Mouse models in non‐alcoholic fatty liver disease and steatohepatitis research
Open accessAbstract
Summary: Non‐alcoholic fatty liver disease (NAFLD) represents a histological spectrum of liver disease associated with obesity, diabetes and insulin resistance that extends from isolated steatosis to steatohepatitis and cirrhosis. As well as being a potential cause of progressive liver disease in its own right, steatosis has been shown to be an important cofactor in the pathogenesis of many other liver diseases. Animal models of NAFLD may be divided into two broad categories: those caused by genetic mutation and those with an acquired phenotype produced by dietary or pharmacological manipulation. The literature contains numerous different mouse models that exhibit histological evidence of hepatic steatosis or, more variably, steatohepatitis; however, few replicate the entire human phenotype. The genetic leptin‐deficient (ob/ob) or leptin‐resistant (db/db) mouse and the dietary methionine/choline‐deficient model are used in the majority of published research. More recently, targeted gene disruption and the use of supra‐nutritional diets to induce NAFLD have gained greater prominence as researchers have attempted to bridge the phenotype gap between the available models and the human disease. Using the physiological processes that underlie the pathogenesis and progression of NAFLD as a framework, we review the literature describing currently available mouse models of NAFLD, highlight the strengths and weaknesses of established models and describe the key findings that have furthered the understanding of disease pathogenesis.
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In publicly available single cell RNA sequencing data of human liver biopsy material, Rorc is predominantly expressed by T cells.
“This showed that Rorc, the transcription factor mediating IL-17A expression, is predominantly expressed by T cells (Fig. S1c).”
From NKG2D-mediated detection of metabolically stressed hepatocytes by innate-like T cells is essential for initiation of NASH and fibrosis (2023) · cites this paper as [24]
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- Authors
- Anstee, Q. M., & Goldin, R. D.
- Affiliations
- Imperial College London (GB)
- Corresponding author
- Goldin, Robert D.
- Venue
- International Journal of Experimental Pathology
- Publisher
- Wiley
- Published
- 2006-01-23
- Volume
- 87
- Issue
- 1
- Pages
- 1-16
- ISSN
- 0959-9673 (ISSN-L)
- 1365-2613
- PMC
- PMC2517349
- OpenAlex
- W1523155649
- Cited by
- 714
- References
- 129
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 23 · 2023: 35 · 2022: 29 · 2021: 34 · 2020: 44 · 2019: 36 · 2018: 44 · 2017: 46 · 2016: 55 · 2015: 48 · 2014: 53 · 2013: 53 · 2012: 43
- FWCI
- 2.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Experimental Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- non-alcoholic fatty liver disease, steatohepatitis, mouse model, hepatic steatosis, leptin-deficient ob/ob mice, methionine-choline-deficient diet, targeted gene disruption, obesity, insulin resistance, NAFLD pathogenesis
- MeSH terms
- Adipose Tissue, Animals, Fatty Acids, Fatty Liver, Mice, Mutant Strains, Triglycerides, Leptin, Models, Animal, Mice
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