A1 Refereed original research article in a scientific journal

Dynamics of gut metabolome and microbiota maturation during early life




AuthorsAatsinki, Anna-Katariina; Lamichhane, Santosh; Isokääntä, Heidi; Sen, Partho; Kråkström, Matilda; Amaral Alves, Marina; Keskitalo, Anniina; Munukka, Eveliina; Karlsson, Hasse; Perasto, Laura; Lukkarinen, Minna; Oresic, Matej; Kailanto, Henna-Maria; Karlsson, Linnea; Lahti, Leo; Dickens, Alex M.

PublisherCell Press

Publication year2025

Journal: iScience

Article number113596

Volume28

Issue11

eISSN2589-0042

DOIhttps://doi.org/10.1016/j.isci.2025.113596

Publication's open availability at the time of reportingOpen Access

Publication channel's open availability Open Access publication channel

Web address https://doi.org/10.1016/j.isci.2025.113596

Self-archived copy’s web addresshttps://research.utu.fi/converis/portal/detail/Publication/505503222


Abstract

Early-life gut microbiome-metabolome crosstalk plays a crucial role in maintaining host physiology. The microbially produced metabolites often convey effects on host health and physiology. This study investigates the gut metabolites, including short-chain fatty acids (SCFAs), bile acids (BAs), and polar metabolites, and their relationship to gut microbiota composition in a birth cohort of 670 children. Samples were collected at 2.5 (n = 272), 6 (n = 232), 14 (n = 289), and 30 months (n = 157) of age.

We identified the trajectories of the fecal metabolome that relate to the maturation of the early-life gut microbiota. We found that prevalent gut microbial abundances were associated with microbial metabolite levels, particularly in 2.5-month-old infants. Here, the abundances of early colonizers, e.g., Bacteroides, Escherichia, and Bifidobacterium, were associated with microbial metabolites, especially secondary BAs, particularly in breastfed infants.

Our results suggest that early-life gut microbiota associates with changes in metabolome composition, particularly BAs, which may have physiological implications.


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Funding information in the publication
This work was supported by the “Inflammation in human early life: targeting impacts on life-course health” (INITIALISE) consortium funded by the Horizon Europe Program of the European Union under Grant Agreement 101094099.
Finnbrain Birth cohort Study (H.K.) has been funded by the Research Council of Finland (grant numbers 253270, 134950), Jane and Aatos Erkko Foundation, as well as Signe and Ane Gyllenberg Foundation. L.K. was funded by the Research Council of Finland (grant numbers 308176 and 325292), Yrjö Jahnsson Foundation (6847, 6976), Signe and Ane Gyllenberg Foundation, Finnish State Grants for Clinical Research (P3654), Jalmari and Rauha Ahokas Foundation, and Waterloo Foundation (2110-3601). A.K.A. was supported by Yrjö Jahnsson Foundation, Psychiatry Research Foundation, Emil Aaltonen Foundation, Brain Foundation, Instrumentarium Science Foundation, Signe and Ane Gyllenberg Foundation, Duodecim Finnish Medical Society, Juho Vainio Foundation, and Research Council of Finland (grant number 347640). H.I. had a grant from Finnish Cultural Foundation [no 00230482]. L.L. was supported by the Research Council of Finland (grant number 330887). E.M. was supported by the government research grant awarded to Turku University Hospital. A.D. has been funded by the Waterloo Foundation and the Research Council of Finland (347924). “Inflammation in human early life: targeting impacts on life-course health” (INITIALISE) consortium funded by the Horizon Europe Program of the European Union under Grant Agreement 101094099 (to M.O., H.K., A.D.).


Last updated on 2025-25-11 at 07:38