POLYCYSTIC OVARY SYNDROME AND FETAL AND NEONATAL BIOMARKERS

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。目的：确定多囊卵巢综合征（PCOS）胎儿和新生儿的标记物。 该项目继续确定雌性恒河猴胎儿在妊娠早期暴露于雄激素过量的胎儿和新生儿后果。目前的研究结果表明，妊娠早期雄激素过多诱导黄体生成素（LH）分泌过多，在胎儿生命后期和婴儿早期，诱导PCOS妇女的生殖异常的一个组成部分。我们的研究结果还表明，LH缺陷可能是由于过度释放促性腺激素释放激素从大脑中的下丘脑和受损的LH负反馈调节。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，在这个非人灵长类动物模型的PCOS。本研究使用WNPRC Assay Services和Animal Services。

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.