RELATIONSHIP BETWEEN INSULIN RESISTANCE & EARLY DEV OF ATHEROGENESIS

胰岛素抵抗之间的关系

• 批准号: 7717843
• 负责人: GERALD M. REAVEN
• 金额: $ 0.5万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7717843
• 关键词: Blood Vessels; Compensatory Hyperinsulinemia; Computer Retrieval of Information on Scientific Projects Database; Coronary heart disease; Defect; Dyslipidemias; Endothelium; Funding; Grant; Hypertension; Institution; Insulin; Insulin Resistance; Link; Mediating; Metabolic; Research; Research Personnel; Resistance; Resources; Risk; Risk Factors; Source; Syndrome; United States National Institutes of Health; Vasodilation; Vasodilation disorder; atherogenesis; glucose disposal; heart disease risk; monocyte

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. The central focus of this study has been on the importance of resistance to insulin-mediated glucose disposal and compensatory hyperinsulinemia in modulation of metabolic changes that increase risk of coronary heart disease (CHD). These can include more obvious well-known CHD risk factors, such as dyslipidemia and hypertension and others leading to the cluster of abnormalities known as Syndrome X. Besides focusing on these risk factors, we will also evaluate changes in endothelium-dependent vasodilation (endothelium-dependent vascular reactivity, EDVR) and determinants of endothelial-monocyte interaction that comprise the earliest steps in atherogenesis. Therefore, we will be attempting to establish a link between insulin resistance and the cluster of metabolic abnormalities associated with this defect in insulin action. We will also try and establish the link with insulin resistance and endothelium-dependent vasodilatation and determinants of endothelium-monocyte interaction.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 这项研究的重点是胰岛素介导的葡萄糖处理抵抗和代偿性高胰岛素血症在调节代谢变化（增加冠心病（CHD）风险）中的重要性。 这些可能包括更明显的众所周知的 CHD 危险因素，例如血脂异常和高血压以及其他导致称为 X 综合征的一系列异常的因素。除了关注这些危险因素外，我们还将评估内皮依赖性血管舒张（内皮-血管舒张）的变化。依赖性血管反应性（EDVR）和内皮-单核细胞相互作用的决定因素，构成动脉粥样硬化形成的最早步骤。 因此，我们将尝试建立胰岛素抵抗和与胰岛素作用缺陷相关的一系列代谢异常之间的联系。 我们还将尝试建立胰岛素抵抗和内皮依赖性血管舒张以及内皮-单核细胞相互作用的决定因素之间的联系。