Abstract
Animal models of human disease are a key component of translational hepatology research, yet there is no consensus on which model is optimal for NAFLD. We generated a database of 3,920 rodent models of NAFLD. Study designs were highly heterogeneous, and therefore, few models had been cited more than once. Analysis of genetic models supported the current evidence for the role of adipose dysfunction and suggested a role for innate immunity in the progression of NAFLD. We identified that high-fat, high-fructose diets 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 variability in preclinical study design, which has wider implications for the reproducibility of in vivo experiments both in the field of hepatology and beyond. This systematic analysis provides a framework for phenotypic assessment of NAFLD models and highlights the need for increased standardization and replication.
Highlights
AND AIMS: Animal models of human disease are a key component of translational hepatology research, yet there is no consensus on which model is optimal for NAFLD
We identified that high-fat, high-fructose diets 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. This analysis demonstrates the variability in preclinical study design, which has wider implications for the reproducibility of in vivo experiments both in the field of hepatology and beyond. This systematic analysis provides a framework for phenotypic assessment of NAFLD models and highlights the need for increased standardization and replication. (Hepatology 2021;0:1-18)
Summary
AND AIMS: Animal models of human disease are a key component of translational hepatology research, yet there is no consensus on which model is optimal for NAFLD. Sex (Weeks) (%kcal) (%weight) Given Dose Obesity Resistance Dyslipidemia Syndrome Liver Overall Yes/No Age No Age Stage Age Yes/No Age Weeks Citations. Leptin deficiency C57BL/6J M (ob/ob) HFD C57BL/6J. Sex (Weeks) Fat (%kcal) (%Weight) (%kcal) (%Weight) Given Dose Obesity Resistance Dyslipidemia Syndrome Liver Overall Yes/No Age Yes/No Age Stage Age Yes/No Age. HFD example studies: PMID C57BL/6? HFD (example studies: PMID Sprague-Dawley M 15761972). HFD (example studies: PMID Wistar 28555525, 23200892).
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