Search

cope A number of findings suggest that zero-calorie d-allulose, also known as d-psicose, has beneficial effects on obesity-related metabolic disturbances. However, it is unclear whether d-allulose can normalize the metabolic status of diet-induced obesity without having an impact on the energy density. We investigated whether 5% d-allulose supplementation in a high fat diet(HFD) could normalize body fat in a diet-induced obesity animal model under isocaloric pair-fed conditions. Methods and results Mice were fed an HFD with or without various sugar substitutes (d-glucose, d-fructose, erytritol, or d-allulose, n = 10 per group) for 16 wk. Body weight and fat-pad mass in the d-allulose group were dramatically lowered to that of the normal group with a simultaneous decrease in plasma leptin and resistin concentrations. d-allulose lowered plasma and hepatic lipids while elevating fecal lipids with a decrease in mRNA expression of CD36, ApoB48, FATP4, in the small intestine in mice. In the liver, activities of both fatty acid synthase and β-oxidation were downregulated by d-allulose to that of the normal group; however, in WAT, fatty acid synthase was decreased while β-oxidation activity was enhanced. Conclusion Taken together, our findings suggest that 5% dietary d-allulose led to the normalization of the metabolic status of diet-induced obesity by altering lipid-regulating enzyme activities and their gene-expression level along with fecal lipids.

Scope The results of recent studies on d-allulose intervention in high-fat diet (HFD)-fed mice suggest that d-allulose has a substantial impact on obesity. In addition, several studies have uncovered bacterial candidates among the gut microbiota associated with obesity and inflammation in mice. To identify the d-allulose-attenuated genes related to the inflammation-associated bacterial candidates, two types of statistical analyses are performed. Methods and results Using liver and epididymal fat tissues, genes with expression levels that recovered from HFD-induced dysregulation are identified through differentially expressed gene (DEG) analysis. Finally, correlation-based network analysis between the diet, microbes, and the candidates identified from DEG analysis reveal 20 genes that showed anti-obesogenic patterns and associations with Lactobacillus and Coprococcus, which are representative bacterial candidates associated with inflammation and obesity. Conclusion The results of the present study suggest that d-allulose closely interacts with the candidate genes and microbes to alleviate weight gain and inflammation, partly via down regulation of Gm12250 expression in multiple tissues and increases the Lactobacillus and Coprococcus in gut microbiota composition.