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Published on: April 13, 2019
Structure-Specific and Individual-Dependent Metabolization of Human Milk Oligosaccharides in Infants: A Longitudinal
Fangjie Gu1, Shuang Wang1, Roseriet Beijers2,3
1Laboratory of Food Chemistry, Wageningen University, P.O. Box 17, 6700 AA Wageningen, The Netherlands.
To follow human milk oligosaccharide (HMO) biosynthesis and in vivometabolization, mother milk and infant feces from 68 mother-infant dyads at 2, 6, and 12 weeks postpartum were analyzed, with 18 major HMOs quantitated. Fucosylated and neutral core HMO levels in milk were dependent on mothers' Lewis/Secretor status, whereas most sialylated HMO levels were independent. Infant fecal excretion of HMOs gradually declined with age, especially for neutral core structures. Although decreasing in absolute concentrations in milk during lactation, the relative abundance of total fucosylated HMOs increased in both milk and feces. Mono-fucosylated HMOs were more consumed than those decorated with two fucose moieties. More (α2-3)-sialylated HMOs were degraded than (α2-6)-sialylated HMOs. The transition speed of HMO metabolization from nonspecific or structure-specific consumption stage to the complete consumption stage was individual-dependent. Variation was associated with mode and place of delivery, where caesarean section or early exposure to hospital environment delayed the transition.
To follow human milk oligosaccharide (HMO) biosynthesis and in vivometabolization, mother milk and infant feces from 68 mother-infant dyads at 2, 6, and 12 weeks postpartum were analyzed, with 18 major HMOs quantitated. Fucosylated and neutral core HMO levels in milk were dependent on mothers' Lewis/Secretor status, whereas most sialylated HMO levels were independent. Infant fecal excretion of HMOs gradually declined with age, especially for neutral core structures. Although decreasing in absolute concentrations in milk during lactation, the relative abundance of total fucosylated HMOs increased in both milk and feces. Mono-fucosylated HMOs were more consumed than those decorated with two fucose moieties. More (α2-3)-sialylated HMOs were degraded than (α2-6)-sialylated HMOs. The transition speed of HMO metabolization from nonspecific or structure-specific consumption stage to the complete consumption stage was individual-dependent. Variation was associated with mode and place of delivery, where caesarean section or early exposure to hospital environment delayed the transition.
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