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Prebiotic Functions of Mannose Oligosaccharides Revealed by Microbiomic and Metabolomic Analyses of Intestinal Digesta (P20-017-19).

Objectives
Mannose oligosaccharides (MOS) are considered to be prebiotics, but MOS-induced changes in the microbiome and metabolome of intestinal digesta were not well characterized. The objective of this study aims to investigate the effects of MOS-induced changes in metabolites and microbiota.


Methods
4 groups of male C57Bl/6 mice were fed AIN93G diet containing 0, 0.2, 1 and 5% of MOS, respectively, for six weeks. The effects of MOS on growth performance was determined by body weight gain and food intake. The effects of MOS on the microbiome and metabolome of intestinal digesta were determined by 16S rRNA sequencing and liquid chromatography-mass spectrometry-based metabolomics analysis of ileal, cecal, colonic digesta and feces samples collected at the end of 6-week MOS feeding, respectively.


Results
MOS feeding did not affect growth performance among different treatments. Microbiomic analysis showed that MOS dose-dependently modulated the microbiome in both cecal and colonic digesta samples. At the phylum level, MOS decreased the abundance of Firmicutes and increased the abundance of Actinobacteria. At the genus level, MOS increased Bacteroides, Parasutterella, Prevotellaceae UCG-001 and decreased Clostridium sensu stricto. Metabolomic analysis showed that MOS dose-dependently affected diverse metabolites from both endogenous and microbial metabolism, including the increases of aspartate, glutamate, lactate, succinate, α-ketoglutarate, butyrate and valerate, and the decreases of many other amino acids. In addition, the correlations between MOS-responsive microbiota and MOS-responsive metabolites were also observed.


Conclusions
Overall, our results revealed the probiotic functions of MOS by identifying MOS-induced changes in gut microbiome and metabolome, which may provide mechanistic insights on the potential beneficial effects of MOS on the whole-body metabolism system.


Funding Sources
N/A.