POLYCYSTIC OVARY SYNDROME AND FETAL AND NEONATAL BIOMARKERS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 目的：确定多囊卵巢综合征(PCOS)胎儿程序化的胎儿和新生儿标志物。 该项目继续确定雌性恒河猴胚胎在怀孕早期暴露于雄激素过剩的胎儿和新生儿的后果。目前的结果表明，妊娠早期雄激素过多导致妊娠晚期胎儿卵泡刺激素过多，以及婴儿早期的高雄激素血症，这可能包括肾上腺高雄激素血症的一个组成部分，反映了成人内分泌疾病的早期生活先兆。我们的发现表明，胎儿促性腺激素过量可能是由于大脑下丘脑促性腺激素释放激素增加和负反馈调节受损所致。这项工作为多囊卵巢综合征的非人类灵长类动物模型中的内分泌缺陷的胎儿编程提供了额外的直接证据。这项研究使用了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 follicle stimulating hormone excess in late gestation fetuses, as well as hyperandrogenism in early infancy that may include a component of adrenal hyperandrogenism, reflecting early life antecedents of adult enodcrinopathy. Our findings suggest that fetal gonadotropin excess may be due to both increased release of gonadotropin-releasing hormone from the hypothalamus in the brain and impaired negative feedback regulation. This work provides additional direct evidence for fetal programming of endocrine defects in this nonhuman primate model of PCOS. This research used WNPRC Assay Services and Animal Services.