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Phenotyping non‐alcoholic fatty liver disease by the gut microbiota: Ready for prime time?
Author(s) -
Demir Münevver,
Lang Sonja,
Martin Anna,
Farowski Fedja,
Wisplinghoff Hilmar,
Vehreschild Maria J.G.T.,
Krawczyk Marcin,
Nowag Angela,
Scholz Claus Jürgen,
Kretzschmar Anne,
Roderburg Christoph,
Lammert Frank,
Goeser Tobias,
Kasper Philipp,
Steffen HansMichael
Publication year - 2020
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.15071
Subject(s) - gut flora , medicine , fatty liver , disease , cohort , cohort study , prospective cohort study , gastroenterology , feces , physiology , immunology , biology , microbiology and biotechnology
Background and Aim Several studies observed alterations in the gut microbiota in patients with non‐alcoholic fatty liver disease (NAFLD). However, analyzed patient populations and methods strongly differ among these studies. The aim of this study was to prove the reproducibility of published results and to provide a detailed overview of all findings in our NAFLD cohort using next generation sequencing methods. Methods The individual taxonomic microbiota composition of fecal samples from 90 NAFLD patients and 21 healthy controls was analyzed using 16S rRNA gene sequencing. Study participants were grouped according to their disease stage and compared regarding their gut microbiota composition. Studies were identified from PubMed listed publications, and the results were compared with the findings in our cohort. Results Results from 13 identified studies were compared with our data. A decreased abundance of the Bacteroidetes and Ruminococcaceae as well as an increased abundance of Lactobacillaceae and Veillonellaceae and Dorea were the most frequently reported changes among NAFLD patients in 4/13, 5/13, 4/13, 2/13, and 3/13 studies, respectively. Even though these alterations in the gut microbiota composition were also observed in our patient cohort, the majority of published differences could not be reproduced, neither in our own nor in other NAFLD cohort studies. Conclusion Despite repeatedly reproduced abundance patterns of specific bacteria, the heterogeneous study results did not reveal a consistent disease specific gut microbiota signature. Further prospective studies with homogenous patient cohorts and standardized methods are necessary to phenotype NAFLD by the gut microbiota.