Many animal models of non-alcoholic steatohepatitis (NASH) have been developed which mirror various aspects of the disease and choosing the most appropriate is a key question faced by the pharmaceutical industry. Dietary-deficient mouse models of NASH present limitations due to their associated weight loss resulting in an altered metabolic profile to man. To resolve this issue we have developed a genetically-obese dietary-induced mouse model (ob/ob H-FFC) of NASH and fibrosis which is more congruent with man. We have evaluated this paradigm with the clinically effective dual peroxisome proliferator activated receptor (PPAR) α/δ agonist elafibranor and the PPARγ agonist pioglitazone.
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