Scientists show how a common zero -calorie sweetener found in many nutrition drinks can damage the brain’s vascular system by increasing oxidative stress and damaging the vital functions of the blood vessel.
Study: Non -religious sweetener redritol adversely affects the function of microvascular endothelial cells of the brain. Credit Picture: Tawan Ramtang/Shutterstock.com
Erythritol, an artificial sweetener, has adversely affected the human brain microvascular endothelial cell in laboratory experiments and can contribute to mechanisms based on an increased risk of ischemic stroke, as mentioned by a study published by a study published in Newspaper of applied physiology.
Background
Erythritol is an organic low -calorie organic compound used more widely as an artificial sweetener in food products and drinks due to its minimum effect on blood glucose and insulin levels. The US Food and Drug Administration (FDA) approved the use of erythritol for people with diabetes, obesity or metabolic syndrome to help reduce calories and intake of sugar and control blood glucose levels.
Erythritol is of course present in various fruits and vegetables and is also produced in the human body of glucose and fructose. Therefore, blood erythritol levels depend on endogenous production and exogenous intake.
Recent elements associate increased levels of blood erythritol with an increased risk of cardiovascular and cerebrospinal events, such as myocardial infarction and stroke. This Union has been observed in men and women and in subgroups in the United States and Europe.
Since endothelial cell dysfunction contributes significantly to cardiovascular and cerebrospinal diseases, researchers at the University of Colorado, USA, explored the effect of erythritol on release of cerebral endothelial cells, and the production of nitrogenic cells.
Design planning
The study used cultivated human brain microvascular endothelial cells to explore the effect of erythritol. Cultivated cells were treated with erythritol six mm, equivalent to the standard amount of artificial sweet drinks, for 24 hours.
Intracellular oxidative stress was determined by measuring the production of reactive oxygen species (ROS) and the expression of antioxidant enzymes. The production of nitric oxide, which helps to regulate blood pressure and blood flow by expanding blood vessels, was measured using a commercial analysis kit.
Endothelin-1 levels, which help regulate blood pressure by reducing blood vessels and the tissue-type plasminogenic, which helps to break down blood clots, were determined using an enzymatic immunoodox test (ELISA).
Basic findings
The study found that the 24-hour treatment of human brain microvascular endothelial cells with erythritol causes the production of ROS, antioxidant enzyme expressions and endothelin-1 production and significantly reduces the release of nitric oxide activator and release.
Erythritol reduced the activation of endothelial nitrate (ENOS) synthesis by reducing phosphorylation in SER1177 (an activation position) and increasing phosphorylation in THR495 (inhibitory position), the mechanisms observed by reduced production of nitrogen.
These findings reveal that non-dystical artificial redricritol sweetener increases oxidative stress, limits the enlargement of blood vessels, promotes the stenosis of blood vessels and prevents the activity of thrombosis (division of the bloodstream). affect the brain vascular, but require confirmation in animal and clinical studies before the risk of the brain.
Importance
The findings of the study emphasize that erythritol, at a concentration that is usually available in commercially available sweet drinks, can cause changes in the phenotype of microvascular endothelial cells of the brain, which in turn can lead to cerebrovascular dysfunction.
Due to the presence of a large number of mitochondria, endothelial cells of the brain are more prone to damage and malfunction with ROS mediation. Excessive production of ROS in these cells, as observed in this study, can lead to a disorder of the integrity of the blood -brain barrier, resulting in increased vascular permeability, which promotes tissue damage and death.
The increased expression of antioxidant enzymes observed in the study indicates cellular defense mechanisms. However, the study noted that despite the response of the enzyme compensatory reaction, ROS levels remained increased, suggesting that these defenses do not completely neutralize the oxidative stress. This finding suggests that although erythritol increases ROS production, it does not suppress the antioxidant defense system. However, researchers could not rule out the possibility that repeated or long -term exposure to Erythritol could suppress antioxidant defense mechanisms.
The production of nitric oxide and endothelin-1 by endothelial cells of the brain is vital to regulating blood flow to the brain. The observed decrease in nitric oxide production and the induction of endothelin-1 production of endothelial cells of the brain indicate that exposure to erythritol causes biochemical displacements that prefer vasoconstriction, leading to weakened brain flow of blood and pervasive blood flow.
The tissue -type plasminogen released by endothelial cells of the brain plays a vital role in maintaining the brain vascular system and in preventing blood clot formation. Therefore, the decrease in erythritol mediated in the release of a tissue -type activator can lead to an increased risk of blood clot and subsequent thrombotic brain injury.
Overall, the study provides experimental indications on the mechanism of action of Erythritol, which supports recent epidemiological data linking the exposure to Erythritol with an increased risk of cerebrospinal events.
The study used laboratory cultivated human brain cells for experimental purposes. Although the findings derived from laboratory experiments provide a valuable picture of the mechanism of reds, further studies are needed to understand these findings in animals and humans for preclinical and clinical risk assessments.
The study examined the immediate exposure of endothelial cells of the human brain in Erythritol. Unlike some reports, Erythritol crosses the blood -brain barrier and can interact with the vascular system of the brain, as noted by the authors. This further emphasizes the need for animal studies to determine the level of exposure and the duration required for brain vascular damage caused by redritol.
