- 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
The FATZO mouse is an inbred polygenic animal model for obesity, metabolic syndrome, and diabetes. The FATZO 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
2017 Pricing (per animal)
|Age (in weeks)||Male||Female|