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 ( = 10) fed a standard diet and an intervention group ( = 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 < 0.001), monocyte chemoattractant protein-1 ( = 0.005), and plasminogen activator inhibitor-1 ( = 0.037) than the control group. Gene expression of miR-33a increased ( = 0.001) and miR-126 ( < 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 ( = 0.007), reduction in the mean area of cardiomyocytes ( = 0.037), and an increase of atrophic cardiomyocytes ( = 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 < 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.
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| http://dx.doi.org/10.4254/wjh.v13.i12.2052 | DOI Listing |
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