Dietary triacyglycerols rich in sn-2 palmitate alter post-prandial lipoprotein and unesterified fatty acids in term infants

Human milk TAG contain 20–25% 16:0, with over 70% of the 16:0 at the TAG sn-2 position. The benefits of TAG sn-2 16:0 have been ascribed to reducing 16:0 excretion as insoluble fatty acid soaps. This study builds on knowledge that infants conserve milk TG sn-2 16:0 post-absorption. Comparison of plasma lipids from 120 day old infants fed formula containing 25–27% 16:0 with 29% 16:0 or 5% 16:0 at the TAG sn-2 position showed higher formula sn-2 16:0 led to lower 18:1n-9, but higher 18:2n-6 and 22:6n-3 in the infant plasma unesterified fatty acids, higher 18:0 in LDL TAG, and higher apo B and lower apo A-1. TAG-sn-2 16:0 may provide 16:0 in remnant particles for hepatic elongation to 18:0, needed for plasma and tissue phospholipids. We suggest attention to the plasma unesterified fatty acids as possible sources of fatty acids for membrane phospholipid synthesis

Polyunsaturated fatty acids and protection of newborn rats from oxygen toxicity

To test whether polyunsaturated fatty acids (PUFA) might be assoclated with protection against oxygen toxicity in newborn experimental animals, we performed two series of experiments. In the first series, adult female rats were fed one of three diets—regular Rat Chow, a high-PUFA (safflower oil-based) diet, or a low-PUFA (paim oil-based) diet—for several weeks before and throughout pregnancy and lactation. Newborn offspring of the three diet groups had similar antioxidant enzyme activities and surfactant development. Offspring of dams fed the high-PUFA diet had total lung lipid fatty acids characterized by increased linoleic acid (18:2ω6) and arachidonic acid (20:4ω6) and a significantly increased PUFA/saturated fatty acid ratio, compared with offspring of dams fed the regular diet or low-PUFA diet; associated with this increased PUFA pattern was markedly superior survival (80 of 84 (95%) vs 56 of 84 (67%) for regular-diet offspring, P95% oxygen. Conversely, offspring born to dams fed the low-PUFA diet had decreased lung PUFA content and inferior tolerance to prolonged high O 2 exposure (survival 38 of 84 (45%)). In the second experimental series, the postnatal provision of high PUFA rat milk to offspring born to dams fed the low-PUFA diet (via “crossnurturing” by high-PUFA diet dams) rapidly increased their lung lipid PUFA and improved their hyperoxic survival (44 of 50 vs 25 of 50 for low-PUFA diet newborn animals kept with their low-PUFA mother rats, P<0.01). These studies suggest that increasing lung lipid PUFA can confer a protective effect against the toxic effects of hyperoxia on the newborn animal lung