Steatosis and gut microbiota dysbiosis induced by high-fat diet are reversed by 1-week chow diet administration.


Journal

Nutrition research (New York, N.Y.)
ISSN: 1879-0739
Titre abrégé: Nutr Res
Pays: United States
ID NLM: 8303331

Informations de publication

Date de publication:
11 2019
Historique:
received: 24 04 2019
revised: 26 08 2019
accepted: 13 09 2019
pubmed: 24 11 2019
medline: 4 11 2020
entrez: 24 11 2019
Statut: ppublish

Résumé

Many studies have recently shown that diet and its impact on gut microbiota are closely related to obesity and metabolic diseases including nonalcoholic fatty liver disease. Gut microbiota may be an important intermediate link, causing gastrointestinal and metabolic diseases under the influence of changes in diet and genetic predisposition. The aim of this study was to assess the reversibility of liver phenotype in parallel with exploring the resilience of the mice gut microbiota by switching high-fat diet (HFD) to chow diet (CD). Mice were fed an HF for 8 weeks. A part of the mice was euthanized, whereas the rest were then fed a CD. These mice were euthanized after 3 and 7 days of feeding with CD, respectively. Gut microbiota composition, serum parameters, and liver morphology were assessed. Eight weeks of HFD treatment induced marked liver steatosis in mice with a perturbed microbiome. Interestingly, only 7 days of CD was enough to recover the liver to a normal status, whereas the microbiome was accordingly reshaped to a close to initial pattern. The abundance of some of the bacteria including Prevotella, Parabacteroides, Lactobacillus, and Allobaculum was reversible upon diet change from HFD to CD. This suggests that microbiome modifications contribute to the metabolic effects of HFD feeding and that restoration of a normal microbiota may lead to improvement of the liver phenotype. In conclusion, we found that steatosis and gut microbiota dysbiosis induced by 8 weeks of high-fat diet can be reversed by 1 week of chow diet administration, and we identified gut bacteria associated with the metabolic phenotype.

Identifiants

pubmed: 31757631
pii: S0271-5317(19)30427-0
doi: 10.1016/j.nutres.2019.09.004
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

72-88

Subventions

Organisme : Austrian Science Fund FWF
ID : W 1226
Pays : Austria

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Zahra Safari (Z)

Institute of Pathology, Medical University of Graz, 8010 Graz, Austria; Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, 78350 Jouy-en-Josas, France.

Magali Monnoye (M)

Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, 78350 Jouy-en-Josas, France.

Peter M Abuja (PM)

Institute of Pathology, Medical University of Graz, 8010 Graz, Austria.

Mahendra Mariadassou (M)

MaIAGE, UR1404, INRA, 78350 Jouy-en-Josas, France.

Karl Kashofer (K)

Institute of Pathology, Medical University of Graz, 8010 Graz, Austria.

Philippe Gérard (P)

Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, 78350 Jouy-en-Josas, France. Electronic address: philippe.gerard@inra.fr.

Kurt Zatloukal (K)

Institute of Pathology, Medical University of Graz, 8010 Graz, Austria. Electronic address: kurt.zatloukal@medunigraz.at.

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Classifications MeSH