771-8. (c) 2012 by American Society for Reproductive Medicine.)

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据