ArticleBMC gastroenterology2020
Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis.
Article in BMC gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
81 citing papers in PubMed.
- Chronic Dietary Stress Is Associated with Early Cardiac Dysfunction and Progressive MASH Accompanied by Systemic Inflammation and Fibrosis.Nutrients · 2026Article
- Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Intestinal lipase inhibition uncouples diet-induced obesity from MASH by remodeling the hepatic lipidome in mice.Journal of lipid research · 2026Article
- Bariatric surgery resolves MASH by enhancing MAT1A-dependent one-carbon metabolism.Nature communications · 2026Article
- Mitochondrial Dysfunction in Metabolic-Syndrome-Related MASLD/MASH: Metabolic Mechanisms and Therapeutic Perspectives.Metabolites · 2026Review
- Article
- Hepatic ketogenesis is not required for exercise training to mitigate diet-induced liver steatosis in male mice.Function (Oxford, England) · 2026Article
- Reduction in Hepatic Phosphatidylcholine Biosynthesis Promotes MASH Through Copper Deficiency.bioRxiv : the preprint server for biology · 2026Article
- Panx1 deficiency exacerbates GAN diet-induced obesity by destabilizing β-catenin via GSK3β.iScience · 2026Article
- Comparison and Characteristics of MASLD Mouse Models.Biomedicines · 2026Review
- Cholesterol-rich diet exacerbates steatohepatitis in the STAM mouse model.Scientific reports · 2026Article
- [Characterization of liver macrophage subsets in different mouse models of metabolic associated steatohepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Sex- and mouse strain-related differences in body weight gain, composition of the gut microbiota, and levels of selected metabolites in response to a Western-style diet.BMC gastroenterology · 2026Article
- Hepatic ketogenesis supports liver lipid homeostasis during acute exercise but is not required for exercise training to mitigate liver steatosis in mice.bioRxiv : the preprint server for biology · 2026Article
- Multi-omics reveals an association of the gut butyrate-IDO1-tryptophan axis with Yinchenhaotang plus Zexietang-ameliorated NASH in a microbiota-dependent manner.Chinese medicine · 2026Article
- CD163 Expression Protects Against Early Hepatic Steatosis in Western Diet-Fed Male Mice.Gastro hep advances · 2026Article
- Article
- Renalase deficiency suppresses hepatic triglyceride accumulation in the progression to MASLD/MASH by GAN diet in male mice.Physiological reports · 2026Article
- Fructose and follistatin potentiate acute MASLD during complete hepatic insulin resistance.Nature communications · 2025Article
- Dehydrotrametenolic acid methyl ester, a triterpenoid of Poria cocos, alleviates non-alcoholic steatohepatitis by suppressing NLRP3 inflammasome activation via targeting Caspase-1 in mice.Acta pharmacologica Sinica · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
backgroundAnimal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients.
methodsC57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH.
resultsLiver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance.
conclusionsThe GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.