EFFECT OF FRUCTOSE ON ENDOTHELIAL FUNCTION

果糖对内皮功能的影响

• 批准号: 7717117
• 负责人: MARK R SEGAL
• 金额: $ 1.08万
• 依托单位: UNIVERSITY OF FLORIDA
• 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 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7717117
• 关键词: Allopurinol; Biological Availability; Blood flow; Computer Retrieval of Information on Scientific Projects Database; Epidemic; Fructose; Funding; Grant; Institution; Insulin; Insulin Resistance; Intake; Link; Maize; Metabolic syndrome; Nitric Oxide; Obesity; Pathway interactions; Rattus; Research; Research Personnel; Resources; Serum; Skeletal Muscle; Source; Sucrose; Syndrome; United States National Institutes of Health; Uric Acid; Zea mays; glucose uptake; prevent; toe corn

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. Fructose intake either as sucrose or High fructose corn syrup has been recently linked with the epidemic of obesity and metabolic syndrome. We have identified a potential pathway by which fructose may cause this syndrome. Specifically, fructose intake results in the rapid increase in serum uric acid over 30- 60 minutes. In turn, we have found that uric acid can inhibit endothelial nitric oxide bioavailability. Blocking NO has been found to be a mechanism for insulin resistance, since insulin stimulates glucose uptake in skeletal muscle in part by increasing blood flow via an NO dependent mechanism. Consistent with this hypothesis, we have found that we can prevent or reverse many features of the metabolic syndrome in rats by lowering their uric acid with allopurinol.

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