Journal of Lipid Research, Vol. 10, 158-165, March 1969
Copyright © 1969 by Lipid Research, Inc.

Lysophosphatidylcholine concentrations and metabolism in aortic intima plus inner media: effect of nutritionally induced atherosclerosis

Oscar W. Portman and Manfred Alexander

Oregon Regional Primate Research Center, Beaverton, Oregon 97005, and University of Oregon Medical School, Portland, Oregon 97201

The concentration of lysophosphatidylcholine (monoacyl sn-glycerol 3-phosphorylcholine) in intima plus inner media of atherosclerotic aorta from squirrel monkeys was nearly eight times that in comparable control tissue. Plasma levels of the same compound were somewhat elevated in the atherosclerotic group.

The metabolism of fatty acyl CoA's and lysophosphatides was studied in cell-free preparations of intima plus inner media from squirrel monkey aorta. Linoleic acid was incorporated predominantly into phosphatidylcholine (as opposed to other phospholipids) when linoleoyl-1-¹⁴C CoA was the substrate. The extent of this reaction was dependent on the concentration of lysophosphatidylcholine. Lysophosphatidylethanolamine (monoacyl sn-glycerol 3-phosphorylethanolamine) stimulated the incorporation of linoleate into phosphatidylethanolamine. 1-Palmitoyl-1'-¹⁴C sn-glycerol 3-phosphorylcholine (¹⁴C-lysophosphatidylcholine) was incorporated into phosphatidylcholine only in the presence of acyl CoA's or ATP plus CoA. Incorporation of ¹⁴C with ¹⁴C-lysophosphatidylcholine plus linoleoyl CoA equaled that with linoleoyl-1-¹⁴C CoA and lysophosphatidylcholine.

Various other lines of evidence are presented to support the importance of the fatty acyl CoA:lysophosphatide fatty acyl transferase mechanism in aortic phospholipid metabolism. Cell-free preparations of aortic intima plus inner media from squirrel monkeys with early, nutritionally-induced atherosclerosis utilized linoleoyl-1-¹⁴C CoA more than preparations from control monkeys when incubations were carried out without added lysophosphatidylcholine and for long periods (30 min). With optimum levels of labeled linoleoyl CoA and unlabeled lysophosphatidylcholine, or unlabeled linoleoyl CoA and labeled lysophosphatidylcholine, there were no differences in substrate utilization between control and atherosclerotic tissues.

We conclude that the concentrations of lysophosphatidylcholine, which are higher in atherosclerotic than in control aortic tissues, could be a factor controlling rates of fatty acid incorporation into phosphatidylcholine.

Supplementary key words squirrel monkeys • linoleoyl CoA • palmitoyl CoA • fatty acyl CoA: lysophosphatide fatty acyl transferase

Submitted on August 7, 1968
Accepted on October 7, 1968

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