Rapidly Progress your Metabolic Disease, Obesity, Diabetes and NAFLD/NASH Research with the Translational MS-NASH Mouse Model
The MS-NASH (formerly called FATZO) mouse model is an inbred polygenic animal model for obesity, metabolic syndrome, diabetes, and NAFLD/NASH research. Unlike other rodent models of metabolic disease, the MS-NASH mouse has a functional leptin pathway, which more closely mimics the human condition, and results in a more translatable choice for testing the efficacy of metabolic disease compounds. Key facts:
- More closely resembles human metabolic syndrome, development of obesity, and diabetes
- Intact leptin pathway like humans
- Rapid weight gain in prediabetic state; hyperglycemia and insulin resistance at an early age
- This strain is valuable in studying the continuum of metabolic disturbances that accompany the conditions that lead to overt diabetes: obesity, metabolic syndrome, and the overt hyperglycemic state
- Responds to GLP-1 agonist – Semaglutide
- Develops NAFLD/NASH on a “Western” diet + fructose; accelerated disease progression and exacerbated pathology with administration of CCl4
The MS-NASH mouse is an inbred polygenic animal model for obesity, metabolic syndrome, and diabetes. The MS-NASH mouse was created by crossing of the AKR/J and C57BL/6J strains followed by selective inbreeding. These two strains are very sensitive to developing obesity and metabolic syndrome under the influence of high fat diets. Both strains develop leptin resistance while gaining adiposity.
However, under the same feeding conditions, AKR/J mice gain more weight, have higher carcass lipid content, plasma leptin, insulin, and triglyceride concentrations, and are more insulin resistant, but are less hyperglycemic and less glucose intolerant than C57BL/6J mice. The crossing of these two strains and the selective inbreeding of the subsequent generations has resulted in a strain exhibiting obesity in a prediabetic state which slowly progresses to overt diabetes.
- Rapid weight gain on standard diet compared to DIO, db/db, and ob/ob rodent models
- Males begin to express and maintain hyperglycemia at 14 weeks of age
- Insulin resistance develops at a rapid rate
- Reduction in body weight, food intake, and blood glucose upon administration of GLP-1 agonist - Semaglutide
- Develops NAFLD/NASH on Western diet + fructose; accelerated disease progression and exacerbated pathology with CCl4