Abstract

Abstract The milk fat globule membrane (MFGM) is instrumental for the fat delivery system into human and bovine milk, but is typically removed during the manufacture of infant formula. MFGM contains components that may impact neurodevelopment, including sialic acid, gangliosides, sphingomyelin, choline, glycerophospholipids, proteins, and cholesterol. This presentation will review the clinical trial evidence linking MFGM supplementation to beneficial outcomes in infants and will describe potential mechanistic evidence linking MFGM with neurocognitive outcomes arising from preclinical studies in piglets. Infants fed formula supplemented with a MFGM (4% total protein) from 2 to 6 months of age had improved neurocognitive development at 1 year of age compared to infants fed standard formula. Infants fed formula with MFGM (5.0 g/L) and lactoferrin (0.6 g/L) for 1 year had an accelerated neurodevelopmental profile at 1 year and improved language subcategories at 18 months compared to infants fed a standard formula. To investigate potential mechanisms, piglets were fed a CONT formula or a TEST formula with MFGM and lactoferrin at the same concentrations from 2 to 31 days of age. Piglets underwent spatial T-maze testing to assess learning and memory, and magnetic resonance imaging to measure brain micro- and macrostructure. TEST piglets had lower radial and mean diffusivities in the internal capsule, suggesting greater myelination. The internal capsule contains motor and sensory projections from the cortex to corticospinal tract. Piglets on the CONT diet displayed shorter latency to choice in the T-maze compared to TEST piglets, potentially indicating anxiety-like behaviors or greater impulsivity. Aspects of the microbiome-gut-brain-axis (MGBA) were investigated to uncover potential mechanisms. TEST piglets had higher protein abundance of tyrosine hydroxylase and vasoactive intestinal peptide, longer villi and greater disaccharidase activity in the small intestine and differences in microbial abundances in the ascending colon and feces, suggesting potential modulation of the MGBA by MFGM.

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