Deficient butyrate metabolism in the intestinal microbiome is a potential risk factor for recurrent kidney stone disease.
Intestinal microbiome
Kidney stone disease
Kidney stones
Oxalate metabolism
Urology
Journal
Urolithiasis
ISSN: 2194-7236
Titre abrégé: Urolithiasis
Pays: Germany
ID NLM: 101602699
Informations de publication
Date de publication:
28 Feb 2024
28 Feb 2024
Historique:
received:
17
10
2023
accepted:
16
01
2024
medline:
28
2
2024
pubmed:
28
2
2024
entrez:
27
2
2024
Statut:
epublish
Résumé
Intestinal microbiome dysbiosis is a known risk factor for recurrent kidney stone disease (KSD) with prior data suggesting a role for dysfunctional metabolic pathways other than those directly utilizing oxalate. To identify alternative mechanisms, the current study analyzed differences in the metabolic potential of intestinal microbiomes of patients (n = 17) and live-in controls (n = 17) and determined their relevance to increased risk for KSD using shotgun metagenomic sequencing. We found no differences in the abundance of genes associated with known oxalate degradation pathways, supporting the notion that dysfunction in other metabolic pathways plays a role in KSD. Further analysis showed decreased abundance of key enzymes involved in butyrate biosynthesis in patient intestinal microbiomes. Furthermore, de novo construction of microbial genomes showed that the majority of genes significantly enriched in non-stone formers are affiliated with Faecalibacterium prausnitzii, a major butyrate producer. Specifically pertaining to butyrate metabolism, the majority of abundant genes mapped back to F. prausnitzii, Alistipes spp., and Akkermansia muciniphila. No differences were observed in ascorbate or glyoxylate metabolic pathways. Collectively, these data suggest that impaired bacterial-associated butyrate metabolism may be an oxalate-independent mechanism that contributes to an increased risk for recurrent KSD. This indicates that the role of the intestinal microbiome in recurrent KSD is multi-factorial, which is representative of the highly intertwined metabolic nature of this complex environment. Future bacteria-based treatments must not be restricted to targeting only oxalate metabolism.
Identifiants
pubmed: 38413462
doi: 10.1007/s00240-024-01534-x
pii: 10.1007/s00240-024-01534-x
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
38Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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