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

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 代谢综合征是心脏病风险因素的聚集性。血管应该对不同的刺激做出反应，如血压升高，以防止血压的剧烈变化。当血管功能不正常时，这通常是内皮功能障碍的结果。胰岛素是一种荷尔蒙，能将血糖或葡萄糖转化为可用能量。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、总肥胖症、腹部肥胖症、缺乏运动、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。氧化应激是指人体细胞暴露在分子(即活性氧物种)下，这些分子在正常新陈代谢的作用下在体内持续产生。活性氧物质会对细胞造成损害，干扰人体的正常功能，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，这项拟议的研究将检验这样一个假设，即抑制炎症可能改善年龄、肥胖、习惯性体力活动水平、血脂和脂蛋白和/或血压不同、但没有临床心血管或代谢性疾病的个体的内皮功能障碍和胰岛素抵抗。此外，拟议的研究将确定这些过程中涉及的分子机制。

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.