1-Palmitoyl-2-linoleoyl
phosphatidylcholine (
PLPC) labeled in either the
choline,
glycerol,
palmitate, or
linoleate component in reconstituted rat
high density lipoprotein (rHDL), was administered by vein to rats with bile
fistula and
taurocholate infusion.
PLPC disappeared from plasma in a monoexponential fashion with a half-life of 50 min. A small fraction, about 14%, of
PLPC disappearance was due to removal of
linoleate from the sn-2
ester bond to form plasma
cholesterol esters, presumably by
lecithin-cholesterol acyltransferase. Otherwise, nearly all of the
PLPC components that disappeared from blood in 1 h were recovered in the liver. The
choline,
glycerol, and
linoleate components appeared predominantly in hepatic
phosphatidylcholine (PC). These three components remained together in the liver with similar fractions of each in individual PC molecular species, most notably 1-stearoyl-2-linoleoyl-PC and dilinoleoyl-PC as well as
PLPC. However, the
palmitate component was spread among hepatic
triglyceride,
free fatty acid, other
phospholipids, and all
palmitate-containing molecular species of PC. Less than 2% of any administered
PLPC component appeared in 1-stearoyl-2-arachidonyl-PC, the major species by mass in the liver. The
palmitate component from plasma
PLPC appeared in biliary PC at a more rapid rate than
glycerol and
linoleate components; the latter components appeared in bile in identical fashion. The results show that about two-thirds of plasma
PLPC disappearance is due to
phospholipase A1 hydrolysis, probably hepatic
lipase. The putative produce, 2-linoleoyl-lysoPC, is efficiently reacylated with a
saturated fatty acid in the liver, conserving PC.