Arachidonate and docosahexaenoate added to infant formula influence fatty acid composition and subsequent eicosanoid production in neonatal pigs.

As natural components of human milk, arachdonic and docosahexaenoic acids play important roles in neonatal development; thus, addition of these fatty acids to infant formula has been suggested. This study examined the effects of supplementation of infant formula with microbial sources of either arachidonate or docosahexaenoate or both on accretion of these fatty acids in phospholipids and subsequent modulation of eicosanoid production in neonatal pig lung. One-day-old piglets received for 25 d one of four diets (n = 5): 1) standard diet containing a fat blend similar to that of conventional infant formula, 2) diet containing 0.9 g/100 g of total fatty acids as arachidonate, 3) diet containing 0.7 g/100 g as docosahexaenoate, or 4) a diet containing both 1.0 g/100 g as arachidonate and 0.8 g/100 g as docosahexaenoate. Arachidonate supplementation resulted in 30-60% significantly greater arachidonate in lung phosphatidylethanolamine and phosphatidylcholine. In phosphatidylinositol, however, arachidonate was resistant to dietary manipulation. Accretion of docosahexaenoate in all three phospholipid classes was 2.6- to 4.7-fold greater in docosahexaenoate-supplemented groups than in the standard group. Inclusion of arachidonate in the diet augmented both prostacyclin and thromboxane production by 25 to 35%. Docosahexaenoate supplementation resulted in the least eicosanoid production among the treatments, and significant suppression was observed for thromboxane when supplementation with both fatty acids was compared with supplementation with arachidonate alone. Thus, dietary arachidonic acid and docosahexaenoic acid at concentrations only slightly greater than those found in human milk tended to exercise opposing effects on lung eicosanoid production.