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: 7604513
• 负责人: LISA LIESNEWSKI
• 金额: $ 1.92万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604513
• 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.

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。 代谢综合征是心脏病危险因素的聚类。 血管应响应不同的刺激（例如升高血压）来扩张或收缩，以防止血压的急剧变化。 当血管无法正常工作时，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。 当人体不再具有产生或释放适量的胰岛素的能力时，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，腹部肥胖，身体不活跃，胆固醇和血压的增加通常与内皮功能障碍和胰岛素抵抗有关。 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。 氧化应激是人体细胞暴露于分子（即活性氧），这些分子是在体内连续产生的，这是正常代谢的函数。 活性氧可能会对细胞产生损害并干扰人体的正常功能，例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：抑制炎症可能会改善年龄，肥胖，习惯性体育活动水平，血浆脂质和/或血压的人的内皮功能障碍和胰岛素抵抗，但没有临床心血管或代谢疾病。 此外，提出的研究将确定这些过程中涉及的分子机制。