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Effects of Sugar-Sweetened Beverage Consumption on Microvascular and Macrovascular Function in a Healthy Population
Jordan Loader1, Cindy Meziat1, Rani Watts1
1From 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.).
Objective:
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.
Approach And Results:
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%, P<0.01) and reduced flow-mediated dilation (0.019±0.002 versus 0.014±0.002%/s, P<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, N-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.
Conclusions:
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.
Clinical Trial Registration:
URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366442&isReview=true. Australian New Zealand Clinical Trials Registry Number: ACTRN12614000614695.