A point mutation in the leptin gene leads ob/ob mice to be obese (even on standard diet), glucose intolerant, and have increased insulin levels. Exacerbated by a HFD containing cholesterol and trans-fats (the AMLN diet), ob/ob mice more quickly develop steatohepatitis and fibrosis than wild-type counterparts fed the same diet. Liver histopathology readily demonstrates the severity of the NASH phenotype.

Model NAFLD and Metabolic Diseases

Recreate the metabolic changes and disorders commonly found in human patients to study the causes and treatments for NAFLD and other conditions.

Accelerate NASH Without a Chemical Insult

Using a genetic model enables increased NASH phenotype development without the need for adding a chemical insult.

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