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J Proteome Res. 2010 Oct 1;9(10):5284-95. doi: 10.1021/pr100554m.

Dietary modulation of gut functional ecology studied by fecal metabonomics.

Author information

1
Nestlé Research Center, Vers-chez-les-Blanc, Lausanne 26, Switzerland. francois-pierre.martin@rdls.nestle.com

Abstract

A major source of intestinal metabolites results from both host and microbial processing of dietary nutrients. (1)H NMR-based metabolic profiling of mouse feces was carried out over time in different microbiome mouse models, including conventional (n = 9), conventionalized (n = 10), and "humanized" gnotobiotic mice inoculated with a model of human baby microbiota (HBM, n = 17). HBM mice were supplemented with Lactobacillus paracasei with (n = 10) and without (n = 7) prebiotics. Animals not supplemented with prebiotics received a diet enriched in glucose and lactose as placebo. In conventionalized animals, microbial populations and activities converged in term of multivariate mapping toward conventional mice. Both groups decreased bacterial processing of dietary proteins when switching to a diet enriched in glucose and lactose, as described with low levels of 5-aminovalerate, acetate, and propionate and high levels of lysine and arginine. The HBM model differs from conventional and conventionalized microbiota in terms of type, proportion, and metabolic activity of gut bacteria (lower short chain fatty acids (SCFAs), lactate, 5-aminovalerate, and oligosaccharides, higher bile acids and choline). The probiotics supplementation of HBM mice was associated with a specific amino acid pattern that can be linked to L. paracasei proteolytic activities. The combination of L. paracasei with the galactosyl-oligosaccharide prebiotics was related to the enhanced growth of bifidobacteria and lactobacilli, and a specific metabolism of carbohydrates, proteins, and SCFAs. The present study describes how the assessment of metabolic changes in feces may provide information for studying nutrient-microbiota relationships in different microbiome mouse models.

PMID:
20806900
DOI:
10.1021/pr100554m
[Indexed for MEDLINE]

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