EFFECT OF FRUCTOSE ON ENDOTHELIAL FUNCTION

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 研究中心，而研究中心不一定是研究者所在的机构。 果糖摄入无论是蔗糖或高果糖玉米糖浆最近已与肥胖症和代谢综合征的流行。 我们已经确定了果糖可能导致这种综合征的潜在途径。具体来说，果糖摄入导致血清尿酸在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。已经发现阻断NO是胰岛素抗性的机制，因为胰岛素通过NO依赖性机制增加血流量部分地刺激骨骼肌中的葡萄糖摄取。 与这一假设相一致，我们已经发现，我们可以通过用别嘌呤醇降低大鼠的尿酸来预防或逆转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.