Surfactant predominantly comprises phosphatidylcholine (PC) species, together with phosphatidylglycerols, phosphatidylinositols, neutral lipids and surfactant proteins SP-A to -D. Together, dipalmitoyl-PC (PC16:0/16:0), palmitoyl-myristoyl-PC (PC16:0/14:0) and palmitoyl-palmitoleoyl-PC (PC16:0/16:1) make up 75-80% of mammalian surfactant PC, the proportions of which vary during development and in chronic lung diseases. PC16:0/14:0, which exerts specific effects on macrophage differentiation in vitro, increases in surfactant during alveolarisation (at the expense of PC16:0/16:0), a prenatal event in humans but postnatal in rats. The mechanisms responsible and the significance of this reversible increase are however not understood. We hypothesized that in rats, myristic acid (C14:0) enriched milk is key to lung specific PC16:0/14:0 increases in surfactant. We found that surfactant PC16:0/14:0 in suckling rats correlates with C14:0 concentration in plasma chylomicrons and lung tissue triglycerides and that PC16:0/14:0 fractions reflect exogenous C14:0 supply. Significantly, C14:0 was neither increased in plasma PC nor in liver triglycerides, free fatty acids or PC. Lauric acid was also abundant in triglycerides, but was not incorporated into surfactant PC. Comparing a C14:0-rich milk diet with a C14:0 poor carbohydrate diet revealed increased C14:0 and decreased C16:0 in plasma and lung triglycerides respectively. PC16:0/14:0-enrichment at the expense of PC16:0/16:0 did not impair surfactant surface tension function. However, the PC profile of the alveolar macrophages from the milk fed animals changed from PC16:0/16:0-rich to PC16:0/14:0-rich. This was accompanied by reduced reactive oxygen species (ROS) production. We propose that nutritional supply with C14:0 and its lung specific enrichment may contribute to decreased ROS production during alveolarization.
- lung development
- myristic acid
- Copyright © 2010, Journal of Applied Physiology