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：探讨多囊卵巢综合征(PCOS)的胎儿和新生儿标志物对妊娠结局的影响。 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，怀孕的恒河猴母亲服用过量的雄激素而导致的高血糖妊娠可能导致婴儿体重的更大增加和产前雄激素诱导的雌性后代胰岛素对血糖的功能亢进。这项工作为多囊卵巢综合征的这种非人类灵长类动物模型中的代谢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。 (请在本报告的研究要点部分阅读更多关于阿博特博士和他的团队的工作。)

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. Objective: 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 a hyperglycemic pregnancy induced by the androgen excess given to pregnant rhesus mothers may contribute to greater increases in infant body weight and hyperfunctional insulin regulation of glucose in prenatally androgenized female offspring. This work provides additional direct evidence for fetal programming of metabolic defects in this nonhuman primate model of PCOS. This research used WNPRC Assay Services and Animal Services. (Please read more on Dr. Abbott and his team's work in the Research Highlights section of this report.)