Gut Dysbiosis and Increased Intestinal Permeability Drive microRNAs, NLRP-3 Inflammasome and Liver Fibrosis in a Nutritional Model of Non-Alcoholic Steatohepatitis in Adult Male Sprague Dawley Rats.

fatty liver disease models fibrosis gut microbiota non-alcoholic fatty liver disease non-alcoholic steatohepatitis

Journal

Clinical and experimental gastroenterology
ISSN: 1178-7023
Titre abrégé: Clin Exp Gastroenterol
Pays: New Zealand
ID NLM: 101532800

Informations de publication

Date de publication:
2020
Historique:
received: 25 05 2020
accepted: 23 07 2020
entrez: 28 9 2020
pubmed: 29 9 2020
medline: 29 9 2020
Statut: epublish

Résumé

The interactions between the gut and liver have been described in the progression of non-alcoholic steatohepatitis (NASH). The aim of this study was to develop an experimental nutritional model of NASH simulating metabolic changes occurring in humans. Adult male Sprague Dawley rats were randomized into two groups: controls (standard diet) and intervention (high-fat and choline-deficient diet) for 16 weeks, each experimental group with 10 animals. Biochemical analysis, hepatic lipid content, microRNAs, inflammatory, gut permeability markers and gut microbiota were measured. Animals in the intervention group showed significantly higher delta Lee index ( This experimental model mimicking human NASH demonstrated gut and liver interaction, with gut microbiota and intestinal permeability changes occurring in parallel with systemic and liver inflammation, miRNAs regulation and liver tissue damage.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
The interactions between the gut and liver have been described in the progression of non-alcoholic steatohepatitis (NASH). The aim of this study was to develop an experimental nutritional model of NASH simulating metabolic changes occurring in humans.
MATERIALS AND METHODS METHODS
Adult male Sprague Dawley rats were randomized into two groups: controls (standard diet) and intervention (high-fat and choline-deficient diet) for 16 weeks, each experimental group with 10 animals. Biochemical analysis, hepatic lipid content, microRNAs, inflammatory, gut permeability markers and gut microbiota were measured.
RESULTS RESULTS
Animals in the intervention group showed significantly higher delta Lee index (
CONCLUSION CONCLUSIONS
This experimental model mimicking human NASH demonstrated gut and liver interaction, with gut microbiota and intestinal permeability changes occurring in parallel with systemic and liver inflammation, miRNAs regulation and liver tissue damage.

Identifiants

pubmed: 32982365
doi: 10.2147/CEG.S262879
pii: 262879
pmc: PMC7509481
doi:

Types de publication

Journal Article

Langues

eng

Pagination

351-368

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2020 Longo et al.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest in this work.

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Auteurs

Larisse Longo (L)

Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Jéssica Tonin Ferrari (J)

Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Pabulo Henrique Rampelotto (PH)

Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.
Graduate Program in Pharmaceutical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Gustavo Hirata Dellavia (G)

School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Amanda Pasqualotto (A)

Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Claudia P Oliveira (C)

Department of Gastroenterology (LIM07), Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.

Carlos Thadeu Schmidt Cerski (C)

Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Unit of Surgical Pathology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Themis Reverbel da Silveira (T)

Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Carolina Uribe-Cruz (C)

Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Mário Reis Álvares-da-Silva (MR)

Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Experimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.
School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Division of Gastroenterology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.

Classifications MeSH