Mariotti François, Huneau Jean François, Szezepanski Isabelle, Petzke Klaus J, Aggoun Yacine, Tomé Daniel, Bonnet Damien
INRA, AgroParisTech, UMR914 Nutrition Physiology and Ingestive Behavior, F-75005 Paris, France.
J Nutr. 2007 Jun;137(6):1383-9. doi: 10.1093/jn/137.6.1383.
Postprandial endothelial dysfunction is a key event mediating the effects of diet on early atherogenesis. The potential effects of protein intake have been overlooked in the past, although amino acids are precursors for homocysteine and nitric oxide (NO). Our objective was to study the effect of amino acids on postprandial vascular function, in relation to the utilization of meal arginine for NO production. In a crossover design, 9 men ingested 50 g of a complete amino acid mixture, trace-labeled with (13)C-glycine and (15)N(2)-arginine, without (meal A) or with (meal B) 3 g extra arginine. The postprandial utilization of meal arginine for NO production was determined from urinary (15)NO(3). We monitored endothelial function of the brachial artery, the stiffness of the common carotid artery, aortic pulse wave velocity and soluble markers related to endothelial function for 8 h. Meal A did not significantly increase plasma homocysteine and did not alter endothelial function markers. The amount of NO synthesized from meal arginine doubled after meal B (107.1 +/- 16.5% increase vs. meal A, P < 0.01) but was very low (271 +/- 84 ppm vs. 332 +/- 73 ppm, P < 0.05, respectively). After meal B, flow-mediated and nitroglycerine-induced dilation decreased but common carotid artery compliance, pulse wave velocity, plasma soluble intercellular adhesion molecule-1, and von Willebrand factor, and urinary cGMP did not differ when compared with meal A. Together, the data indicate that, in healthy men, meal amino acids do not adversely affect endothelial function, and meal arginine only slightly enters the NO pathway. Unexpectedly, arginine in physiological amounts may acutely lessen smooth muscle cell reactivity to a high dynamic NO release.
餐后内皮功能障碍是介导饮食对早期动脉粥样硬化影响的关键事件。尽管氨基酸是同型半胱氨酸和一氧化氮（NO）的前体，但过去蛋白质摄入的潜在影响一直被忽视。我们的目的是研究氨基酸对餐后血管功能的影响，以及膳食精氨酸用于生成NO的情况。在一项交叉设计中，9名男性摄入50克完全氨基酸混合物，用（13）C-甘氨酸和（15）N（2）-精氨酸进行微量标记，一种情况是没有额外的精氨酸（餐A），另一种情况是添加3克额外精氨酸（餐B）。通过尿（15）NO（3）来测定膳食精氨酸用于生成NO的餐后利用率。我们监测肱动脉的内皮功能、颈总动脉的僵硬度、主动脉脉搏波速度以及与内皮功能相关的可溶性标志物，持续8小时。餐A没有显著增加血浆同型半胱氨酸，也没有改变内皮功能标志物。餐B后，膳食精氨酸合成的NO量增加了一倍（与餐A相比增加了107.1±16.5%，P<0.01），但仍然非常低（分别为271±84 ppm和332±73 ppm，P<0.05）。餐B后，血流介导的和硝酸甘油诱导的血管舒张功能下降，但与餐A相比，颈总动脉顺应性、脉搏波速度、血浆可溶性细胞间黏附分子-1、血管性血友病因子以及尿cGMP没有差异。总体而言，数据表明，在健康男性中，膳食氨基酸不会对内皮功能产生不利影响，膳食精氨酸仅少量进入NO生成途径。出乎意料的是，生理量的精氨酸可能会急性降低平滑肌细胞对高动态NO释放的反应性。
