Cited by 587Liver Disease Diagnosis and TreatmentLiver physiology and pathologyDrug-Induced Hepatotoxicity and Protection

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A simple diet- and chemical-induced murine NASH model with rapid progression of steatohepatitis, fibrosis and liver cancer

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Tsuchida, Takuma, Lee, Youngmin A., Fujiwara, Naoto, Ybanez, Maria, Allen, Brittany, Martins, Sebastiao, Fiel, M. Isabel, Goossens, Nicolas, Chou, Hsin-I., Hoshida, Yujin, Friedman, Scott L.·2018·Journal of Hepatology

DOI 10.1016/j.jhep.2018.03.011PMC PMC6054570

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Abstract

Background and Aims Although the majority of patients with non-alcoholic fatty liver disease (NAFLD) have only steatosis without progression, a sizeable fraction develop non-alcoholic steatohepatitis (NASH), which can lead to cirrhosis and hepatocellular carcinoma (HCC). Many established diet-induced mouse models for NASH require 24–52 weeks, which makes testing for drug response costly and time consuming. Methods We have sought to establish a murine NASH model with rapid progression of extensive fibrosis and HCC by using a western diet (WD), which is high-fat, high-fructose and high-cholesterol, combined with low weekly dose of intraperitoneal carbon tetrachloride (CCl 4 ), which serves as an accelerator. Results C57BL/6J mice were fed a normal chow diet ± CCl 4 or WD ± CCl 4 for 12 and 24 weeks. Addition of CCl 4 exacerbated histological features of NASH, fibrosis, and tumor development induced by WD, which resulted in stage 3 fibrosis at 12 weeks and HCC development at 24 weeks. Furthermore, whole liver transcriptomic analysis indicated that dysregulated molecular pathways in WD/CCl 4 mice and immunologic features were similar to those of human NASH. Conclusions Our mouse NASH model exhibits rapid progression of advanced fibrosis and HCC, and mimics histological, immunological and transcriptomic features of human NASH, suggesting that it will be a useful experimental tool for preclinical drug testing. Lay summary A carefully characterized model has been developed in mice that recapitulates the progressive stages of human fatty liver disease, from simple steatosis, to inflammation, fibrosis and cancer. The functional pathways of gene expression and immune abnormalities in this model closely resemble human disease. The ease and reproducibility of this model make it ideal to study disease pathogenesis and test new treatments.

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Authors: Tsuchida, T., Lee, Y. A., Fujiwara, N., Ybanez, M., Allen, B., Martins, S., Fiel, M. I., Goossens, N., Chou, H.-I., Hoshida, Y., & Friedman, S. L.
Affiliations: Tanabe Pharma Corporation (Japan) (JP)
Icahn School of Medicine at Mount Sinai (US)
Mount Sinai Hospital (US)
Corresponding author: Friedman, Scott L.
ORCID: Lee, Youngmin A.
Fujiwara, Naoto
Fiel, M. Isabel
Goossens, Nicolas
Hoshida, Yujin
Friedman, Scott L.
Venue: Journal of Hepatology
Publisher: Elsevier BV
Published: 2018-08
Volume: 69
Issue: 2
Pages: 385-395
ISSN: 0168-8278 (ISSN-L)
DOI: 10.1016/j.jhep.2018.03.011
PMC: PMC6054570
OpenAlex: W2790198401
Cited by: 583
References: 56
Citations by year: 2026: 65 · 2025: 86 · 2024: 90 · 2023: 91 · 2022: 93 · 2021: 62 · 2020: 52 · 2019: 34 · 2018: 10
FWCI: 30.84
Type: journal article
Language: en
Update notices: erratum (2018-10-01)
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (am, 349 d)
Locations: Journal of Hepatology (acceptedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
HAL (submittedVersion)
Funders: NIH
NIDDK (DK099558)
European Commission (ERC-2014-AdG-671231)
Topics: Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords: nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, mouse model, Western diet, carbon tetrachloride, liver fibrosis, hepatocellular carcinoma, liver transcriptome, immune abnormalities, preclinical drug testing
MeSH terms: Animals, Carbon Tetrachloride, Disease Models, Animal, Fatty Liver, Inflammation, Liver Cirrhosis, Liver Neoplasms, Mice, Inbred C57BL, Reproducibility of Results, Disease Progression, Gene Expression Profiling, Mice, Diet, Western

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A simple diet- and chemical-induced murine NASH model with rapid progression of steatohepatitis, fibrosis and liver cancer

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