Fricker Ashwana D, Sejane Kristija, Desai Mina, Snyder Michael W, Duran Luis, Mackelprang Rachel, Bode Lars, Ross Michael G, Flores Gilberto E
Department of Biology, California State University, Northridge, CA 91330, USA.
Biology Department, Adelphi University, Garden City, NY 11530, USA.
Nutrients. 2025 Jan 18;17(2):338. doi: 10.3390/nu17020338.
Maternal obesity may contribute to childhood obesity in a myriad of ways, including through alterations of the infant gut microbiome. For example, maternal obesity may contribute both directly by introducing a dysbiotic microbiome to the infant and indirectly through the altered composition of human milk that fuels the infant gut microbiome. In particular, indigestible human milk oligosaccharides (HMOs) are known to shape the composition of the infant gut microbiome. The goal of this study was to characterize the HMO profiles of normal-weight and overweight mothers and to quantitatively link HMO concentrations to the taxonomic composition and functional potential of the infant gut microbiome.
Normal-weight (BMI = 18.5-24.9; = 9) and overweight/obese (OW/OB; BMI > 25; = 11) breastfeeding mothers and their infants were enrolled in this single-center, cross-sectional pilot study. Human milk from the mothers and rectal stool swabs from the infants were collected 7-9 weeks postpartum. The HMO composition, microbiome composition, and microbial functions were assessed using HPLC, 16S rRNA gene sequencing, and metagenomic sequencing, respectively.
Neither the HMO profiles nor the infant microbiome composition varied according to maternal BMI status. Taxonomically, the gut microbiota of infants were dominated by typical gut lineages including . Significant correlations between individual HMOs and bacterial genera were identified, including for , a genus of the Bacteroidota phylum that was positively correlated with the concentrations of lacto--neotetraose (LNnT) and lacto--hexaose (LNH). Using metagenomic assembled genomes, we were also able to identify the broad HMO-degradative capacity across the and genera.
These results suggest that the maternal BMI status does not impact the HMO profiles of human milk. However, select HMOs were correlated with specific bacterial taxa, suggesting that the milk composition influences both the taxonomic composition and the functional capacity of the infant gut microbiome.
母亲肥胖可能通过多种方式导致儿童肥胖，包括改变婴儿肠道微生物群。例如，母亲肥胖可能直接通过将失调的微生物群传递给婴儿，以及间接通过改变为婴儿肠道微生物群提供养分的母乳成分来发挥作用。特别是，已知难消化的人乳寡糖（HMOs）会影响婴儿肠道微生物群的组成。本研究的目的是描述正常体重和超重母亲的HMO谱，并将HMO浓度与婴儿肠道微生物群的分类组成和功能潜力进行定量关联。
本单中心横断面试点研究纳入了正常体重（BMI = 18.5 - 24.9；n = 9）和超重/肥胖（OW/OB；BMI > 25；n = 11）的母乳喂养母亲及其婴儿。在产后7 - 9周收集母亲的母乳和婴儿的直肠粪便拭子。分别使用高效液相色谱法、16S rRNA基因测序和宏基因组测序评估HMO组成、微生物群组成和微生物功能。
HMO谱和婴儿微生物群组成均未因母亲BMI状态而有所不同。在分类学上，婴儿的肠道微生物群以典型的肠道谱系为主，包括 。确定了个体HMO与细菌属之间的显著相关性，包括与拟杆菌门的一个属 ，该属与乳糖 - N - 新四糖（LNnT）和乳糖 - N - 六糖（LNH）的浓度呈正相关。使用宏基因组组装基因组，我们还能够确定 和 属的广泛HMO降解能力。
这些结果表明，母亲BMI状态不会影响母乳的HMO谱。然而，特定的HMO与特定的细菌分类群相关，表明母乳成分会影响婴儿肠道微生物群的分类组成和功能能力。
