POLYCYSTIC OVARY SYNDROME AND FETAL AND NEONATAL BIOMARKERS

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。目的：探讨多囊卵巢综合征（PCOS）胎儿程序设计的胎儿和新生儿标志物。该项目继续确定在妊娠早期将雌性恒河猴胎儿暴露于雄激素过量对胎儿和新生儿的影响。目前的研究结果表明，妊娠早期雄激素过量会导致胎儿晚期和婴儿早期黄体生成素（LH）分泌过多，这是PCOS女性生殖异常的一个组成部分。我们的研究结果还表明，黄体生成素缺陷可能是由于大脑下丘脑的促性腺激素释放激素过度释放和黄体生成素负反馈调节受损所致。这项工作提供了第一个直接的证据，胎儿编程的关键生殖缺陷，在这种非人灵长类动物多囊卵巢综合征模型。本研究使用了WNPRC化验服务和动物服务。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. To determine fetal and neonatal markers for fetal programming of polycystic ovary syndrome (PCOS). This project continues to determine fetal and neonatal consequences of exposing female rhesus monkey fetuses to androgen excess during early gestation. Current results indicate that early gestation androgen excess induces luteinizing hormone (LH) hypersecretion in late fetal life and early infancy, inducing one component of the reproductive abnormalities found in PCOS women. Our findings also suggest that the LH defect may be due to both excessive release of gonadotropin-releasing hormone from the hypothalamus in the brain and impaired negative feedback regulation of LH. This work provides the first direct evidence for fetal programming of key reproductive defects in this nonhuman primate model of PCOS. This research used WNPRC Assay Services and Animal Services.