摘要
近年研究认为,多囊卵巢综合征(polycystic ovary syndrome,PCOS)是一种胎源性疾病。胎儿暴露于宫内高雄激素环境,可能引起多个组织内基因表观遗传修饰状态的改变,如基因DNA甲基化、子代基因印迹的改变,干扰胎儿下丘脑-垂体-卵巢轴和内脏靶器官的生理发育过程,导致下丘脑对类固醇激素的负反馈调节敏感性下降和胰腺功能受损,造成青春期或成年后出现各种PCOS症状。明确PCOS的早期发病机制,对预防高危人群PCOS的发生与发展具有临床意义。
Clinical,experimental and genetic evidence suggested that polycystic ovary syndrome(PCOS) could have an fetal origin of adult disease.During fetal development,prenatal androgens excess may intervene the epigenome,such as the altered DNA methylation and genomic imprinting,which may increase the later risk of PCOS.Exposure to androgens in utero induces a permanent PCOS-like phenotype characterized by hyperandrogenism,abnormal follicle development,luteinizing hormone hypersecretion from the reduced hypothalamic sensitivity to steroid negative feedback,and insulin resistance from the increased abdominal adiposity.The ability of prenatal androgens excess to alter the developmental trajectory of multiple organ systems could be one of early mechanisms of PCOS pathogenesis,which could be valuable for PCOS prevention in groups with high risks.
出处
《国际生殖健康／计划生育杂志》
CAS
2013年第2期136-139,共4页
Journal of International Reproductive Health/Family Planning
基金
国家973计划项目(2012CB944902
2012CB944703)
国家自然科学基金项目(81070465)
关键词
多囊卵巢综合征
雄激素类
环境暴露
表现遗传
Polycystic ovary syndrome
Androgens
Environmental exposure
Epigenetics
