Non-targeted metabolomics was utilized to investigate the differential metabolites in feces among the four groups. The score scatter plots generated by the OPLS-DA model displayed clear differentiation between normal mice, T2DM mice, and CMPs-treated T2DM mice (Fig. 7A). The reliability of the model was validated through a permutations test (Fig. 7B). PLS-DA analysis of metabolic profiles showed complete separation between normal and T2DM groups, while partial overlap was observed for D, DH, and DL groups, indicating that T2DM induced metabolic disorders and CMPs altered metabolites in T2DM mice (Fig. 7C). A volcano plot was used to display differential metabolites screened based on VIP＞1.0, p＜0.05, FC＞2 or FC＜0.05 criteria (Fig. 7D). A total of 84 different metabolites were identified as potential biomarkers between the T2DM group and CMPs-treated groups (Table S2), of which 58 were significantly up-regulated (e.g., ureidopropionic acid and (S)-ureidoglycine) and 26 were significantly down-regulated (e.g., beta-leucine, dodecanedioic acid, and 3,4-methylenedioxyamphetamine) by CMPs intervention. Specifically, CMPs mainly altered organic acids (21), alcohols (10), amino acids (9), and amines (7) in T2DM mice. To understand the metabolic alterations caused by CMP intervention, metabolic pathway enrichment analysis was performed revealing three significant pathways including pantothenate and CoA biosynthesis, phenylalanine metabolism, and linoleic acid metabolism (p＜0.05) (Fig. 7E). Notably, specific metabolites such as ®-Pantoate, pantetheine, pantothenic acid, and ureidopropionic acid were involved in pantothenate and CoA biosynthesis while linoleic acid, 9(S)-HPODE, and 9,12,13-TriHOME were involved in linoleic acid metabolism (Table S3).
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