ArticlePloS one2017
Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Syndrome Nonalcoholic Steatohepatitis Male Mouse With Adeno-Associated Viral Renin as a Novel Model for Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2024Article
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- Mouse models of nonalcoholic steatohepatitis and their application to new drug development.Archives of pharmacal research · 2022Review
- Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice.PloS one · 2022Article
- In Vitro and In Vivo Models of Non-Alcoholic Fatty Liver Disease: A Critical Appraisal.Journal of clinical medicine · 2020Review
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- Carbon tetrachloride (CClBMC gastroenterology · 2020Article
- Herring Milt Protein Hydrolysate Improves Insulin Resistance in High-Fat-Diet-Induced Obese Male C57BL/6J Mice.Marine drugs · 2019Article
- The FATZO mouse, a next generation model of type 2 diabetes, develops NAFLD and NASH when fed a Western diet supplemented with fructose.BMC gastroenterology · 2019Article
- Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction.World journal of gastroenterology · 2018Article
- Glucose dysregulation and response to common anti-diabetic agents in the FATZO/Pco mouse.PloS one · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity in many current pre-clinical animal models of obesity and diabetes is mediated by monogenic mutations; these are rarely associated with the development of human obesity. A new mouse model, the FATZO mouse, has been developed to provide polygenic obesity and a metabolic pattern of hyperglycemia and hyperinsulinemia, that support the presence of insulin resistance similar to metabolic disease in patients with insulin resistance/type 2 diabetes. The FATZO mouse resulted from a cross of C57BL/6J and AKR/J mice followed by selective inbreeding for obesity, increased insulin and hyperglycemia. Since many clinical studies have established a close link between higher body weight and the development of type 2 diabetes, we investigated whether time to progression to type 2 diabetes or disease severity in FATZO mice was dependent on weight gain in young animals. Our results indicate that lighter animals developed metabolic disturbances much slower and to a lesser magnitude than their heavier counterparts. Consumption of a diet containing high fat, accelerated weight gain in parallel with disease progression. A naturally occurring and significant variation in the body weight of FATZO offspring enables these mice to be identified as low, mid and high body weight groups at a young age. These weight groups remain into adulthood and correspond to slow, medium and accelerated development of type 2 diabetes. Thus, body weight inclusion criteria can optimize the FATZO model for studies of prevention, stabilization or treatment of type 2 diabetes.
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