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Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants
Maternal secretor status has been shown to be associated with the presence of specific fucosylated human milk oligosaccharides (HMOs), and the impact of maternal secretor status on infant gut microbiota measured through 16s sequencing has previously been reported. None of those studies have confirme...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10519369/ https://www.ncbi.nlm.nih.gov/pubmed/37741856 http://dx.doi.org/10.1080/19490976.2023.2257273 |
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author | Wang, Aidong Diana, Aly Rahmannia, Sofa Gibson, Rosalind S Houghton, Lisa A Slupsky, Carolyn M |
author_facet | Wang, Aidong Diana, Aly Rahmannia, Sofa Gibson, Rosalind S Houghton, Lisa A Slupsky, Carolyn M |
author_sort | Wang, Aidong |
collection | PubMed |
description | Maternal secretor status has been shown to be associated with the presence of specific fucosylated human milk oligosaccharides (HMOs), and the impact of maternal secretor status on infant gut microbiota measured through 16s sequencing has previously been reported. None of those studies have confirmed exclusive breastfeeding nor investigated the impact of maternal secretor status on gut microbial fermentation products. The present study focused on exclusively breastfed (EBF) Indonesian infants, with exclusive breastfeeding validated through the stable isotope deuterium oxide dose-to-mother (DTM) technique, and the impact of maternal secretor status on the infant fecal microbiome and metabolome. Maternal secretor status did not alter the within-community (alpha) diversity, between-community (beta) diversity, or the relative abundance of bacterial taxa at the genus level. However, infants fed milk from secretor (Se+) mothers exhibited a lower level of fecal succinate, amino acids and their derivatives, and a higher level of 1,2-propanediol when compared to infants fed milk from non-secretor (Se-) mothers. Interestingly, for infants consuming milk from Se+ mothers, there was a correlation between the relative abundance of Bifidobacterium and Streptococcus, and between each of these genera and fecal metabolites that was not observed in infants receiving milk from Se- mothers. Our findings indicate that the secretor status of the mother impacts the gut microbiome of the exclusively breastfed infant. |
format | Online Article Text |
id | pubmed-10519369 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-105193692023-09-26 Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants Wang, Aidong Diana, Aly Rahmannia, Sofa Gibson, Rosalind S Houghton, Lisa A Slupsky, Carolyn M Gut Microbes Research Paper Maternal secretor status has been shown to be associated with the presence of specific fucosylated human milk oligosaccharides (HMOs), and the impact of maternal secretor status on infant gut microbiota measured through 16s sequencing has previously been reported. None of those studies have confirmed exclusive breastfeeding nor investigated the impact of maternal secretor status on gut microbial fermentation products. The present study focused on exclusively breastfed (EBF) Indonesian infants, with exclusive breastfeeding validated through the stable isotope deuterium oxide dose-to-mother (DTM) technique, and the impact of maternal secretor status on the infant fecal microbiome and metabolome. Maternal secretor status did not alter the within-community (alpha) diversity, between-community (beta) diversity, or the relative abundance of bacterial taxa at the genus level. However, infants fed milk from secretor (Se+) mothers exhibited a lower level of fecal succinate, amino acids and their derivatives, and a higher level of 1,2-propanediol when compared to infants fed milk from non-secretor (Se-) mothers. Interestingly, for infants consuming milk from Se+ mothers, there was a correlation between the relative abundance of Bifidobacterium and Streptococcus, and between each of these genera and fecal metabolites that was not observed in infants receiving milk from Se- mothers. Our findings indicate that the secretor status of the mother impacts the gut microbiome of the exclusively breastfed infant. Taylor & Francis 2023-09-23 /pmc/articles/PMC10519369/ /pubmed/37741856 http://dx.doi.org/10.1080/19490976.2023.2257273 Text en © 2023 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent. |
spellingShingle | Research Paper Wang, Aidong Diana, Aly Rahmannia, Sofa Gibson, Rosalind S Houghton, Lisa A Slupsky, Carolyn M Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title | Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title_full | Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title_fullStr | Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title_full_unstemmed | Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title_short | Impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
title_sort | impact of milk secretor status on the fecal metabolome and microbiota of breastfed infants |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10519369/ https://www.ncbi.nlm.nih.gov/pubmed/37741856 http://dx.doi.org/10.1080/19490976.2023.2257273 |
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