Functional hyperemia during metabolic syndrome

代谢综合征期间的功能性充血

• 批准号: 6994569
• 负责人: Jay S Naik
• 金额: $ 4.06万
• 依托单位: UNIVERSITY OF MISSISSIPPI MED CTR
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-08-01 至 2006-05-24
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6994569
• 关键词: NAD(P)H dehydrogenase; blood circulation; cardiovascular disorder; cardiovascular disorder therapy; exercise; free radical oxygen; laboratory rat; metabolic syndrome; muscle contraction; nonhuman therapy evaluation; noninsulin dependent diabetes mellitus; obesity; oxidative stress; postdoctoral investigator; striated muscles; vascular endothelium; vasodilation; xanthine oxidase

DESCRIPTION (provided by applicant): The long-term goal of our laboratory is to define the physiological mechanisms linking muscle blood flow to the metabolic state of the tissue, and how these mechanisms are altered under pathophysiological conditions. For example, obesity is associated with hypertension, dyslipidemia, and type II diabetes, a collection of conditions often referred to as metabolic syndrome affecting approximately 45 million US residents. Endothelial dysfunction is major component of metabolic syndrome. Impaired blood glucose homeostasis and elevated reactive oxygen species generation may be important factors in the endothelial dysfunction seen in these individuals. The present proposal employs an animal model, the obese Zucker rat which exhibits increased food consumption, and rapidly develops obesity, type II diabetes, and hypertension (i.e., metabolic syndrome). Thus, the Zucker rat provides a useful tool for the study of vascular function during a cohort of pathophysiological conditions that are rapidly growing in prevalence in western society. The experiments in this proposal will provide important new information concerning the cellular mechanism(s) of impaired functional hyperemia in a model of metabolic syndrome, and the cellular mechanisms by which exercise training improves endothelial function.

描述（由申请人提供）：我们实验室的长期目标是定义将肌肉血流与组织的代谢状态联系起来的生理机制，以及在病理生理条件下如何改变这些机制。例如，肥胖与高血压，血脂异常和II型糖尿病有关，这是一系列通常称为代谢综合征，影响了约4500万美国居民。内皮功能障碍是代谢综合征的主要组成部分。在这些个体中看到的内皮功能障碍中，血糖稳态受损和活性氧的产生升高可能是重要因素。本提案采用动物模型，肥胖的扎克大鼠，表现出增加的食物消耗，并迅速发展肥胖，II型糖尿病和高血压（即代谢综合征）。因此，扎克大鼠为研究西方社会患病率迅速增长的病理生理状况的研究提供了一种有用的工具。该提案中的实验将提供有关代谢综合征模型中功能性充血受损的细胞机制以及运动训练改善内皮功能的细胞机制的重要新信息。