Polycystic ovary syndrome and oocyte developmental competence

被引:108
作者
Dumesic, Daniel A. [1 ,2 ,3 ]
Padmanabhan, Vasantha [4 ,5 ,6 ,7 ]
Abbott, David H.
机构
[1] Reprod Med Infertil Assoc, Woodbury, MN 55125 USA
[2] Univ Wisconsin, Dept Obstet & Gynecol, Madison, WI 53706 USA
[3] Univ Wisconsin, Wisconsin Natl Primate Res Ctr, Madison, WI USA
[4] Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA
[6] Univ Michigan, Dep Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
[7] Univ Michigan, Reprod Sci Program, Ann Arbor, MI 48109 USA
关键词
D O I
10.1097/OGX.0b013e31815e85fc
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Folliculogenesis is a complex process, in which multiple endocrine and intraovarian paracrine interactions create a changing intrafollicular microenvironment for appropriate oocyte development. Within this microenvironment, bidirectional cumulus cell-oocyte signaling governs the gradual acquisition of developmental competence by the oocyte, defined as the ability of the oocyte to complete meiosis and undergo fertilization, embryogenesis, and term development. These regulatory mechanisms of follicle growth, controlled in part by the oocyte itself, are susceptible to derangement in polycystic ovary syndrome (PCOS), a heterogeneous syndrome characterized by ovarian hyperandrogenism, insulin resistance, and paracrine dysregulation of follicle development. Consequently, only a subset of PCOS patients experience reduced pregnancy outcome after ovarian stimulation for in vitro fertilization. Recent data implicate functional associations between endocrine/paracrine abnormalities, metabolic dysfunction, and altered oocyte gene expression with impaired oocyte developmental competence in women with PCOS. Therefore, an understanding of how developmentally relevant endocrine/paracrine factors interact to promote optimal oocyte developmental is crucial to identify those PCOS patients who might benefit from long-term correction of follicle growth to improve fertility, optimize follicular responsiveness to gonadotropin therapy, and enhance pregnancy outcome by in vitro fertilization.
引用
收藏
页码:39 / 48
页数:10
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