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Specific synbiotics in early life protect against diet‐induced obesity in adult mice
Author(s) -
Mischke Mona,
Arora Tulika,
Tims Sebastian,
Engels Eefje,
Sommer Nina,
van Limpt Kees,
Baars Annemarie,
Oozeer Raish,
Oosting Annemarie,
Bäckhed Fredrik,
Knol Jan
Publication year - 2018
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.13240
Subject(s) - synbiotics , biology , microbiome , gut flora , prebiotic , obesity , bifidobacterium , physiology , immunology , endocrinology , bioinformatics , probiotic , lactobacillus , genetics , bacteria
Aims The metabolic state of human adults is associated with their gut microbiome. The symbiosis between host and microbiome is initiated at birth, and early life microbiome perturbation can disturb health throughout life. Here, we determined how beneficial microbiome interventions in early life affect metabolic health in adulthood. Methods Postnatal diets were supplemented with either prebiotics (scGOS/lcFOS) or synbiotics (scGOS/lcFOS with Bifidobacterium breve M‐16 V) until post‐natal (PN) day 42 in a well‐established rodent model for nutritional programming. Mice were subsequently challenged with a high‐fat Western‐style diet (WSD) for 8 weeks. Body weight and composition were monitored, as was gut microbiota composition at PN21, 42 and 98. Markers of glucose homeostasis, lipid metabolism and host transcriptomics of 6 target tissues were determined in adulthood (PN98). Results Early life synbiotics protected mice against WSD‐induced excessive fat accumulation throughout life, replicable in 2 independent European animal facilities. Adult insulin sensitivity and dyslipidaemia were improved and most pronounced changes in gene expression were observed in the ileum. We observed subtle changes in faecal microbiota composition, both in early life and in adulthood, including increased abundance of Bifidobacterium . Microbiota transplantation using samples collected from synbiotics‐supplemented adolescent mice at PN42 to age‐matched germ‐free recipients did not transfer the beneficial phenotype, indicating that synbiotics‐modified microbiota at PN42 is not sufficient to transfer long‐lasting protection of metabolic health status. Conclusion Together, these findings show the potential and importance of timing of synbiotic interventions in early life during crucial microbiota development as a preventive measure to lower the risk of obesity and improve metabolic health throughout life.