Myricetin supplementation decreases hepatic lipid synthesis and inflammation by modulating gut microbiota

The relationship between poor in vivo bioavailability and effective pharmacological activity are not yet fully clarified for many flavonoids. The analysis of flavonoids-induced alterations in the gut microbiota represents a promising approach to provide useful clues to elucidate the mechanism of act...

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Veröffentlicht in:Cell reports (Cambridge) 2021-08, Vol.36 (9), p.109641-109641, Article 109641
Hauptverfasser: Sun, Wen-Long, Li, Xin-Yu, Dou, Hao-Yue, Wang, Xu-Dong, Li, Jing-Da, Shen, Liang, Ji, Hong-Fang
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Sprache:eng
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Zusammenfassung:The relationship between poor in vivo bioavailability and effective pharmacological activity are not yet fully clarified for many flavonoids. The analysis of flavonoids-induced alterations in the gut microbiota represents a promising approach to provide useful clues to elucidate the mechanism of action. Here, we investigate the effect of myricetin supplementation on high-fat-diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in rats and explore the associations with the gut microbiota through high-throughput analyses. The 12-week myricetin supplementation and fecal microbiota transplantation outcomes suggest that myricetin significantly slows the development of NAFLD. Meanwhile, the anti-NAFLD effects of myricetin are associated with the modulation of the gut microbiota composition. Myricetin reduces hepatic lipid synthesis and inflammation through modulations in fecal butyric-acid-related gut microbiota and protection of the gut barrier function. This study may facilitate the elucidation of the action mechanism of flavonoids with low bioavailability. [Display omitted] •Myricetin slows the development of NAFLD in HFD-fed rat•Myricetin reduces hepatic lipid synthesis and inflammation•Myricetin modulates the fecal butyric acid-related gut microbiota•Myricetin protects the gut barrier function Sun et al. find that myricetin reduces hepatic lipid synthesis and inflammation through modulations in fecal butyric acid-related gut microbiota and protection of the gut barrier function.
ISSN:2211-1247
2211-1247
DOI:10.1016/j.celrep.2021.109641