Plasma lipoprotein fatty acids are altered by the positional distribution of fatty acids in infant formula triacylglycerols and human milkpresented by a grant from the Medical Research Council of Canada, Industry Award, with industrysupport from Ross Laboratories, Columbus, OH.rted by a grant from the Medical Research Council of Canada, Industry Award, with industrysupport from Ross Laboratories, Columbus, OH.rted by a

Abstract

Triacylglycerol digestion involves hydrolysis of fatty acids esterified at the glycerol 1,3 positions by gastric and pancreatic lipase to produce 2-monoacylglycerols and unesterified fatty acids, which are then absorbed, reesterified to triacylglycerol, and secreted in chylomicrons. Palmitic acid (16:0) is predominantly esterified to the 2 position of human milk triacylglycerol but to the 1,3 positions in the oils used in infant formulas. We aimed to determine whether the position of 16:0 in human milk and infant formula triacylglycerol influences the position of fatty acids in postprandial plasma chylomicron triacylglycerol. Full-term infants were fed formula with 25-27% 16:0 with either 39% of the 16:0(synthesized triacylglycerol) or 6% of the 16:0 (standard formula) esterified at the triacylglycerol 2 position, or were breast-fed (23% 16:0, 81% at the triacylglycerol 2 position) from birth to 120 d of age. Chylomicron fatty acids and plasma lipids were assessed at 30 and 120 d of age. Infants fed the synthesized triacylglycerol formula, standard formula, or breast milk had 15.8%,8.3%, and 28.0% 16:0 in the chylomicron triacylglycerol 2 position (P < 0.05). These results suggest that >/=50% of the dietary triacylglycerol 2-position 16:0 is conserved through digestion, absorption, and chylomicron triacylglycerol synthesis in breast-fed and formula-fed infants. Infants fed the synthesized triacylglycerol formula had significantly lower HDL-cholesterol and apolipoprotein A-I and higher apolipoprotein B concentrations than infants fed the standard formula. Dietary triacylglycerol fatty acid distribution may alter lipoprotein metabolism in young infants.