Tracing the Anti‐Inflammatory Mechanism/Triggers of d‐Allulose: A Profile Study of Microbiome Composition and mRNA Expression in Diet‐Induced Obese Mice

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. Recently, there has been a global shift in diet toward increased intake of energy‐dense foods that are high in sugars. Allulose, which is sweet but has no calories, has received attention as a sugar substitute. Mice are divided into three dietary groups and are fed a normal diet, a high‐fat diet (HFD, 20% fat, 1% cholesterol, w/w), HFD with 5% d‐allulose supplement for 16 weeks. A pair‐feeding approach is used so that all groups receiving the HFD will have the same calorie intake. As a result, allulose supplement improves the obesity‐related inflammation by regulating microbial community and mRNA expression.