The aim of the present study was to investigate whether unsaturated 2‐acyl‐lysophosphatidylcholine bound to plasma albumin is a relevant delivery form of unsaturated fatty acids to the developing brain. Twenty‐day‐old rats were perfused for 30 s with labeled palmitic, oleic, linoleic, and arachidonic acids in either their unesterified form or esterified in 2‐acyl‐lysophosphatidylcholine labeled on the choline and fatty acid moieties. Both forms were bound to albumin. Incorporation in brain lipid classes was followed within 1 h. The brain uptake of the unesterified fatty acids reached a plateau at 5–155 mim and was maximal for arachidonic acid (0.45% of the perfused dose). The brain uptake of palmitoyl‐lysophosphatidylcholine was similar to that of palmitic acid, whereas that of other lysophosphatidylcholines increased with the degree of unsaturation (rate and maximal uptake) and was six‐ to 10‐fold higher than that of the corresponding unesterified fatty acid. 2‐Acyl‐lysophosphatidylcholines were taken up without prior hydrolysis and reacylated into doubly labeled phosphatidylcholine, which was the most labeled lipid class, whereas lipid distribution of the unesterified fatty acid was more diversi fied. Partial hydrolysis of 2‐acyl‐lysophosphatidylcholine occurred in the brain tissue, and redistribution of the fatty acyl moiety into other phospholipid classes was also observed and was the highest for arachidonic acid. In this case, the percentage of esterification of this fatty acid in phosphatidylinositol (expressed as a percentage of the total lipid fraction) was relatively lower than that observed when the unesterified form was used. 1‐Acyl‐lysophosphatidylcholine (palmitoyl) was taken at the same extent that 2‐acyllysophosphatidylcholine but was more hydrolyzed and reesterified in other lipid classes than 2‐acyl isomer. All these results suggest that 2‐acyl‐lysophosphatidylcholine bound to albumin could be an efficient delivery form of unsaturated fatty acids to the developing rat brain and that the fatty acid delivery form could modulate their fate in the tissue.

Utilization of very long chain saturated fatty acids by brain was studied by injecting 20-day-old and adult rats with high-density lipoprotein containing [stearic or lignoceric acid-14C, (methyl-3H)choline]sphingomyelin. Labeling was followed for 24 h. Very small amounts of 14C were recovered in the brain of all rats, and there was no preferential uptake of lignoceric acid. Approximately 20% of the entrapped 14C was located in the form of unchanged sphingomyelin 24 h after injection. This result shows that the rat brain utilizes very little very long chain fatty acids (greater than or equal to 20 C atoms) from high-density lipoprotein sphingomyelin, even during the myelinating period. The [3H]choline moiety from sphingomyelin was recovered in brain phosphatidylcholine in a higher proportion in comparison with the 14C uptake. The brain 3H increased throughout the studied period in all experiments, but was much higher in the myelinating brain than in the mature brain. From the radioactivity distribution in liver and plasma lipids, it is clear that the choline 3H in the brain originates from either double-labeled phosphatidylcholine of lipoproteins or tritiated lysophosphatidylcholine bound to albumin, both synthesized by the liver.

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The metabolic fate of high density lipoprotein (HDL) sphingomyelin in plasma was studied in rats over a 24-hr period after injection of HDL containing sphingomyelin which was 14C-labeled in the stearic (18:0) or lignoceric acid (24:0) moiety and 3H-labeled in the choline methyl groups. Decay of label in plasma followed three phases. The first two phases were similar for both isotopes and both types of sphingomyelin (t1/2 approximately 10 and 110 min). However, during the third phase (from 10 hr after injection), 3H label disappeared more slowly than 14C label from 18:0 sphingomyelin, whereas the 3H/14C ratio remained relatively constant when 24:0 sphingomyelin was used. Intact, doubly-labeled 18:0 sphingomyelin disappeared from HDL rapidly (t1/2 = 38 min) by tissue uptake and by transfer to very low density lipoprotein (VLDL). VLDL contained up to 12% of the sphingomyelin 1 hr after injection. This is the first demonstration of a transfer in vivo of sphingomyelin from HDL to VLDL. A similarly rapid transfer was also observed in vitro. Some nontritiated, [14C]18:0 or [14C]24:0 sphingomyelin was redistributed more slowly into HDL. Doubly-labeled phosphatidylcholine appeared in VLDL and HDL within 1 hr after injection and reached 1.8 and 2.1% of the injected 14C and 3H in VLDL at 1 hr, and 4.8 and 6.9% in HDL at 3 hr, respectively.