IMPACT OF MATERNAL OBESITY AND DIETARY EXCESS ON FETAL ADIPOSITY

母亲肥胖和饮食过量对胎儿肥胖的影响

• 批准号: 8167813
• 负责人: NATHAN P LONG
• 金额: $ 12.41万
• 依托单位: UNIVERSITY OF WYOMING
• 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/8167813
• 关键词: 3 year old; Adipocytes; Adipose tissue; Angiogenic Factor; Animal Model; Arteries; Birth Weight; Blood Pressure; Blood Vessels; Body Composition; Characteristics; Computer Retrieval of Information on Scientific Projects Database; Data; Deposition; Development; Diet; Fatty Acids; Fatty acid glycerol esters; Funding; Grant; Growth; Hormones; Hypertension; Institution; Insulin Resistance; Life; Muscle; National Heart, Lung, and Blood Institute; National Institute of Diabetes and Digestive and Kidney Diseases; Obesity; Organ; Physiological; Pregnancy; Property; Research; Research Personnel; Resistance; Resources; Sheep; Skeletal Muscle; Source; Tissues; United States National Institutes of Health; Weight; Woman; angiogenesis; comparative; dietary excess; fatty acid transport; feeding; fetal; fetal blood; insight; mortality; neonatal morbidity; offspring; postnatal; receptor; research study; skeletal

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. Maternal obesity (MO) is a major cause if fetal and neonatal morbidity and mortality. Increased pre-pregnancy maternal weight in women correlates with increased offspring weight and the potential for persistent and damaging consequences resulting from changes in body composition and developing tissue and organ function. A recent NIDDK and NHLBI RFA acknowledges that animal models of MO are needed to gain insight into the physiologic consequences. We hypothesize that MO and a highly palatable obesogenic diet (HPD) in sheep: 1) increases fatty acid transport from the maternal to the fetal compartment resulting in increased fetal fat deposition, 2) shifts vascular development away from skeletal muscle towards adipose tissue depots through alterations in angiogenesis and vascular reactivity, 3) increases fetal fat to lean body mass which will result in obesity, insulin resistance and hypertension in offspring in postnatal life. Experiment 1 will characterize the impacts of MO/HPD on fetal hormone levels and fatty acid profiles in fetal blood and adipose tissue depots, and evaluate maternal diet-induced changes in vascularity, fatty acid transport activity and adipocyte characteristics in selected fetal fat depots. Experiment 2 will determine the Impact of MO/HPD on fetal adipose and skeletal muscle tissue angiogenic factor/receptor activity and relate these data to comparative vascularity, as well as evaluate alterations in the contractile/relaxant properties of resistance arteries supplying adipose tissue and skeletal muscle. Experiment 3 will compare postnatal characteristics of lambs born to MO/HPD and Control fed ewes, including lamb birth weight and morphometrics, adiposity, growth rate, hormone secretion profiles, insulin resistance and blood pressures to 3 years of age.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 如果胎儿和新生儿发病率和死亡率，孕产妇肥胖（MO）是主要原因。女性孕前孕妇体重的增加与后代体重的增加以及由于身体组成以及发展组织和器官功能的变化而产生的持续和破坏性后果的潜力相关。最近的NIDDK和NHLBI RFA承认，需要MO的动物模型来深入了解生理后果。我们假设绵羊中的mo和高度可口的肥胖饮食（HPD）：1）增加脂肪酸从母体到胎儿室的传递，导致胎儿脂肪沉积增加，2）将血管发育从骨骼肌肉中转移到骨骼肌肉向脂肪组织的变化，从而使肥胖的变化会导致血管生成和血管反应的改变，3）和产后生活中后代的高血压。实验1将表征MO/HPD对胎儿血液和脂肪组织库中胎儿激素水平和脂肪酸谱的影响，并评估所选胎儿脂肪库中孕妇饮食诱导的血管饮食诱导的血管变化，脂肪酸转运活性以及脂肪细胞的特征。实验2将确定mo/hpd对胎儿脂肪和骨骼肌组织血管生成因子/受体活性的影响，并将这些数据与比较血管性联系起来，并评估供应脂肪组织和骨骼肌的收缩/松弛特性的改变。实验3将比较MO/HPD所生的羔羊的产后特征和对照喂养母羊，包括羔羊的出生体重和形态图，肥胖，生长速度，激素分泌谱，胰岛素抵抗和血液压力到3岁。