Please use this identifier to cite or link to this item: https://doi.org/10.20517/2394-5079.2020.134
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dc.titleGut microbiota and their metabolites in the progression of non-alcoholic fatty liver disease
dc.contributor.authorZhou, J
dc.contributor.authorTripathi, M
dc.contributor.authorSinha, RA
dc.contributor.authorSingh, BK
dc.contributor.authorYen, PM
dc.date.accessioned2022-06-08T03:17:13Z
dc.date.available2022-06-08T03:17:13Z
dc.date.issued2021-01-01
dc.identifier.citationZhou, J, Tripathi, M, Sinha, RA, Singh, BK, Yen, PM (2021-01-01). Gut microbiota and their metabolites in the progression of non-alcoholic fatty liver disease. Hepatoma Research 7. ScholarBank@NUS Repository. https://doi.org/10.20517/2394-5079.2020.134
dc.identifier.issn23945079
dc.identifier.issn24542520
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/226697
dc.description.abstractNon-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disorder worldwide. It comprises a spectrum of conditions that range from steatosis to non-alcoholic steatohepatitis, with progression to cirrhosis and hepatocellular carcinoma. Currently, there is no FDA-approved pharmacological treatment for NAFLD. The pathogenesis of NAFLD involves genetic and environmental/host factors, including those that cause changes in intestinal microbiota and their metabolites. In this review, we discuss recent findings on the relationship(s) of microbiota signature with severity of NAFLD and the role(s) microbial metabolites in NAFLD progression. We discuss how metabolites may affect NAFLD progression and their potential to serve as biomarkers for NAFLD diagnosis or therapeutic targets for disease management.
dc.publisherOAE Publishing Inc.
dc.sourceElements
dc.typeReview
dc.date.updated2022-06-07T06:22:16Z
dc.contributor.departmentDEAN'S OFFICE (DUKE-NUS MEDICAL SCHOOL)
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.20517/2394-5079.2020.134
dc.description.sourcetitleHepatoma Research
dc.description.volume7
dc.published.statePublished
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