CHRONIC LOW-GRAD INFLAMMATION, VASCULAR ENDOTHELIAL FUNCTION AND INSULIN SENSITI

慢性低度炎症、血管内皮功能和胰岛素敏感性

• 批准号: 7719556
• 负责人: LISA LIESNEWSKI
• 金额: $ 0.37万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7719556
• 关键词: Age; Blood Glucose; Blood Pressure; Blood Vessels; Cardiovascular system; Cells; Central obesity; Cholesterol; Chronic; Clinical; Computer Retrieval of Information on Scientific Projects Database; Contracts; Functional disorder; Funding; Glucose; Grant; Heart Diseases; Hormones; Human; Individual; Inflammation; Institution; Insulin; Insulin Resistance; Lipids; Lipoproteins; Metabolic Diseases; Metabolic syndrome; Metabolism; Molecular; Obesity; Oxidative Stress; Physical activity; Plasma; Process; Reactive Oxygen Species; Research; Research Personnel; Resources; Risk Factors; Source; Stimulus; Testing; United States National Institutes of Health; improved; neuronal cell body; prevent; response; vascular inflammation

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. Metabolic syndrome is a clustering of risk factors for heart disease. Blood vessels should dilate or contract in response to different stimuli, such as increased blood pressure, to prevent drastic changes in blood pressure. When the blood vessels do not function properly this is usually the result of endothelial dysfunction. Insulin is a hormone that converts blood sugar, or glucose, into useable energy. Insulin resistance occurs when the body no longer has the ability to produce or release the right amount of insulin. Endothelial dysfunction and insulin resistance are two key components of the metabolic syndrome. Increases in age, total and abdominal obesity, physical inactivity, cholesterol, and blood pressure are generally associated with endothelial dysfunction and insulin resistance. Importantly, we know that inflammation and oxidative stress are associated with endothelial function and insulin resistance. Oxidative stress is the exposure of the body's cells to molecules (i.e. reactive oxygen species) that are generated continuously in the body as a function of normal metabolism. Reactive oxygen species can produce damage to cells and interfere with the body's normal function, such as the ability of blood vessels to dilate or produce insulin. In humans we are unable to block oxidative stress, but we can block inflammation. Accordingly, the proposed research will test the hypothesis that inhibition of inflammation may improve endothelial dysfunction and insulin resistance in individuals varying in age, adiposity, habitual physical activity levels, plasma lipids and lipoproteins, and/or blood pressure, but without clinical cardiovascular or metabolic diseases. Furthermore, the proposed research will determine the molecular mechanisms involved in these processes.

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。 代谢综合征是心脏病危险因素的聚集。 血管应该扩张或收缩，以应对不同的刺激，如血压升高，以防止血压急剧变化。 当血管不能正常工作时，这通常是内皮功能障碍的结果。 胰岛素是一种将血糖或葡萄糖转化为可用能量的激素。 当身体不再有能力产生或释放适量的胰岛素时，就会发生胰岛素抵抗。 内皮功能障碍和胰岛素抵抗是代谢综合征的两个关键组成部分。 年龄的增加、总体和腹部肥胖、缺乏体力活动、胆固醇和血压通常与内皮功能障碍和胰岛素抵抗相关。 重要的是，我们知道炎症和氧化应激与内皮功能和胰岛素抵抗有关。 氧化应激是身体细胞暴露于分子（即活性氧物质），这些分子作为正常代谢的功能在体内连续产生。 活性氧会对细胞产生损伤，干扰身体的正常功能，如血管扩张或产生胰岛素的能力。 在人类中，我们无法阻止氧化应激，但我们可以阻止炎症。 因此，拟议的研究将检验以下假设：抑制炎症可能改善年龄、肥胖、习惯性体力活动水平、血浆脂质和脂蛋白和/或血压不同但无临床心血管或代谢疾病的个体的内皮功能障碍和胰岛素抵抗。 此外，拟议的研究将确定参与这些过程的分子机制。