ArticlePloS one2017
Glucose dysregulation and response to common anti-diabetic agents 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 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Colonic metabolomic and transcriptomic alterations in a mouse model of metabolic syndrome.bioRxiv : the preprint server for biology · 2026Article
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- 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
- Enhanced Oral Efficacy of Semaglutide via an Ionic Nanocomplex with Organometallic Phyllosilicate in Type 2 Diabetic Rats.Pharmaceutics · 2024Article
- Association of Uroguanylin, Body Mass Index, and Waist Circumference: Sex Differences and Obesity Implications among a Sample of Iraqi Adults in Baghdad City.Journal of pharmacy & bioallied sciences · 2024Article
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- Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice.PloS one · 2022Article
- Obese mice weight loss role on nonalcoholic fatty liver disease and endoplasmic reticulum stress treated by a GLP-1 receptor agonist.International journal of obesity (2005) · 2022Article
- In Vitro and In Vivo Models of Non-Alcoholic Fatty Liver Disease: A Critical Appraisal.Journal of clinical medicine · 2020Review
- FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia.Blood advances · 2020Article
- Carbon tetrachloride (CClBMC gastroenterology · 2020Article
- NAFLD Preclinical Models: More than a Handful, Less of a Concern?Biomedicines · 2020Review
- Farewell, FATZO: a NASH mouse update.Lab animal · 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
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The FATZO/Pco mouse is the result of a cross of the C57BL/6J and AKR/J strains. The crossing of these two strains and the selective inbreeding for obesity, insulin resistance and hyperglycemia has resulted in an inbred strain exhibiting obesity in the presumed presence of an intact leptin pathway. Routinely used rodent models for obesity and diabetes research have a monogenic defect in leptin signaling that initiates obesity. Given that obesity and its sequelae in humans are polygenic in nature and not associated with leptin signaling defects, the FATZO mouse may represent a more translatable rodent model for study of obesity and its associated metabolic disturbances. The FATZO mouse develops obesity spontaneously when fed a normal chow diet. Glucose intolerance with increased insulin levels are apparent in FATZO mice as young as 6 weeks of age. These progress to hyperglycemia/pre-diabetes and frank diabetes with decreasing insulin levels as they age. The disease in these mice is multi-faceted, similar to the metabolic syndrome apparent in obese individuals, and thus provides a long pre-diabetic state for determining the preventive value of new interventions. We have assessed the utility of this new model for the pre-clinical screening of agents to stop or slow progression of the metabolic syndrome to severe diabetes. Our assessment included: 1) characterization of the spontaneous development of disease, 2) comparison of metabolic disturbances of FATZO mice to control mice and 3) validation of the model with regard to the effectiveness of current and emerging anti-diabetic agents; rosiglitazone, metformin and semaglutide.
conclusionMale FATZO mice spontaneously develop significant metabolic disease when compared to normal controls while maintaining hyperglycemia in the presence of high leptin levels and hyperinsulinemia. The disease condition responds to commonly used antidiabetic agents.
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