POLYCYSTIC OVARY SYNDROME AND FETAL AND NEONATAL BIOMARKERS

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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.