Pathology of hyperandrogenemia in the oocyte of polycystic ovary syndrome

被引:8
|
作者
Chappell, Neil R. [1 ,2 ]
Gibbons, William E. [1 ,2 ]
Blesson, Chellakkan S. [1 ,2 ]
机构
[1] Baylor Coll Med, Reprod Endocrinol & Infertil Div, Dept Obstet & Gynecol, One Baylor Plaza,MS BCM610, Houston, TX 77030 USA
[2] Texas Childrens Hosp, Family Fertil Ctr, Houston, TX 77030 USA
关键词
PCOS; Polycystic ovary syndrome; Hyperandrogenemia; Oocyte; Embryo; ANTI-MULLERIAN HORMONE; PRENATAL ANDROGEN EXPOSURE; GENOME-WIDE ASSOCIATION; BODY-MASS INDEX; IN-VITRO; INSULIN-RESISTANCE; MITOCHONDRIAL DYSFUNCTION; MISCARRIAGE RATE; EMBRYO-TRANSFER; SYNDROME PCOS;
D O I
10.1016/j.steroids.2022.108989
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Polycystic ovary syndrome (PCOS) is the most common ovulatory disorder in the world and is associated with multiple adverse outcomes. The phenotype is widely varied, with several pathologies contributing to the spec-trum of the disease including insulin resistance, obesity and hyperandrogenemia. Of these, the role of hyper-androgenemia and the mechanism by which it causes dysfunction remains poorly understood. Early studies have shown that androgens may affect the metabolic pathways of a cell, and this may pose hazards at the level of the mitochondria. As mitochondria are strictly maternally inherited, this would provide an exciting explanation not only to the pathophysiology of PCOS as a disease, but also to the inheritance pattern. This review seeks to summarize what is known about PCOS and associated adverse outcomes with focus on the role of hyper-androgenemia and specific emphasis on the oocyte.
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页数:7
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