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

Autor: Oscar W. Portman, Manfred Alexander
Jazyk: angličtina
Rok vydání: 1969
Předmět:
Zdroj: Journal of Lipid Research, Vol 10, Iss 2, Pp 158-165 (1969)
Druh dokumentu: article
ISSN: 0022-2275
DOI: 10.1016/S0022-2275(20)42662-8
Popis: 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.
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