4.7 Article

Flavonoids from Whole-Grain Oat Alleviated High-Fat Diet-Induced Hyperlipidemia via Regulating Bile Acid Metabolism and Gut Microbiota in Mice

Journal

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 69, Issue 27, Pages 7629-7640

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.1c01813

Keywords

whole-grain oat; flavonoids; hyperlipidemia; gut microbiota; bile acid metabolism; lipid metabolism

Funding

  1. Capacity-Building Project of Local Universities of SSTC [20060502100]
  2. Dawn Program of Shanghai Education Commission [19SG45]
  3. National Natural Science Foundation of China [31901609]

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Whole-grain oat flavonoids can improve hyperlipidemia induced by high-fat diet by regulating lipid metabolism, promoting bile acid synthesis, and enhancing the efflux of fat through the FXR pathway. Additionally, they can significantly alter the composition of gut microbiota, reducing harmful bacteria and increasing beneficial bacteria.
A high-fat diet (HFD) causes hyperlipidemia, which worsens disturbances in bile acid (BA) metabolism and gut microbiota. This study aimed to investigate the regulation of flavonoids from whole-grain oat (FO) on BA metabolism and gut microbiota in HFD-induced hyperlipidemic mice. The experiment results showed that FO improved serum lipid profiles and decreased body weight and lipid deposition in HFD-fed mice. Through real-time qualitative polymerase chain reaction (RT-qPCR) and Western blot assays, by up-regulating the expression of PPARa, CPT-1, CYP7A1, FXR, TGR5, NTCP, and BSTP, and downregulating those of SREBP-1c, FAS, and ASBT, FO suppressed lipogenesis, promoted lipolysis and BA synthesis, and efflux to faeces via the FXR pathway. 16s rRNA sequencing revealed that FO significantly increased Akkermansia and significantly decreased Lachnoclostridium, Blautia, Colidextribacter, and Desulfovibrio. Spearman's correlation analysis showed that these bacteria were strongly correlated with hyperlipidemia-related parameters. Therefore, our results indicated that FO possessed an antihyperlipidemic effect via regulating the gut-liver axis, i.e., BA metabolism and gut microbiota.

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