Fecal Microbiota Transplant from Human to Mice Gives Insights into the Role of the Gut Microbiota in Non-Alcoholic Fatty Liver Disease (NAFLD).
NAFL
NAFLD
gut microbiome
health
high-fat diet
high-fructose
human
liver
Journal
Microorganisms
ISSN: 2076-2607
Titre abrégé: Microorganisms
Pays: Switzerland
ID NLM: 101625893
Informations de publication
Date de publication:
19 Jan 2021
19 Jan 2021
Historique:
received:
22
12
2020
revised:
11
01
2021
accepted:
12
01
2021
entrez:
22
1
2021
pubmed:
23
1
2021
medline:
23
1
2021
Statut:
epublish
Résumé
Non-alcoholic fatty liver diseases (NAFLD) are associated with changes in the composition and metabolic activities of the gut microbiota. However, the causal role played by the gut microbiota in individual susceptibility to NAFLD and particularly at its early stage is still unclear. In this context, we transplanted the microbiota from a patient with fatty liver (NAFL) and from a healthy individual to two groups of mice. We first showed that the microbiota composition in recipient mice resembled the microbiota composition of their respective human donor. Following administration of a high-fructose, high-fat diet, mice that received the human NAFL microbiota (NAFLR) gained more weight and had a higher liver triglycerides level and higher plasma LDL cholesterol than mice that received the human healthy microbiota (HR). Metabolomic analyses revealed that it was associated with lower and higher plasma levels of glycine and 3-Indolepropionic acid in NAFLR mice, respectively. Moreover, several bacterial genera and OTUs were identified as differently represented in the NAFLR and HR microbiota and therefore potentially responsible for the different phenotypes observed. Altogether, our results confirm that the gut bacteria play a role in obesity and steatosis development and that targeting the gut microbiota may be a preventive or therapeutic strategy in NAFLD management.
Identifiants
pubmed: 33477939
pii: microorganisms9010199
doi: 10.3390/microorganisms9010199
pmc: PMC7833443
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Agence Nationale de la Recherche
ID : ANR-15-CE14-0021-03
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