LaforestLapointeBeckerMandhaneEtAl2021

Référence

Laforest-Lapointe, I., Becker, A.B., Mandhane, P.J., Turvey, S.E., Moraes, T.J., Sears, M.R., Subbarao, P., Sycuro, L.K., Azad, M.B., Arrieta, M.-C. (2021) Maternal consumption of artificially sweetened beverages during pregnancy is associated with infant gut microbiota and metabolic modifications and increased infant body mass index. Gut Microbes, 13(1):1-15. (Scopus )

Résumé

Artificial sweetener consumption by pregnant women has been associated with an increased risk of infant obesity, but the underlying mechanisms are unknown. We aimed to determine if maternal consumption of artificially sweetened beverages (ASB) during pregnancy is associated with modifications of infant gut bacterial community composition and function during the first year of life, and whether these alterations are linked with infant body mass index (BMI) at one year of age. We studied 100 infants from the prospective Canadian CHILD Cohort Study, selected based on maternal ASB consumption during pregnancy (50 non-consumers and 50 daily consumers). BMI was higher among ASB-exposed infants. Infant stool (16S rRNA gene sequencing) and urine (untargeted metabolomics) were acquired in early (3–4 months) and late (12 months) infancy. We identified four microbiome clusters, of which two recapitulated the maturation trajectory of the infant gut bacterial communities from immature (Cluster 1) to mature (Cluster 4) and two deviated from this trajectory (Clusters 2 and 3). Maternal ASB consumption did not differ between clusters, but was associated with community-level shifts in infant gut bacterial taxonomy structure and depletion of several Bacteroides sp. in Cluster 2. In the complete dataset, urine succinate and spermidine levels at 3 months were higher in ASB-exposed infants, and urine succinate was positively associated with BMI at one-year-old. Overall, gestational exposure to ASB was associated with gut microbiota structure in infants from Cluster 2, and gut microbiota structure was associated with infant BMI. Gestational exposure to ASB was positively associated with infant urine succinate and spermidine. Succinate was found to mediate 29% of the effect of ASB exposure on BMI at one-year-old, revealing a potential role of this metabolite in increased infant weight linked to gestational ASB consumption. As we face an unprecedented rise in childhood obesity, future studies should evaluate the causal relationships between maternal ASB consumption (a modifiable exposure), gut microbiota and metabolites, infant metabolism, and body composition. © 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.

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@ARTICLE { LaforestLapointeBeckerMandhaneEtAl2021,
    AUTHOR = { Laforest-Lapointe, I. and Becker, A.B. and Mandhane, P.J. and Turvey, S.E. and Moraes, T.J. and Sears, M.R. and Subbarao, P. and Sycuro, L.K. and Azad, M.B. and Arrieta, M.-C. },
    JOURNAL = { Gut Microbes },
    TITLE = { Maternal consumption of artificially sweetened beverages during pregnancy is associated with infant gut microbiota and metabolic modifications and increased infant body mass index },
    YEAR = { 2021 },
    NOTE = { cited By 1 },
    NUMBER = { 1 },
    PAGES = { 1-15 },
    VOLUME = { 13 },
    ABSTRACT = { Artificial sweetener consumption by pregnant women has been associated with an increased risk of infant obesity, but the underlying mechanisms are unknown. We aimed to determine if maternal consumption of artificially sweetened beverages (ASB) during pregnancy is associated with modifications of infant gut bacterial community composition and function during the first year of life, and whether these alterations are linked with infant body mass index (BMI) at one year of age. We studied 100 infants from the prospective Canadian CHILD Cohort Study, selected based on maternal ASB consumption during pregnancy (50 non-consumers and 50 daily consumers). BMI was higher among ASB-exposed infants. Infant stool (16S rRNA gene sequencing) and urine (untargeted metabolomics) were acquired in early (3–4 months) and late (12 months) infancy. We identified four microbiome clusters, of which two recapitulated the maturation trajectory of the infant gut bacterial communities from immature (Cluster 1) to mature (Cluster 4) and two deviated from this trajectory (Clusters 2 and 3). Maternal ASB consumption did not differ between clusters, but was associated with community-level shifts in infant gut bacterial taxonomy structure and depletion of several Bacteroides sp. in Cluster 2. In the complete dataset, urine succinate and spermidine levels at 3 months were higher in ASB-exposed infants, and urine succinate was positively associated with BMI at one-year-old. Overall, gestational exposure to ASB was associated with gut microbiota structure in infants from Cluster 2, and gut microbiota structure was associated with infant BMI. Gestational exposure to ASB was positively associated with infant urine succinate and spermidine. Succinate was found to mediate 29% of the effect of ASB exposure on BMI at one-year-old, revealing a potential role of this metabolite in increased infant weight linked to gestational ASB consumption. As we face an unprecedented rise in childhood obesity, future studies should evaluate the causal relationships between maternal ASB consumption (a modifiable exposure), gut microbiota and metabolites, infant metabolism, and body composition. © 2020 The Author(s). Published with license by Taylor & Francis Group, LLC. },
    AFFILIATION = { Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada; University of Calgary, Calgary, AB, Canada; Université De Sherbrooke, Sherbrooke, QC, Canada; Alberta Children’s Hospital Research Institute (ACHRI), Calgary, AB, Canada; Snyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada; Pediatrics and Child Health, University of Manitoba, Winnipeg, MB, Canada; University of Alberta, Edmonton, AB, Canada; British Columbia Children’s Hospital, The University of British Columbia, Vancouver, BC, Canada; Hospital for Sick Children, Toronto, ON, Canada; University of Toronto, Toronto, ON, Canada; Medicine, McMaster University, Hamilton, ON, Canada; Microbiology, Immunology, and Infectious Diseases, University of Calgary, Calgary, AB, Canada },
    AUTHOR_KEYWORDS = { 16s rRNA; artificial sweeteners; BMI; breastfeeding; Child cohort; genomics; gestational exposure; Gut microbiota; metabolomics; obesity },
    DOCUMENT_TYPE = { Article },
    DOI = { 10.1080/19490976.2020.1857513 },
    SOURCE = { Scopus },
    URL = { https://www.scopus.com/inward/record.uri?eid=2-s2.0-85098621046&doi=10.1080%2f19490976.2020.1857513&partnerID=40&md5=ca4e9967bb42bbe35006be604f235118 },
}

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