Fig. 3: Alteration of microbial functions in children with T1D.
From: Functional and metabolic alterations of gut microbiota in children with new-onset type 1 diabetes
a Total gene count in the NC and T1D groups (p < 0.001). b, c The microbial community richness (Chao 1 index; b, p = 0.002) and diversity (Shannon index; c). d, e PCoA based on weighted UniFrac distance (d) and inner-group distance by ANOSIM (e, p < 0.001). f, g PCoA plot based on the Bray-Curtis distances of KOs (f) and inner-group distance by ANOSIM (g, p < 0.001). h The abundance of carbohydrate-active enzymes (CAZy) genes (p < 0.001). i The five most differential expressed CAZy genes. j The abundance of the most differential expressed genes involved in butyrate metabolism (EefB, p = 0.044; HgCoAd_A, p = 0.002; But, p < 0.001; KamA, p < 0.001; AtoA, p = 0.009). k The metabolic pathways for butyrate synthesis. The upward and downward red arrows represent upregulation and downregulation in the T1D group compared to the NC group. l The contribution of Faecalibacterium prausnitzii to genes involved in butyrate metabolism (p < 0.001). m The abundance of genes involved in lipopolysaccharide synthesis based on the KEGG database (p = 0.019). n The abundance of genes involved in BSHs based on the UniProt database (p < 0.001). o, p The abundance of genes involved in bile acid metabolism based on the EggNOG database (COG0385, p < 0.001). NC: n = 77, T1D: n = 64. Violin plots show the median, quartiles, and min/max values. Two-sided Wilcoxon rank-sum test. *p < 0.05, **p < 0.01, ***p < 0.001. Source data are provided as a Source Data file.
