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Review
. 2022 Dec 13;23(24):15791.
doi: 10.3390/ijms232415791.

Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research

Affiliations
Review

Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research

Christina-Maria Flessa et al. Int J Mol Sci. .

Abstract

A rapidly increasing incidence of non-alcoholic fatty liver disease (NAFLD) is noted worldwide due to the adoption of western-type lifestyles and eating habits. This makes the understanding of the molecular mechanisms that drive the pathogenesis of this chronic disease and the development of newly approved treatments of utmost necessity. Animal models are indispensable tools for achieving these ends. Although the ideal mouse model for human NAFLD does not exist yet, several models have arisen with the combination of dietary interventions, genetic manipulations and/or administration of chemical substances. Herein, we present the most common mouse models used in the research of NAFLD, either for the whole disease spectrum or for a particular disease stage (e.g., non-alcoholic steatohepatitis). We also discuss the advantages and disadvantages of each model, along with the challenges facing the researchers who aim to develop and use animal models for translational research in NAFLD. Based on these characteristics and the specific study aims/needs, researchers should select the most appropriate model with caution when translating results from animal to human.

Keywords: NAFLD; NASH; animal models; cirrhosis; mouse; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis.

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Conflict of interest statement

The authors declare no conflict of interest.

References

    1. Powell E.E., Wong V.W., Rinella M. Non-alcoholic fatty liver disease. Lancet. 2021;397:2212–2224. doi: 10.1016/S0140-6736(20)32511-3. - DOI - PubMed
    1. Younossi Z., Anstee Q.M., Marietti M., Hardy T., Henry L., Eslam M., George J., Bugianesi E. Global burden of NAFLD and NASH: Trends, predictions, risk factors and prevention. Nat. Rev. Gastroenterol. Hepatol. 2018;15:11–20. doi: 10.1038/nrgastro.2017.109. - DOI - PubMed
    1. Makri E., Goulas A., Polyzos S.A. Epidemiology, Pathogenesis, Diagnosis and Emerging Treatment of Nonalcoholic Fatty Liver Disease. Arch. Med. Res. 2021;52:25–37. doi: 10.1016/j.arcmed.2020.11.010. - DOI - PubMed
    1. Brunt E.M., Neuschwander-Tetri B.A., Burt A.D. 6—Fatty liver disease: Alcoholic and non-alcoholic. In: Burt A.D., Portmann B.C., Ferrell L.D., editors. MacSween’s Pathology of the Liver. 6th ed. Churchill Livingstone; Edinburgh, UK: 2012. pp. 293–359. - DOI
    1. Buzzetti E., Pinzani M., Tsochatzis E.A. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD) Metabolism. 2016;65:1038–1048. doi: 10.1016/j.metabol.2015.12.012. - DOI - PubMed