MECHANISMS OF HEPATIC PHOSPHATIDYLCHOLINE SYNTHESIS IN THE DEVELOPING GUINEA-PIG - CONTRIBUTIONS OF ACYL REMODELING AND OF N-METHYLATION OF PHOSPHATIDYLETHANOLAMINE

Hepatic phosphatidylcholine (PC) from the immature fetal guinea pig at day 55 of gestation comprised mainly unsaturated molecular species containing C18:2(n-6) and C22:6(n-3) at the sn-2 position, reflecting placental permeability to essential fatty acids. At both day 55 and term (day 68), [Me-C-14]choline was incorporated in utero over 3 h largely into sn-1-C-16:0 PC species, with incorporation into sn-1-C18:0 PC species increasing by 18 h of incubation. Comparison of specific radioactivities after 3 h and 18 h suggests PC acyl remodelling by phospholipase A1. No incorporation into C20:4(n-6)-containing PC species could be detected of either [Me-C-14]choline in vivo or CDP-[Me-C-14]choline in isolated microsomes. The major phosphatidyl-ethanolamine (PE) species were 16:0/22:6 and 18:0/22:6. Although [C-14]ethanolamine was initially incorporated mainly into sn-1-C-16:0 species, specific-radioactivity analysis suggested differential turnover rather than acyl remodelling. [1,2-C-14]Ethanolamine and [Me-C-14]methionine incorporation into PC molecular species indicated that both newly synthesized and total PE pools were available for N-methylation. Since the PC pool synthesized from PE included C20:4- and C22:6-containing species, N-methylation may provide a mechanism for supplying essential long-chain fatty acids to developing tissues that can be regulated independently from bulk PC synthesis.