POLYCYSTIC OVARY SYNDROME (PCOS) AND FETAL, NEONATAL AND ADULT BIOMARKERS

多囊卵巢综合症 (PCOS) 和胎儿、新生儿和成人生物标志物

• 批准号: 8173071
• 负责人: DAVID H ABBOTT
• 金额: $ 3.1万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173071
• 关键词: Adolescent; Adult; Androgenization; Androgens; Animals; Biological Assay; Biological Markers; Computer Retrieval of Information on Scientific Projects Database; Defect; Female; Fetus; Funding; Grant; Hyperglycemia; Infant; Institution; Insulin; Islets of Langerhans; Macaca mulatta; Mediating; Metabolic; Modeling; Morphology; Mothers; Neonatal; Ovarian; Pathology; Phenotype; Polycystic Ovary Syndrome; Pregnancy; Research; Research Personnel; Resources; Services; Source; United States National Institutes of Health; Work; blood glucose regulation; fetal; fetal programming; nonhuman primate; pregnant; prenatal

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, neonatal and adult markers reflecting mechanism of 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 altered morphology of pancreatic islets in exposed female infants that may explain functional alterations in insulin-mediated regulation of glucose. 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, Pathology Services and Animal Services. PUBLICATIONS: Abbott DH, Dumesic DA. 2009. Adult polycystic ovary. Highlights 17:13-18. Abbott DH, Tarantal AF, Dumesic DA. 2009 Fetal, infant, adolescent and adult phenotypes of polycystic ovary syndrome in prenatally androgenized female rhesus monkeys. Am J Primatol. 71:776-784. Dumesic DA, Patankar M, Barnett DK, Lesnick TG, Hutcherson BA, Abbott DH. 2009 Early prenatal androgenization results in diminished ovarian reserve in adult female rhesus monkeys. Hum Reprod. 24:3188-3195.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。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 研究中心，而研究中心不一定是研究者所在的机构。 目的：探讨多囊卵巢综合征（PCOS）胎儿、新生儿和成人的胎儿编程机制。 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，高血糖妊娠诱导雄激素过量给予怀孕的恒河猴母亲可能有助于改变胰岛的形态学暴露的女婴，这可能解释胰岛素介导的葡萄糖调节功能的改变。这项工作提供了额外的直接证据，胎儿编程的代谢缺陷，在这个非人灵长类动物模型的多囊卵巢综合征。 本研究使用了WNPRC Assay Services、Pathology Services和Animal Services。 出版物： Abbott DH，Dumesic DA. 2009.多囊卵巢综合征亮点17：13-18. Abbott DH，Tarantal AF，Dumesic DA. 2009产前雄激素化雌性恒河猴中多囊卵巢综合征的胎儿、婴儿、青少年和成人表型。《美国医学杂志》71：776-784。 Dumesic DA，Patankar M，巴内特DK，Lesnick TG，Hutcherson BA，Abbott DH. 2009年早期产前雄激素化导致成年雌性恒河猴卵巢储备减少。Reprod. 24：3188-3195。