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The non-nutritive sweetener erythritol adversely affects brain microvascular endothelial cell function
Auburn R Berry1, Samuel T Ruzzene1, Emily I Ostrander1
1Integrative Vascular Biology Laboratory, Department of Integrative PhysiologyUniversity of Colorado, Boulder, Colorado, United States.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 3, 2025
Summary
Erythritol, a common sweetener, increases oxidative stress and impairs nitric oxide (NO) production in brain cells. This in vitro study suggests erythritol may contribute to cerebrovascular risks.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Erythritol is a widely used non-nutritive sweetener linked to cardiovascular and cerebrovascular events.
- Understanding erythritol's cellular mechanisms is crucial for assessing its health implications.
Purpose of the Study:
- To investigate the in vitro effects of erythritol on human brain microvascular endothelial cells (hCMECs).
- To determine erythritol's impact on oxidative stress, nitric oxide (NO), endothelin (ET)-1, and tissue-type plasminogen activator (t-PA) release.
Main Methods:
- hCMECs were cultured and treated with 6 mM erythritol, a concentration found in typical artificially sweetened beverages.
- Assessed intracellular reactive oxygen species (ROS) production, antioxidant protein expression (superoxide dismutase-1, catalase), and eNOS phosphorylation.
- Measured NO and ET-1 production, and thrombin-induced t-PA release.
Main Results:
- Erythritol significantly increased ROS production and antioxidant protein expression in hCMECs.
- Erythritol reduced the phosphorylation of eNOS at Ser1177 and increased it at Thr495, leading to lower NO production.
- Erythritol elevated Big ET-1 expression and production, and significantly blunted t-PA release.
Conclusions:
- Erythritol adversely affects key functions of brain microvascular endothelial cells, including oxidative stress regulation, NO bioavailability, and vascular tone.
- These in vitro findings suggest a potential cellular mechanism linking erythritol consumption to an increased risk of ischemic stroke.
