Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis

Figure 1 Gene expression of circulating microRNAs. A: miR-33a (P = 0.001); B: miR-126 (P < 0.001); C: miR-499 (P = 0.171); D: miR-186 (P = 0.151); E: miR-146a (P = 0.151). ^aP < 0.05, Significant effect of the high-fat and choline-deficient diet. Data are medians (25^th-75^th percentile), Mann-Whitney U test.

Figure 2 Cardiomyocytes morphometric analysis. The area and cross-sectional shape of cardiomyocytes were determined from images of hematoxylin and eosin-stained tissue. A: Dot plot of cardiomyocyte area vs cardiomyocyte irregularity index in control (blue) and intervention (red) groups. Each dot represents a population of cardiomyocytes with different morphometry. N–normal area and shape, Ir–normal area and irregular shape, HR–hypertrophic and regular cardiomyocytes, HIr–hypertrophic and irregular cardiomyocytes, AR–atrophic and regular cardiomyocytes, AIr–atrophic and irregular cardiomyocyte; B: Average area of cardiomyocytes; C: Percentage of normal cardiomyocytes; D: Percentage of atrophic cardiomyocytes; E-G: We segregated the animals in the intervention group into two subgroups and the data were compared. IL: Interleukin; TNF: Tumor necrosis factor.

Figure 3 Gut microbiota changes in intervention and control groups. A: Shannon diversity index; B: Principal coordinate analysis based on Bray-Curtis distance metric; C: Relative abundance of gut microbiota at the family level; D: Differential abundance by linear discriminant analysis; E: Heatmap distribution of the 41 families among the samples. LDA: Linear discriminant analysis.

Figure 4 Sixteen predicted functional Kyoto Encyclopedia of Genes and Genomes lipid metabolism pathways in intervention and control group. A: Principal coordinate analysis; B: Heatmap distribution; C: Linear discriminant analysis (LDA) of the 16 differentially abundant KEGG lipid metabolism pathways.