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A point mutation in the leptin gene leads ob/ob mice to exhibit obesity, hyperphagia, transient hyperglycemia, glucose intolerance, and elevated plasma insulin. Exacerbated by a HFD  to best fit the study goals, ob/ob mice more quickly develop steatohepatitis and fibrosis than wild-type counterparts fed the same diet, expediting your study timelines. 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 clinically relevant conditions such as diabetes and obesity.

Accelerate NASH Without a Chemical Insult

Using a genetic model enables increased NAFLD phenotype development without the need for adding a chemical insult, allowing this animal model to closer mimic the human disease process.

Key features for your best outcomes using this model

  • Longer study durations mimic chronic timeline to develop in people
  • Steatosis is a main feature, leading to good early-stage NASH interventions
  • Diets and animals are readily available for a quick study start timeline

Want more information?

Contact one of our scientists!