In this study, we have investigated the mechanisms of improvement of glucose intolerance via changes in gut microbiota using db/db mice. Eight-week-old db/m and db/db mice were divided into 5 groups and housed for eight weeks (n=6 for each group): db/m group without RJ (db/m), db/db mice without RJ (db/db), db/db mice with 0.2% RJ (db/db + 0.2% RJ), db/db mice with 1% RJ (db/db + 1% P), db/db mice with 5% RJ (db/db + 5% RJ) (Figure A). Body weight of db/db mice was higher than that of db/db mice fed with RJ (Figure B). Moreover, glucose tolerance evaluated by iPGTT and ITT were improved by RJ (Figure C-F). Next, the expression of inflammation-related genes (Tnfa, Ifng) and nutrient transporter genes (Cd36, Sglt1, and Pept1) in small intestine were increased in db/db mice more than in db/m mice, nevertheless significantly decreased by RJ (Figure G-K). In the gut microbiota analyses by 16S rRNA sequencing, it was found that seven taxa, including Firmicutes, were overexpressed in db/db mice, while seven taxa including short-chain fatty acid-producing bacteria such as the family Ruminococcaceae, the genus Butyricioccus, and the genus Acetiviblio were overexpressed in db/db +5%RJ mice in the LEfSe algorithm (Figure L).

In summary, it is suggested that RJ might altere the gut microbiota and contributed to the improvement of metabolic disorders by changing the expression of genes related to nutrient absorption in the small intestine.


T. Okamura: Research Support; Yamada Bee Company, Inc. M. Hamaguchi: Research Support; Yamada Bee Company, Inc. H. Okamoto: Employee; Yamada Bee Company, Inc. N. Okumura: Employee; Yamada bee company, Inc. M. Fukui: None.

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