PRENATAL STRESS EFFECTS ON GLUCOSE METABOLISM

产前应激对葡萄糖代谢的影响

• 批准号: 2680251
• 负责人: ANIL P D'MELLO
• 金额: $ 9.92万
• 依托单位: UNIVERSITY OF THE SCIENCES PHILADELPHIA
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-08-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2680251
• 关键词: animal birth weight; corticosterone; diabetes mellitus; dietary carbohydrates; disease /disorder etiology; early experience; embryo /fetus pharmacology; enzyme activity; fructose; gestational age; glucose metabolism; glucose tolerance test; hydroxysteroid dehydrogenases; insulin; ketones; laboratory rat; nutrition related tag; prenatal stress

DESCRIPTION: The overall objective of the research proposal is to determine th role of prenatal stress in the etiology of diabetes. The aim of this proposal is to examine the effect of chronic maternal immobilization stress of rats on glucose metabolism in the offspring. Specific Aim 1 is designed to identify th gestational period during which prenatal stress has maximal effect on birth weight and glucose metabolism of the offspring. Glucose metabolism will be evaluated by measuring basal fetal glucose and insulin levels and by the glucose tolerance test. Specific Aim 2 is designed to determine the ability of prenatally stressed rats to cope with chronic metabolic stress administered during adulthood by measuring their glucose metabolism after a chronic high fructose diet. The final studies are mechanistic in design, and will establish the role of maternal corticosterone in mediating the effects of prenatal stres on glucose metabolism in the offspring. Stress-induced increases in maternal corticosterone will be inhibited with cyanoketone and glucose metabolism will be examined in the offspring. Finally, the activity of placental 11b-hydroxysteroid dehydrogenase, which inactivates corticosterone, will be measured in chronically stressed pregnant rats to test the hypothesis that chronic prenatal stress decreases the placental level of this enzyme.

描述：研究计划的总体目标是确定 产前应激在糖尿病病因中的作用。 此举的目的 建议检查孕产妇长期固定压力的影响 大鼠对后代葡萄糖代谢的影响。 设计具体目标1 确定产前应激最大的妊娠期 对后代出生体重和糖代谢的影响。 葡萄糖 通过测量基础胎儿葡萄糖和胰岛素来评估新陈代谢 水平和葡萄糖耐量试验。 具体目标 2 旨在 确定产前应激大鼠应对慢性疾病的能力 通过测量血糖来管理成年期间的代谢压力 长期高果糖饮食后的新陈代谢。 最终的研究结果是 机械设计，并将确立母亲的角色 皮质酮介导产前应激对血糖的影响 后代的新陈代谢。 压力引起的产妇体重增加 皮质酮会受到氰酮和葡萄糖代谢的抑制 将在后代中进行检查。 最后，胎盘的活性 11b-羟基类固醇脱氢酶可灭活皮质酮， 在长期应激的怀孕大鼠中进行测量，以检验以下假设： 慢性产前应激会降低这种酶的胎盘水平。