Loader Jordan, Meziat Cindy, Watts Rani, Lorenzen Christian, Sigaudo-Roussel Dominique, Stewart Simon, Reboul Cyril, Meyer Gregory, Walther Guillaume
From the Avignon University, LAPEC EA4278, F-84000, Avignon, France (J.L., C.M., C.R., G.M., G.W.); Centre of Research Excellence to Reduce Inequality in Heart Disease, Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne (J.L.); School of Exercise Science, Australian Catholic University, Melbourne (J.L., R.W., C.L., G.W.); Laboratory of Tissue Biology and Therapeutic Engineering, UMR5305, University of Lyon 1, France (D.S.-R.); and The Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne (S.S.).
Arterioscler Thromb Vasc Biol. 2017 Jun;37(6):1250-1260. doi: 10.1161/ATVBAHA.116.308010. Epub 2017 Apr 13.
To assess vascular function during acute hyperglycemia induced by commercial sugar-sweetened beverage (SSB) consumption and its effect on underlying mechanisms of the nitric oxide pathway.
In a randomized, single-blind, crossover trial, 12 healthy male participants consumed 600 mL (20 oz.) of water or a commercial SSB across 2 visits. Endothelial and vascular smooth muscle functions were assessed in the microcirculation using laser speckle contrast imaging coupled with iontophoresis and in the macrocirculation using brachial artery ultrasound with flow- and nitrate-mediated dilation. Compared with water, SSB consumption impaired microvascular and macrovascular endothelial function as indicated by a decrease in the vascular response to acetylcholine iontophoresis (208.3±24.3 versus 144.2±15.7%, <0.01) and reduced flow-mediated dilation (0.019±0.002 versus 0.014±0.002%/s, <0.01), respectively. Systemic vascular smooth muscle remained preserved. Similar decreases in endothelial function were observed during acute hyperglycemia in an in vivo rat model. However, function was fully restored by treatment with the antioxidants, -acetylcysteine and apocynin. In addition, ex vivo experiments revealed that although the production of reactive oxygen species was increased during acute hyperglycemia, the bioavailability of nitric oxide in the endothelium was decreased, despite no change in the activation state of endothelial nitric oxide synthase.
To our knowledge, this is the first study to assess the vascular effects of acute hyperglycemia induced by commercial SSB consumption alone. These findings suggest that SSB-mediated endothelial dysfunction is partly due to increased oxidative stress that decreases nitric oxide bioavailability.
URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366442&isReview=true. Australian New Zealand Clinical Trials Registry Number: ACTRN12614000614695.
评估饮用市售含糖饮料（SSB）诱发急性高血糖期间的血管功能及其对一氧化氮途径潜在机制的影响。
在一项随机、单盲、交叉试验中，12名健康男性参与者分两次饮用600毫升（20盎司）水或市售SSB。使用激光散斑对比成像结合离子电渗法评估微循环中的内皮和血管平滑肌功能，使用肱动脉超声结合血流介导的扩张和硝酸盐介导的扩张评估大循环中的内皮和血管平滑肌功能。与饮水相比，饮用SSB损害了微血管和大血管内皮功能，表现为对乙酰胆碱离子电渗的血管反应降低（分别为208.3±24.3对144.2±15.7%，<0.01）和血流介导的扩张减少（0.019±0.002对0.014±0.002%/秒，<0.01）。全身血管平滑肌功能保持正常。在体内大鼠模型的急性高血糖期间也观察到类似的内皮功能下降。然而，使用抗氧化剂N-乙酰半胱氨酸和载脂蛋白处理后，功能完全恢复。此外，体外实验表明，尽管急性高血糖期间活性氧的产生增加，但内皮中一氧化氮的生物利用度降低，尽管内皮型一氧化氮合酶的激活状态没有变化。
据我们所知，这是第一项单独评估饮用市售SSB诱发急性高血糖对血管影响的研究。这些发现表明，SSB介导的内皮功能障碍部分归因于氧化应激增加，氧化应激会降低一氧化氮的生物利用度。
