Table 1: Zebrafish gastrointestinal models of pathology.

ModelMechanism of pathologyHuman relevancy/key featuresKey references

Pan-GI neoplasiasHeterozygotic APC mutationAPC mutations drive spontaneous and genetic intestinal adenocarcinomas.Haramis et al., 2006 [24]
Hepatocellular carcinomaThioacetamide ± HCV-core-protein-zebrafishHuman genetic overlap. Rising prevalence of HCV-driven HCC in humans.Lam and Gong, 2006 [25]
Rekha et al., 2008 [26]
Pancreatic cancerTransgenic ptf1a-KRAS zebrafishRecapitulates hedgehog signaling aberrations found in humans. Elucidates a potential cellular origin for pancreatic cancers.Park et al., 2008 [27]
Inflammatory bowel diseaseTNBS in the media of zebrafish larvaeModel inflammatory and goblet cell hypertrophy. Responds to bacterial status and IBD medications.Flemming et al., 2010 [28]
Oehlers et al., 2011 [29]
Inflammatory bowel diseaseOxazolone enema in adult zebrafishGoblet cell depletion and eosinophil infiltration. Responds to antibiotic therapy.Brugman et al., 2009 [30]
NAFLDMutation in a novel gene: foigrhi1532b.
Alternative model involves chemical induction with thioacetamide
Large lipid filled hepatocytes and cellular apoptosis; pathology linked to ER stress responses. Alternative model generates a fatty liver and hepatocyte apoptosis.Cinaroglu et al., 2011 [31]
Amali et al., 2006 [32] (alternative model)
Alcoholic liver disease2% ethanol to the water of 4 dpf zebrafish for 32 daysHepatomegaly and steatosis, with upregulation of genes involved in toxic alcohol metabolism. Model is sensitive to sterol regulatory binding protein, important in human disease.Passeri et al., 2009 [33]

Abbreviations: GI: gastrointestinal; APC: adenomatous polyposis coli; HCV: hepatitis C virus; TNBS: 2,4,6-trinitrobenzene sulfonic acid; IBD: inflammatory bowel diseases; NAFLD: nonalcoholic fatty liver disease; ER: endoplasmic reticulum.