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Tissue arachidonic acid (AA) pools originate from the diet, and from hepatic and extrahepatic desaturation-elongation of dietary linoleic acid (LA). This review summarizes the roles of absorption, transport, and formation of AA in the buildup of tissue AA pools. In humans who ingest 0.2-0.3 g of AA and 10-20 g of LA per day on a Western diet, the formation of AA from LA exceeds the dietary supply of AA. A number of factors favor the partitioning of AA to tissue phospholipids rather than adipose tissue and plasma triglycerides. The characteristics of AA transport with lipoproteins are discussed with focus on the role of lipoprotein lipase, lecithin:cholesterol acyltransferase, hepatic lipase, and the scavenger receptor BI and LDL receptors in tissue uptake of AA. Liver-derived 2-acyl-lysophosphatidylcholine and plasma free AA are two important sources of AA for extrahepatic tissues which exhibit a low rate of uptake of lipoprotein AA. Desaturation-elongation of LA to produce AA occurs both in liver and in extrahepatic tissues, plasma free LA being an important substrate particularly during fasting. The AA preference of the reacylation and transacylation reactions is crucial for the selective retention of AA in phospholipids.
Zhou et al. (Mon,) studied this question.
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