LEP and metabolic dysfunction-associated steatohepatitis: Dietary models gain weight, develop steatosis, and become insulin-resistant, but exhibit much less liver injury than human NASH patients, suggesting fundamental differences in rodent and human livers.[5], [48] Indeed, metabolic profiling of rats fed a methionine-choline-deficient diet—which inhibits fatty acid oxidation, thereby leading to NASH—identified species differences in bile acid, insulin, and leptin levels,6 limiting this model’s utility for studies of biomarkers or disease progression.