A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Dynamics of gut metabolome and microbiota maturation during early life
Tekijät: Aatsinki, 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.
Kustantaja: Cell Press
Julkaisuvuosi: 2025
Lehti: iScience
Artikkelin numero: 113596
Vuosikerta: 28
Numero: 11
eISSN: 2589-0042
DOI: https://doi.org/10.1016/j.isci.2025.113596
Julkaisun avoimuus kirjaamishetkellä: Avoimesti saatavilla
Julkaisukanavan avoimuus : Kokonaan avoin julkaisukanava
Verkko-osoite: https://doi.org/10.1016/j.isci.2025.113596
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/505503222
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.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
Julkaisussa olevat rahoitustiedot:
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.).
