Dietary regulation of dipalmitoyl phosphatidylcholine in the lung. Effects of essential fatty acid deficiency

Abstract

An essential fatty acid deficiency resulted in a significant decrease of saturated phosphatidylcholine in rat lung tissue, with the reduction being mainly due to that of dipalmitoyl species. This decrease was almost completely reversed by administration of a diet containing linoleate from seven days. The features of saturated phosphatidylcholine synthesis in the deficient rat lung slices were studied with labeled precursors in the presence of different concentrations of linoleate and oleate in the medium. Labeling patterns of saturated phosphatidylcholine using [2-3H]glycerol and [Me-14C]choline were unaffected in all ratios of linoleate to oleate examined. The incorporation rates of both [3H]acetate and [1-14C]palmitate into saturated phosphatidylcholine decreased in the deficient state, but that of the palmitate label increased markedly with increase in the concentration of linoleate in the medium. This stimulatory effect due to the increased linoleate concentration, however, was not found with the acetate label. While the utilization of 1-[1-14C]palmitoyl glycerophosphocholine by lung tissue was enhanced in the deficient state, in the presence of linoleate it showed almost the same level as that of the controls. The essential fatty acid deficiency resulted in an increase in the activity of liver choline kinase by 46%. However, other enzyme activities involved in phosphatidylcholine synthesis in the lung and liver were unaffected by the deficient state.