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Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids

It has been reported that Akkermansia muciniphila improves host metabolism and reduces inflammation; however, its potential effects on bile acid metabolism and metabolic patterns in metabolic‐associated fatty liver disease (MAFLD) are unknown. In this study, we have analysed C57BL/6 mice under three...

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Autores principales: Wu, Wenrui, Kaicen, Wang, Bian, Xiaoyuan, Yang, Liya, Ding, Shi, Li, Yating, Li, Shengjie, Zhuge, Aoxiang, Li, Lanjuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10527187/
https://www.ncbi.nlm.nih.gov/pubmed/37377410
http://dx.doi.org/10.1111/1751-7915.14293
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author Wu, Wenrui
Kaicen, Wang
Bian, Xiaoyuan
Yang, Liya
Ding, Shi
Li, Yating
Li, Shengjie
Zhuge, Aoxiang
Li, Lanjuan
author_facet Wu, Wenrui
Kaicen, Wang
Bian, Xiaoyuan
Yang, Liya
Ding, Shi
Li, Yating
Li, Shengjie
Zhuge, Aoxiang
Li, Lanjuan
author_sort Wu, Wenrui
collection PubMed
description It has been reported that Akkermansia muciniphila improves host metabolism and reduces inflammation; however, its potential effects on bile acid metabolism and metabolic patterns in metabolic‐associated fatty liver disease (MAFLD) are unknown. In this study, we have analysed C57BL/6 mice under three feeding conditions: (i) a low‐fat diet group (LP), (ii) a high‐fat diet group (HP) and (iii) a high‐fat diet group supplemented with A. muciniphila (HA). The results found that A. muciniphila administration relieved weight gain, hepatic steatosis and liver injury induced by the high‐fat diet. A. muciniphila altered the gut microbiota with a decrease in Alistipes, Lactobacilli, Tyzzerella, Butyricimonas and Blautia, and an enrichment of Ruminiclostridium, Osclibacter, Allobaculum, Anaeroplasma and Rikenella. The gut microbiota changes correlated significantly with bile acids. Meanwhile, A. muciniphila also improved glucose tolerance, gut barriers and adipokines dysbiosis. Akkermansia muciniphila regulated the intestinal FXR‐FGF15 axis and reshaped the construction of bile acids, with reduced secondary bile acids in the caecum and liver, including DCA and LCA. These findings provide new insights into the relationships between probiotics, microflora and metabolic disorders, highlighting the potential role of A. muciniphila in the management of MAFLD.
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spelling pubmed-105271872023-09-28 Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids Wu, Wenrui Kaicen, Wang Bian, Xiaoyuan Yang, Liya Ding, Shi Li, Yating Li, Shengjie Zhuge, Aoxiang Li, Lanjuan Microb Biotechnol Research Articles It has been reported that Akkermansia muciniphila improves host metabolism and reduces inflammation; however, its potential effects on bile acid metabolism and metabolic patterns in metabolic‐associated fatty liver disease (MAFLD) are unknown. In this study, we have analysed C57BL/6 mice under three feeding conditions: (i) a low‐fat diet group (LP), (ii) a high‐fat diet group (HP) and (iii) a high‐fat diet group supplemented with A. muciniphila (HA). The results found that A. muciniphila administration relieved weight gain, hepatic steatosis and liver injury induced by the high‐fat diet. A. muciniphila altered the gut microbiota with a decrease in Alistipes, Lactobacilli, Tyzzerella, Butyricimonas and Blautia, and an enrichment of Ruminiclostridium, Osclibacter, Allobaculum, Anaeroplasma and Rikenella. The gut microbiota changes correlated significantly with bile acids. Meanwhile, A. muciniphila also improved glucose tolerance, gut barriers and adipokines dysbiosis. Akkermansia muciniphila regulated the intestinal FXR‐FGF15 axis and reshaped the construction of bile acids, with reduced secondary bile acids in the caecum and liver, including DCA and LCA. These findings provide new insights into the relationships between probiotics, microflora and metabolic disorders, highlighting the potential role of A. muciniphila in the management of MAFLD. John Wiley and Sons Inc. 2023-06-28 /pmc/articles/PMC10527187/ /pubmed/37377410 http://dx.doi.org/10.1111/1751-7915.14293 Text en © 2023 The Authors. Microbial Biotechnology published by Applied Microbiology International and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Research Articles
Wu, Wenrui
Kaicen, Wang
Bian, Xiaoyuan
Yang, Liya
Ding, Shi
Li, Yating
Li, Shengjie
Zhuge, Aoxiang
Li, Lanjuan
Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title_full Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title_fullStr Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title_full_unstemmed Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title_short Akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
title_sort akkermansia muciniphila alleviates high‐fat‐diet‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10527187/
https://www.ncbi.nlm.nih.gov/pubmed/37377410
http://dx.doi.org/10.1111/1751-7915.14293
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