ObjectivesSugar-sweetened beverages are the largest source of added sugar, and the largest single source of calories, in the American diet. Consumption of added sugars is a dietary factor linked to risk of chronic disease, including obesity, type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD). One of the metabolic fates of glucose, particularly in individuals with metabolic syndrome, is conversion to other sugars and polyols. Recently, the polyol erythritol was identified as a product of glucose in humans and other mammals. Excitingly, elevated circulating erythritol can predict T2DM and CVD development up to 20 years before disease onset. The relationship between diet and erythritol synthesis is unknown. We hypothesized that high sugar intake may promote erythritol synthesis from glucose. The purpose of this study was to determine if sugar in drinking water increases circulating erythritol in mice. MethodsWe fed 8-week-old C57BL/6J mice a high-fat diet with 60% fat-derived calories for two weeks. Mice were randomly divided into two treatment groups: water, or water with 30% sucrose (w/v). After two weeks of treatment, we recorded body weight, food and water intake, and fasting blood glucose. Fasting plasma erythritol and non-fasted urine erythritol were measured by gas chromatography-mass spectrometry (GC-MS). All data were analyzed using an unpaired t-test. ResultsAfter two weeks, we found that urine erythritol was 50% higher in mice treated with sucrose compared to water controls (p < 0.05). As expected, mice treated with sucrose water consumed more total calories and calories from carbohydrates than controls (p < 0.01 and p < 0.0001, respectively). There was no difference in body weight or fasting blood glucose between groups. Contrary to our expectation, there was also no significant difference in plasma erythritol between groups. ConclusionsOur findings demonstrate that erythritol synthesis and excretion are elevated in response to sugar in drinking water. This suggests that erythritol synthesis may be a mechanism to dispose of glucose during caloric excess. Funding SourcesThis work is supported by the Education and Workforce Development Predoctoral Fellowship from the USDA National Institute of Food and Agriculture.