ArticleBMC gastroenterology2019
The FATZO mouse, a next generation model of type 2 diabetes, develops NAFLD and NASH when fed a Western diet supplemented with fructose.
Article in BMC gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 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
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- Heterogeneous effects of individual high-fat diet compositions on phenotype, metabolic outcome, and hepatic proteome signature in BL/6 male mice.Nutrition & metabolism · 2023Article
- Anti-Inflammatory and Therapeutic Effects of a Novel Small-Molecule Inhibitor of Inflammation in a Male C57BL/6J Mouse Model of Obesity-Induced NAFLD/MAFLD.Journal of inflammation research · 2023Article
- Thermoneutral housing promotes hepatic steatosis in standard diet-fed C57BL/6N mice, with a less pronounced effect on NAFLD progression upon high-fat feeding.Frontiers in endocrinology · 2023Article
- ALS-L1023 fromLife (Basel, Switzerland) · 2022Article
- Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research.International journal of molecular sciences · 2022Review
- Mouse models of nonalcoholic steatohepatitis and their application to new drug development.Archives of pharmacal research · 2022Review
- A novel nanobody-heavy chain antibody against Angiopoietin-like protein 3 reduces plasma lipids and relieves nonalcoholic fatty liver disease.Journal of nanobiotechnology · 2022Article
- Liver Protein Expression in NASH Mice on a High-Fat Diet: Response to Multi-Mineral Intervention.Frontiers in nutrition · 2022Article
- Mouse models of nonalcoholic fatty liver disease (NAFLD): pathomechanisms and pharmacotherapies.International journal of biological sciences · 2022Review
- Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice.PloS one · 2022Article
- Considerations When Choosing High-Fat, High-Fructose, and High-Cholesterol Diets to Induce Experimental Nonalcoholic Fatty Liver Disease in Laboratory Animal Models.Current developments in nutrition · 2021Article
- Differential Effects of Dietary Components on Glucose Intolerance and Non-Alcoholic Steatohepatitis.Nutrients · 2021Article
- Role of 2‑series prostaglandins in the pathogenesis of type 2 diabetes mellitus and non‑alcoholic fatty liver disease (Review).International journal of molecular medicine · 2021Review
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9 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundMetabolic disorders such as insulin resistance, obesity, and hyperglycemia are prominent risk factors for the development of non-alcoholic fatty liver disease (NAFLD)/steatohepatitis (NASH). Dietary rodent models employ high fat, high cholesterol, high fructose, methionine/choline deficient diets or combinations of these to induce NAFLD/NASH. The FATZO mice spontaneously develop the above metabolic disorders and type 2 diabetes (T2D) when fed with a normal chow diet. The aim of the present study was to determine if FATZO mice fed a high fat and fructose diet would exacerbate the progression of NAFLD/NASH.
methodsMale FATZO mice at the age of 8 weeks were fed with high fat Western diet (D12079B) supplemented with 5% fructose in the drinking water (WDF) for the duration of 20 weeks. The body weight, whole body fat content, serum lipid profiles and liver function markers were examined monthly along with the assessment of liver histology for the development of NASH. In addition, the effects of obeticholic acid (OCA, 30 mg/kg, QD) on improvement of NASH progression in the model were evaluated.
resultsCompared to normal control diet (CD), FATZO mice fed with WDF were heavier with higher body fat measured by qNMR, hypercholesterolemia and had progressive elevations in AST (~ 6 fold), ALT (~ 6 fold), liver over body weight (~ 2 fold) and liver triglyceride (TG) content (1.4-2.9 fold). Histological examination displayed evidence of NAFLD/NASH, including hepatic steatosis, lobular inflammation, ballooning and fibrosis in FATZO mice fed WDF. Treatment with OCA for 15 weeks in FATZO mice on WDF significantly alleviated hypercholesterolemia and elevation of AST/ALT, reduced liver weight and liver TG contents, attenuated hepatic ballooning, but did not affect body weight and blood TG levels.
conclusionWDF fed FATZO mice represent a new model for the study of progressive NAFLD/NASH with concurrent metabolic dysregulation.
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