HMOs: Shaping the infant gut microbiota and supporting health

Breast milk is the optimal nutrition for infants, and its composition has been shaped by thousands of years of human evolution in order to provide tailor-made nutrition and protection to the developing neonate, all at an energetic cost to the mother.

Recent advances in analytical tools and the development and integration of “-omics” technologies have offered valuable insights into the composition of human breast milk, while reinforcing our understanding of the health benefits associated with breastfeeding.

One of the most remarkable features of breast milk is the diversity and abundance of complex sugars (glycans) including human milk oligosaccharides (HMOs), which are indigestible to the infant and for this reason reach the colon intact.

The composition of HMO varies between lactating mothers and is impacted significantly by maternal genetics. This variability is largely driven by polymorphisms in the fucosyltransferases FUT2 (Se) and FUT3 (Le). If both genes are active then all fucose-borne HMO species can be synthesized. Mothers with an inactive FUT2 gene cannot synthesize α1-2 fucosylated HMOs (such as 2′-fucosyllactose [2′-FL] and lacto-N-fucopentaose I [LNFP I]) while mothers with an inactive FUT3 gene cannot synthesize α1-3 or α1-4 fucosylated HMOs (such as LNFP II and LNFP III). Based on these fucosyltransferase polymorphisms, four milk groups can be defined: 1) Lewis positive secretors (Le+Se+) 2) Lewis negative secretors (LeSe+) 3) Lewis positive non-secretors (Le+Se) 4) Lewis negative non-secretors (LeSe).

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