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: 8358196
• 负责人: DAVID H ABBOTT
• 金额: $ 0.25万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8358196
• 关键词: Adult; Androgens; Animals; Biological Assay; Biological Markers; Defect; Female; Fetus; Funding; Grant; Hyperglycemia; Infant; Insulin; Islets of Langerhans; Macaca mulatta; Mediating; Metabolic; Modeling; Morphology; Mothers; National Center for Research Resources; Neonatal; Pathology; Polycystic Ovary Syndrome; Pregnancy; Primates; Principal Investigator; Printing; Research; Research Infrastructure; Resources; Services; Source; United States National Institutes of Health; Wisconsin; Work; blood glucose regulation; cost; fetal; fetal programming; nonhuman primate; offspring; pregnant

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 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, Bruns CM, Barnett DK, Dunaif A, Goodfriend TL, Dumesic DA, Tarantal AF. 2010 Experimentally-induced gestational androgen excess disrupts glucoregulation in rhesus monkey dams and their female offspring. Am J Physiol Endocrinol Metab. 299:E741-751. PMID 20682841. Pasquali R, Stener-Victorin E, Yildiz BO, Duleba AJ, Hoeger K, Mason H, Homburg R, Hickey T, Franks S, Tapanainen J, Balen A, Abbott DH, Diamanti-Kandarakis E, Legro RS. PCOS Forum: Research in Polycystic Ovary Syndrome Today and Tomorrow. Clin Endocrinol (Oxf). 2010 Dec 15. doi: 10.1111/j.1365-2265.2010.03956.x. [Epub ahead of print] PMID 21158892.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的首席研究员可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 目的：确定反映多囊卵巢综合征（PCOS）胎儿编程机制的胎儿、新生儿和成人标志物。 该项目继续确定雌性恒河猴胎儿在妊娠早期暴露于过量雄激素的情况下对胎儿和新生儿的影响。目前的结果表明，怀孕的恒河猴母亲雄激素过多引起的高血糖妊娠可能会导致暴露的雌性婴儿胰岛形态的改变，这可能解释胰岛素介导的葡萄糖调节的功能改变。这项工作为这种非人灵长类多囊卵巢综合症模型中代谢缺陷的胎儿编程提供了额外的直接证据。 本研究使用了 WNPRC 检测服务、病理学服务和动物服务。 出版物： Abbott DH、Bruns CM、Barnett DK、Dunaif A、Goodfriend TL、Dumesic DA、Tarantal AF。 2010 年，实验诱导的妊娠期雄激素过多扰乱了恒河猴母猴及其雌性后代的葡萄糖调节。 Am J 生理内分泌代谢杂志。 299：E741-751。 PMID 20682841。 Pasquali R、Stener-Victorin E、Yildiz BO、Duleba AJ、Hoeger K、Mason H、Homburg R、Hickey T、Franks S、Tapanainen J、Balen A、Abbott DH、Diamanti-Kandarakis E、Legro RS。 PCOS 论坛：多囊卵巢综合症的今天和明天的研究。临床内分泌（Oxf）。 2010 年 12 月 15 日。doi：10.1111/j.1365-2265.2010.03956.x。 [印刷前的电子版] PMID 21158892。