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Journal Article
Review
Gut microbiota and non-alcoholic fatty liver disease.
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a common disorder with poorly understood pathogenesis. Beyond environmental and genetic factors, cumulative data support the causative role of gut microbiota in disease development and progression.
DATA SOURCE: We performed a PubMed literature search with the following key words: "non-alcoholic fatty liver disease", "non-alcoholic steatohepatitis", "fatty liver", "gut microbiota" and "microbiome", to review the data implicating gut microbiota in NAFLD development and progression.
RESULTS: Recent metagenomic studies revealed differences in the phylum and genus levels between patients with fatty liver and healthy controls. While bacteroidetes and firmicutes remain the dominant phyla among NAFLD patients, their proportional abundance and genera detection vary among different studies. New techniques indicate a correlation between the methanogenic archaeon (methanobrevibacter smithii) and obesity, while the bacterium akkermanshia municiphila protects against metabolic syndrome. Among NAFLD patients, small intestinal bacterial overgrowth detected by breath tests might induce gut microbiota and host interactions, facilitating disease development.
CONCLUSIONS: There is evidence that gut microbiota participates in NAFLD development through, among others, obesity induction, endogenous ethanol production, inflammatory response triggering and alterations in choline metabolism. Further studies with emerging techniques are needed to further elucidate the microbiome and host crosstalk in NAFLD pathogenesis.
DATA SOURCE: We performed a PubMed literature search with the following key words: "non-alcoholic fatty liver disease", "non-alcoholic steatohepatitis", "fatty liver", "gut microbiota" and "microbiome", to review the data implicating gut microbiota in NAFLD development and progression.
RESULTS: Recent metagenomic studies revealed differences in the phylum and genus levels between patients with fatty liver and healthy controls. While bacteroidetes and firmicutes remain the dominant phyla among NAFLD patients, their proportional abundance and genera detection vary among different studies. New techniques indicate a correlation between the methanogenic archaeon (methanobrevibacter smithii) and obesity, while the bacterium akkermanshia municiphila protects against metabolic syndrome. Among NAFLD patients, small intestinal bacterial overgrowth detected by breath tests might induce gut microbiota and host interactions, facilitating disease development.
CONCLUSIONS: There is evidence that gut microbiota participates in NAFLD development through, among others, obesity induction, endogenous ethanol production, inflammatory response triggering and alterations in choline metabolism. Further studies with emerging techniques are needed to further elucidate the microbiome and host crosstalk in NAFLD pathogenesis.
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