EFFECT OF FRUCTOSE ON ENDOTHELIAL FUNCTION

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。 作为蔗糖或高果糖玉米糖浆的果糖摄入量最近被认为与肥胖和代谢综合征的流行有关。我们已经确定了果糖可能导致这种综合征的潜在途径。具体地说，摄入果糖会导致血尿酸在30-60分钟内迅速增加。反过来，我们发现尿酸可以抑制内皮细胞一氧化氮的生物利用度。阻断NO被发现是胰岛素抵抗的一种机制，因为胰岛素刺激骨骼肌摄取葡萄糖的部分原因是通过依赖NO的机制增加血流量。与这一假设一致，我们发现我们可以通过用别嘌醇降低大鼠的尿酸来预防或逆转大鼠代谢综合征的许多特征。

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.