Selecting and designing an optimal animal model is a key component of translational science, though there is often no consensus on which model is optimal for a particular disease. Here, we generated a database of 3920 rodent models of non-alcoholic fatty liver disease (NAFLD). Due to high heterogeneity in design, few models had been cited more than once. Analysis of genetic models provided evidence for the role of adipose dysfunction and perturbation of the innate immune system in the progression of NAFLD. We identified that high fat, high fructose diet models most closely recapitulate the human phenotype of NAFLD. There was substantial variability in the nomenclature of animal models; a consensus on terminology of specialist diets is needed. More broadly, this analysis demonstrates the variation in preclinical study design and how this may limit the reproducibility of animal studies.

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