Erythritol and high-glucose stress in human endothelial cells
What it found
In lab tests on human endothelial cells, erythritol protected the cells from death caused by high glucose and a peroxynitrite-generating chemical.
Under normal glucose, erythritol had minimal effects.
What they found
Animal and lab studies
Cell death
High glucose increased the percentage of dead cells almost 4-fold. Adding erythritol completely prevented this increase. Erythritol also reduced cell death caused by SIN-1.
Oxidative stress markers
High glucose did not increase malondialdehyde or 8-hydroxydeoxyguanosine. There was a trend toward higher protein carbonyls with high glucose, and erythritol showed a trend toward lower protein carbonyls.
Nitric oxide release
High glucose caused a 3-fold increase in nitric oxide release. Erythritol showed a trend toward lower nitric oxide production. Erythritol did not affect NOS3 activity.
Eicosanoids
In cells exposed to high glucose plus erythritol, thromboxane B2 increased while 8-HETE and 12-HETE decreased compared to high glucose alone. Erythritol also changed levels of other eicosanoids in the culture medium.
Gene expression
High glucose changed 434 transcripts. Adding erythritol reversed the direction of change in 148 of 153 transcripts that changed in common with high glucose alone. Erythritol also affected transcripts related to the TCA cycle and electron transport chain.
What the authors conclude
“Overall, these data indicate a therapeutically important endothelial protective effect of erythritol under hyperglycemic conditions.”
Also in their conclusions
- They conclude that erythritol protects endothelial cells during high glucose conditions via effects on multiple targets.
- They state that erythritol by itself under non-diabetic conditions has minimal effects on endothelial cells.
- They suggest that erythritol could be important for people with diabetes to reduce their risk of developing diabetic complications.
How it was done
The authors previously found that erythritol prevented endothelial dysfunction in diabetic rats. They wanted to find mechanisms beyond radical scavenging that could explain this protective effect.
They grew human umbilical vein endothelial cells in normal glucose (7 mM) or high glucose (30 mM) for 24 hours, with or without erythritol (5 mM). They also tested cells exposed to SIN-1, a peroxynitrite generator, and measured cell death, oxidative stress markers, nitric oxide release, eicosanoids, and gene expression.
What it can’t tell you
- These are lab tests on human cells grown in a dish. They cannot show what happens in the human body.
- The study used a single cell type and short exposure times. It cannot show long-term effects or effects on whole organs.
- The authors note that many effects were small and often did not reach statistical significance.
Who paid
- Conflicts
- Competing Interests: Research was financially supported by Cargill, the employer of Alvin Berger and Peter de Cock. Erythritol was provided by Cargill. There are no further patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.
- Authors work at
- Maastricht University, The Netherlands
The paper
- Title
- Multi-targeted mechanisms underlying the endothelial protective effects of the diabetic-safe sweetener erythritol
- Type
- Study
- Evidence
- Animals and lab studies
- Summarised from
- Full text
- Cite
- Boesten DM, Berger A, de Cock P, et al (2013). Multi-targeted mechanisms underlying the endothelial protective effects of the diabetic-safe sweetener erythritol. PloS one. doi:10.1371/journal.pone.0065741Free full textPubMed 23755276DOI
Summary written 26 Sep 2026. Check it against the paper before it changes what you eat. How we summarise papers · Report an error