{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Juarez-Fernandez M"],"funding":["Junta de Castilla y León cofunded by the European Social Fund","Departamento de Industria del Gobierno Vasco","Ayudas Ramón y Cajal de la Agencia Estatal de Investigación","Ministerio de Ciencia, Innovación y Universidades MICINN integrado en el Plan Estatal de Investigación Científica y Técnica y de Innovación, cofinanciado con Fondos FEDER","Junta de Castilla y León","Ministerio de Economía y Competitividad/FEDER","Proyecto Desarrollo Tecnologico CIBERehd","BIOEF (Basque Foundation for Innovation and Health Research)","Instituto de Salud Carlos III, Proyectos de Investigación en Salud","Junta de Castilla y León (FEDER)","Ministerio de Ciencia e Innovación, Programa Retos-Colaboración","Fundación Científica de la Asociación Española Contra el Cancer (AECC Scientific Foundation) Rare Tumor Calls 2017","Ministerio de Ciencia, Innovación y Universidades","Asociación Española contra el Cáncer","Berrikuntza + Ikerketa + Osasuna Eusko Fundazioa","Ministerio de Economía y Competitividad","La Caixa Foundation Program"],"pagination":["1654-1669"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10113004"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["77(5)"],"pubmed_abstract":["Background and aims
Recent studies suggest that mitochondrial dysfunction promotes progression to NASH by aggravating the gut-liver status. However, the underlying mechanism remains unclear. Herein, we hypothesized that enhanced mitochondrial activity might reshape a specific microbiota signature that, when transferred to germ-free (GF) mice, could delay NASH progression.Approach and results
Wild-type and methylation-controlled J protein knockout (MCJ-KO) mice were fed for 6 weeks with either control or a choline-deficient, L-amino acid-defined, high-fat diet (CDA-HFD). One mouse of each group acted as a donor of cecal microbiota to GF mice, who also underwent the CDA-HFD model for 3 weeks. Hepatic injury, intestinal barrier, gut microbiome, and the associated fecal metabol"],"journal":["Hepatology (Baltimore, Md.)"],"pubmed_title":["Enhanced mitochondrial activity reshapes a gut microbiota profile that delays NASH progression."],"pmcid":["PMC10113004"],"funding_grant_id":["PID2020-120363RB-I0","DTS20/00138","LE063U16","BFU2017-87960-R","GRS2126/A/2020","PID2020‐120363RB‐I0","FPU18/06257","LE017P20","RTC2019-007125-1","PID2020-117116RB-I00","BFU2017‐87960‐R","RY2013-13666"],"pubmed_authors":["Delgado TC","Rodriguez H","Bravo M","Simon J","Lorenzo O","Garcia-Mediavilla MV","Lachiondo-Ortega S","Serrano-Macia M","Anguita J","Abecia L","Juarez-Fernandez M","Rincon M","Martinez-Chantar ML","Sanchez-Campos S","Martinez-Florez S","Goikoetxea-Usandizaga N","Porras D","Varela-Rey M","Nistal E"],"additional_accession":[]},"is_claimable":false,"name":"Enhanced mitochondrial activity reshapes a gut microbiota profile that delays NASH progression.","description":"Background and aims
Recent studies suggest that mitochondrial dysfunction promotes progression to NASH by aggravating the gut-liver status. However, the underlying mechanism remains unclear. Herein, we hypothesized that enhanced mitochondrial activity might reshape a specific microbiota signature that, when transferred to germ-free (GF) mice, could delay NASH progression.Approach and results
Wild-type and methylation-controlled J protein knockout (MCJ-KO) mice were fed for 6 weeks with either control or a choline-deficient, L-amino acid-defined, high-fat diet (CDA-HFD). One mouse of each group acted as a donor of cecal microbiota to GF mice, who also underwent the CDA-HFD model for 3 weeks. Hepatic injury, intestinal barrier, gut microbiome, and the associated fecal metabol","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2025-04-04T08:28:54.988Z","creation":"2025-04-04T08:28:54.988Z"},"accession":"S-EPMC10113004","cross_references":{"pubmed":["35921199"],"doi":["10.1002/hep.32705"]}}