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Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis
BACKGROUND: 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. ME...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8727214/ https://www.ncbi.nlm.nih.gov/pubmed/35070008 http://dx.doi.org/10.4254/wjh.v13.i12.2052 |
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author | Longo, Larisse Rampelotto, Pabulo Henrique Filippi-Chiela, Eduardo de Souza, Valessa Emanoele Gabriel Salvati, Fernando Cerski, Carlos Thadeu da Silveira, Themis Reverbel Oliveira, Cláudia P Uribe-Cruz, Carolina Álvares-da-Silva, Mário Reis |
author_facet | Longo, Larisse Rampelotto, Pabulo Henrique Filippi-Chiela, Eduardo de Souza, Valessa Emanoele Gabriel Salvati, Fernando Cerski, Carlos Thadeu da Silveira, Themis Reverbel Oliveira, Cláudia P Uribe-Cruz, Carolina Álvares-da-Silva, Mário Reis |
author_sort | Longo, Larisse |
collection | PubMed |
description | BACKGROUND: 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. |
format | Online Article Text |
id | pubmed-8727214 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-87272142022-01-20 Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis Longo, Larisse Rampelotto, Pabulo Henrique Filippi-Chiela, Eduardo de Souza, Valessa Emanoele Gabriel Salvati, Fernando Cerski, Carlos Thadeu da Silveira, Themis Reverbel Oliveira, Cláudia P Uribe-Cruz, Carolina Álvares-da-Silva, Mário Reis World J Hepatol Basic Study BACKGROUND: 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. Baishideng Publishing Group Inc 2021-12-27 2021-12-27 /pmc/articles/PMC8727214/ /pubmed/35070008 http://dx.doi.org/10.4254/wjh.v13.i12.2052 Text en ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/ |
spellingShingle | Basic Study Longo, Larisse Rampelotto, Pabulo Henrique Filippi-Chiela, Eduardo de Souza, Valessa Emanoele Gabriel Salvati, Fernando Cerski, Carlos Thadeu da Silveira, Themis Reverbel Oliveira, Cláudia P Uribe-Cruz, Carolina Álvares-da-Silva, Mário Reis Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title_full | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title_fullStr | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title_full_unstemmed | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title_short | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
title_sort | gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8727214/ https://www.ncbi.nlm.nih.gov/pubmed/35070008 http://dx.doi.org/10.4254/wjh.v13.i12.2052 |
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