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We describe the impact of a choline-deficient amino acid defined high fat diet (CDAHFD) on the gut microbiota in a male Göttingen Minipig model and on selected pathways involved in the development of NASH. Eight weeks of CDAHFD resulted in a significantly altered colon microbiota mainly driven by the bacterial families Lachnospiraceae and Enterobacteriaceae, being decreased and increased in abundance, respectively. CDAHFD decreased colon content of SCFA and increased colonic pH. In addition, serum imidazole propionate was significantly elevated as a consequence of CDAHFD feeding. Hepatic gene expression analysis indicated upregulation of ras homolog enriched in brain and mechanistic target of rapamycin (mTOR) and downregulation of insulin receptor substrate 1 and insulin receptor substrate 2 in CDAHFD fed minipigs. Furthe consequences of CDAHFD was increased serum cholesterol, increased serum bile acids (BA) and hyperglucagonemia, but not hyperaminoacidemia. In Göttingen Minipigs, CDAHFD introduced a shift in the colon microbiota resulting in a bacterial community with a decreased capacity for SCFA production. Consequently, the pH rises creating an environment with the potential to activate the bacterial enzymes urocanate reductase facilitating production imidazole propionate. We speculate that imidazole propionate activates hepatic mTORC1 resulting in impaired insulin sensitivity in the liver. Moreover, we suggest that imidazole propionate has the ability to activate mTOR in α-cells and contribute to an hyperglucagonemic state through α-cell hyperplasia. Additionally, the changed colon microbiota could be linked to a changed BA profile and hepatic fibrosis, further contributing to the NASH development."],"repository":["ENA"],"name_synonyms":["Dysbacteriosis, imidazole acetate, digestive canal, Microbial Community Composition, Dys symbiosis, Community Composition, Bowel, Dysbioses, Propionate, nonalcoholic steatohepatitis, non alcoholic steatohepatitis, enteric tract, NASH - nonalcoholic steatohepatitis, non-alcoholic steatohepatitis., Microbial, supernumerary, Propanoic Acid, Nonalcoholic Steatohepatitis, Human, Propanoate, gut tube, Gus, Gur, imidazole conjugate monoacid, Gut, Propanoic Acids, imidazole monohydrochloride, imidazole citrate, H2im(+), Propanoates, Propanoic Acid Derivatives, alimentary canal, Microbial Communities, Dysbacterioses, Microbiome, increased, AI747421, gut, Microbiomes, Microbial Community Compositions, MASH, Microbial Community, increased number, Microbial Community Structure, Gus-u, alimentary tract, Community Structure, Gus-t, Gus-s, Gus-r, Propionic Acid, imidazolium, Disbacteriosis, Composition, present in greater numbers in organism, Dys-symbioses, imidazolium chloride, g, Propionic, gastrointestinal system, Disbioses, Derivatives, NASH, metabolic dysfunction-associated steatohepatitis, Disbiosis, Microbial Community Structures, digestive tube, Microbiotas, asd, imidazolium ion, Cu-imidazole, Acids, adult alimentary canal, alimentary system, Dys-symbiosis, imidazole sodium, Propionic Acids, Propionic Acid Derivatives, intestines, Human Microbiomes, IMIDAZOLE, Propanoic, Disbacterioses, accessory, Al-imidazole, Community, Human Microbiome, imidazole monophosphonate"],"description_synonyms":["Dysbacteriosis, digestive canal, Dys symbiosis, Bowel, Dysbioses, pig, nonalcoholic steatohepatitis, pigs, non alcoholic steatohepatitis, enteric tract, NASH - nonalcoholic steatohepatitis, Sus scrofus, Nonalcoholic Steatohepatitis, gut tube, Gus, Gur, Gut, wild boar, Smn, Lap18., alimentary canal, DmelCG15914, Dysbacterioses, non-alcoholic steatohepatitis, 19k, Pr22, AI747421, gut, MASH, Op18, Gus-u, alimentary tract, Gus-t, Gus-s, Gus-r, Pp17, Disbacteriosis, Pp18, Dys-symbioses, g, gastrointestinal system, Disbioses, NASH, metabolic dysfunction-associated steatohepatitis, Pp19, Disbiosis, Pig, PIG, swine, digestive tube, asd, Lag, P18, adult alimentary canal, alimentary system, Dys-symbiosis, P19, intestines, Disbacterioses"],"additional_accession":[]},"is_claimable":false,"name":"Marked gut microbiota dysbiosis and increased imidazole propionate are associated with a NASH Göttingen Minipig model","description":"Gut dysbiosis contributes to NASH in a pig model","dates":{"last_updated":"2022-07-07","first_public":"2022-07-07"},"accession":"PRJEB54561","cross_references":{}}