Abstract

Background: Aspartame is an artificial sweetener that has been widely used in beverages and foods. Recently, higher intake of artificially sweetened beverages was shown to be associated with increased risk of stroke. Objective: To investigate if short-term high consumption of aspartame could increase cerebral infarct volume and mortality in mouse models of focal ischemic stroke. Methods: Eleven-week-old male C57BL/6N mice (n=90) received one of the following three treatments for 7 days: phosphate-buffered saline (PBS), aspartame 200 mg/kg in PBS, and aspartame in Zero Coke (with the final dose of aspartame being 200 mg/kg). Thereafter, either transient middle cerebral artery occlusion for 1 hour (1h-tMCAO; n=27, 9/group) or common carotid artery occlusion (CCAO)-related hemispheric ischemia with cerebral autoregulatory dysfunction (CCAO+CAD; n=63, 21/group) was induced. To measure the infarct volume, 2,3,5-Triphenyltetrazolium chloride staining was performed at 24 hours after tMCAO and 6 days after CCAO+CAD. Results: 1h-tMCAO-related 24-hour mortality and infarct volume (of survived animals) did not differ significantly among the three groups (both p>0.05): PBS (5/9 death and 93.7±30.0mm 3 ), aspartame in PBS (2/9 death and 102±50.0mm 3 ), and aspartame in Zero Coke (4/9 death and 111.4±17.4mm 3 ). CCAO+CAD-related mortality 6-day mortality did not show inter-group differences (p>0.05): PBS (n=9/21, 42.9 %), aspartame in PBS (n=12/21, 57.1 %), and aspartame in Zero Coke (n=8/21, 38 %). Among the survived, infarct volume did not significantly differ, either (p>0.05): PBS (60.8±68.0mm 3 ), aspartame in PBS (58.5±68.0mm 3 ), and aspartame in Zero Coke (54.2±48.3mm 3 ). Conclusions: Short-term high consumption of aspartame did not increase cerebral infarct volume and stroke-related mortality in our experimental setting. Category: Peripheral Artery Disease, Carotid Artery Disease and Stroke

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