Abstract

Sialic acid (Sia), a carboxylated 9‐carbon monosaccharide, is a crucial constituent of brain glycoproteins and glycolipids associated with brain development and enhanced cognitive function. Brain Sia concentrations rapidly increase after birth and are significantly higher in breast‐fed than in formula‐fed infants. Compared to formula, human breast milk contains a high amount of sialylated oligosaccharides; yet their direct role in brain Sia accrual is unknown. Our objective was to determine whether sialylated milk oligosaccharides contribute to brain Sia accumulation in mice between birth and weaning. To overcome problems with artificial feeding in newborn pups, we used a cross‐foster approach with pups reared on dams normal or genetically deficient in 3′sialyllactose (3′SL), one of the major sialylated milk oligosaccharides. Urine 3′SL and brain Sia were derivatized and measured by HPLC. While pups reared on dams with normal milk 3′SL had significantly higher urine 3′SL levels than pups fed on 3′SL deficient milk (460 vs. 40 uM at day 7, P<0.001), there was no significant difference in brain Sia one week (6.0±1.1 vs. 6.0±1.2 pmol/ug protein) and three weeks after birth (19.0±9.7 vs. 15.0±4.9 pmol/ug protein). The data indicate that 3′SL, one of the major sialylated milk oligosaccharides, does not contribute to postnatal brain Sia accumulation – at least in mice.Grant Funding Source: NIH

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