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dc.contributor.authorLongo, Larissept_BR
dc.contributor.authorRampelotto, Pabulo Henriquept_BR
dc.contributor.authorChiela, Eduardo Cremonese Filippipt_BR
dc.contributor.authorSouza, Valessa Emanoele Gabriel dept_BR
dc.contributor.authorSalvati, Fernandopt_BR
dc.contributor.authorCerski, Carlos Thadeu Schmidtpt_BR
dc.contributor.authorSilveira, Themis Reverbel dapt_BR
dc.contributor.authorOliveira, Claudia Pinto Marques Souza dept_BR
dc.contributor.authorCruz, Carolina Uribept_BR
dc.contributor.authorÁlvares-da-Silva, Mário Reispt_BR
dc.date.accessioned2023-11-18T03:24:35Zpt_BR
dc.date.issued2021pt_BR
dc.identifier.issn1948-5182pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/267213pt_BR
dc.description.abstractBACKGROUND Cardiovascular disease is the main cause of death in metabolic-associated fatty liver disease, and gut microbiota dysbiosis is associated with both of them. AIM To assess the relationship between gut dysbiosis and cardiovascular risk (CVR) in an experimental model of steatohepatitis. METHODS Adult male Sprague-Dawley rats were randomized to a control group (n = 10) fed a standard diet and an intervention group (n = 10) fed a high-fat choline-deficient diet for 16 wk. Biochemical, molecular, hepatic, and cardiac histopathology. Gut microbiota variables were evaluated. RESULTS The intervention group had a significantly higher atherogenic coefficient, Castelli’s risk index (CRI)-I and CRI-II, interleukin-1β, tissue inhibitor of metalloproteinase- 1 (all P < 0.001), monocyte chemoattractant protein-1 (P = 0.005), and plasminogen activator inhibitor-1 (P = 0.037) than the control group. Gene expression of miR-33a increased (P = 0.001) and miR-126 (P < 0.001) decreased in the intervention group. Steatohepatitis with fibrosis was seen in the intervention group, and heart computerized histological imaging analysis showed a significant decrease in the percentage of cardiomyocytes with a normal morphometric appearance (P = 0.007), reduction in the mean area of cardiomyocytes (P = 0.037), and an increase of atrophic cardiomyocytes (P = 0.007). There were significant correlations between the cardiomyocyte morphometry markers and those of progression and severity of liver disease and CVR. The intervention group had a lower Shannon diversity index and fewer changes in the structural pattern of gut microbiota (both P < 0.001) than controls. Nine microbial families that are involved in lipid metabolism were differentially abundant in intervention group and were significantly correlated with markers of liver injury and CVR. CONCLUSION The study found a link between gut dysbiosis and significant cardiomyocyte abnormalities in animals with steatohepatitis.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofWorld journal of hepatology. Pleasanton. Vol. 13, no. 12 (2021), p. 2052-2070pt_BR
dc.rightsOpen Accessen
dc.subjectAnimal modelen
dc.subjectModelos animaispt_BR
dc.subjectDoenças cardiovascularespt_BR
dc.subjectCardiovascular diseasesen
dc.subjectGut microbiotaen
dc.subjectMicrobioma gastrointestinalpt_BR
dc.subjectMetabolic-associated fatty liver diseaseen
dc.subjectPrognósticopt_BR
dc.subjectPredicted lipid metabolismen
dc.subjectFatores de riscopt_BR
dc.subjectHepatopatia gordurosa não alcoólicapt_BR
dc.subjectRisk cardiovascularen
dc.subjectMetabolismopt_BR
dc.subjectSteatohepatitisen
dc.subjectLipídeospt_BR
dc.titleGut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitispt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001186994pt_BR
dc.type.originEstrangeiropt_BR


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