4.7 Article

Butyrate in Human Milk: Associations with Milk Microbiota, Milk Intake Volume, and Infant Growth

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NUTRIENTS
卷 15, 期 4, 页码 -

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MDPI
DOI: 10.3390/nu15040916

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human milk butyrate; human milk microbiota; human milk intake volume; butyrate intake; infant growth; infant adiposity; infant weight gain

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This study investigated the origins and determining factors of butyrate in human milk and its influence on infant weight gain. The results showed that higher concentrations of butyrate in human milk were associated with lower infant weight and adiposity, especially in younger infants. Furthermore, the study found an inverse correlation between butyrate concentration and milk intake volume, suggesting a potential mechanism involving appetite regulation and modulation of milk intake.
Butyrate in human milk (HM) has been suggested to reduce excessive weight and adipo-sity gains during infancy. However, HM butyrate's origins, determinants, and its influencing mechanism on weight gain are not completely understood. These were studied in the prospective longitudinal Cambridge Baby Growth and Breastfeeding Study (CBGS-BF), in which infants (n = 59) were exclusively breastfed for at least 6 weeks. Infant growth (birth, 2 weeks, 6 weeks, 3 months, 6 months, and 12 months) and HM butyrate concentrations (2 weeks, 6 weeks, 3 months, and 6 months) were measured. At age 6 weeks, HM intake volume was measured by deuterium-labelled water technique and HM microbiota by 16S sequencing. Cross-sectionally at 6 weeks, HM butyrate was associated with HM microbiota composition (p = 0.036) although no association with the abundance of typical butyrate producers was detected. In longitudinal analyses across all time points, HM butyrate concentrations were overall negatively associated with infant weight and adiposity, and associations were stronger at younger infant ages. HM butyrate concentration was also inversely correlated with HM intake volume, supporting a possible mechanism whereby butyrate might reduce infant growth via appetite regulation and modulation of HM intake.

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