Gender and gut microbiota composition determine hepatic bile acid, metabolic and inflammatory response to a single fast-food meal in healthy adults.


Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
05 2021
Historique:
received: 09 12 2020
revised: 16 03 2021
accepted: 02 04 2021
pubmed: 3 5 2021
medline: 28 8 2021
entrez: 2 5 2021
Statut: ppublish

Résumé

Regular consumption of fast-food (FF) as a form of typical Western style diet is associated with obesity and the metabolic syndrome, including its hepatic manifestation nonalcoholic fatty liver disease. Currently, it remains unclear how intermittent excess FF consumption may influence liver metabolism. The study aimed to characterize the effects of a single FF binge on hepatic steatosis, inflammation, bile acid (BA), glucose and lipid metabolism. Twenty-five healthy individuals received a FF meal and were asked to continue eating either for a two-hour period or until fully saturated. Serum levels of transaminases, fasting BA, lipid profile, glucose and cytokine levels as well as transient elastography and controlled attenuation parameter (CAP; to assess hepatic steatosis) were analyzed before (day 0) and the day after FF binge (day 1). Feces was collected prior and after the FF challenge for microbiota analysis. The FF meal induced a modest increase in CAP, which was accompanied by a robust increase of fasting serum BA levels. Surprisingly, levels of cholesterol and bilirubin were significantly lower after the FF meal. Differentiating individuals with a relevant delta BA (>1 μmol/l) increase vs. individuals without (delta BA ≤1 μmol/l), identified several gut microbiota, as well as gender to be associated with the BA increase and the observed alterations in liver function, metabolism and inflammation. A single binge FF meal leads to a robust increase in serum BA levels and alterations in parameters of liver injury and metabolism, indicating a novel metabolic aspect of the gut-liver axis.

Sections du résumé

BACKGROUND & AIMS
Regular consumption of fast-food (FF) as a form of typical Western style diet is associated with obesity and the metabolic syndrome, including its hepatic manifestation nonalcoholic fatty liver disease. Currently, it remains unclear how intermittent excess FF consumption may influence liver metabolism. The study aimed to characterize the effects of a single FF binge on hepatic steatosis, inflammation, bile acid (BA), glucose and lipid metabolism.
METHODS
Twenty-five healthy individuals received a FF meal and were asked to continue eating either for a two-hour period or until fully saturated. Serum levels of transaminases, fasting BA, lipid profile, glucose and cytokine levels as well as transient elastography and controlled attenuation parameter (CAP; to assess hepatic steatosis) were analyzed before (day 0) and the day after FF binge (day 1). Feces was collected prior and after the FF challenge for microbiota analysis.
RESULTS
The FF meal induced a modest increase in CAP, which was accompanied by a robust increase of fasting serum BA levels. Surprisingly, levels of cholesterol and bilirubin were significantly lower after the FF meal. Differentiating individuals with a relevant delta BA (>1 μmol/l) increase vs. individuals without (delta BA ≤1 μmol/l), identified several gut microbiota, as well as gender to be associated with the BA increase and the observed alterations in liver function, metabolism and inflammation.
CONCLUSION
A single binge FF meal leads to a robust increase in serum BA levels and alterations in parameters of liver injury and metabolism, indicating a novel metabolic aspect of the gut-liver axis.

Identifiants

pubmed: 33933727
pii: S0261-5614(21)00200-4
doi: 10.1016/j.clnu.2021.04.008
pii:
doi:

Substances chimiques

Bile Acids and Salts 0
Transaminases EC 2.6.1.-
Bilirubin RFM9X3LJ49

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2609-2619

Informations de copyright

Copyright © 2021 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest All authors declare that they do not have a conflict of interests.

Auteurs

A Figge (A)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.

S Sydor (S)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.

C Wenning (C)

Department of Gastroenterology and Hepatology, University Hospital Essen, Hufelandstrasse 55, 45147 Essen, Germany.

P Manka (P)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany; Department of Gastroenterology and Hepatology, University Hospital Essen, Hufelandstrasse 55, 45147 Essen, Germany.

S Assmuth (S)

Department of Gastroenterology and Hepatology, University Hospital Essen, Hufelandstrasse 55, 45147 Essen, Germany.

R Vilchez-Vargas (R)

Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke-University Hospital Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany.

A Link (A)

Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke-University Hospital Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany.

A Jähnert (A)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.

S Brodesser (S)

CECAD Research Center, CECAD Lipidomics Facility, University of Cologne Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.

C Lucas (C)

CECAD Research Center, CECAD Lipidomics Facility, University of Cologne Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.

Y A Nevzorova (YA)

Department of Immunology, Opthalmology and ORL, Complutense University School of Medicine, Avenida de Séneca 2, 28040 Madrid, Spain; 12 de Octubre Health Research Institute (imas 12), Madrid, Spain.

K N Faber (KN)

Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands; Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands.

H Moshage (H)

Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands; Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands.

M Porsch-Özcürümez (M)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.

G Gerken (G)

Department of Gastroenterology and Hepatology, University Hospital Essen, Hufelandstrasse 55, 45147 Essen, Germany.

F J Cubero (FJ)

Department of Immunology, Opthalmology and ORL, Complutense University School of Medicine, Avenida de Séneca 2, 28040 Madrid, Spain; 12 de Octubre Health Research Institute (imas 12), Madrid, Spain.

A Canbay (A)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.

L P Bechmann (LP)

Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany. Electronic address: lars.bechmann@rub.de.

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