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Biochim Biophys Acta. 2006 Sep;1761(9):1050-9. Epub 2006 Jul 8.

Brain elongation of linoleic acid is a negligible source of the arachidonate in brain phospholipids of adult rats.

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  • 1Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S 126, Bethesda, MD 20892-1582, USA.


The extent to which the adult brain can derive some of its arachidonic acid (AA) through internalized synthesis from linoleic acid (LA) is uncertain. Thus, we determined for plasma-derived LA in vivo rates for brain incorporation, beta-oxidation, and conversion to AA. Adult male unanesthetized rats, reared on a diet enriched in LA but low in AA, were infused intravenously for 5 min with [1-(14)C]LA. Timed arterial samples were collected until the animals were killed at 5 min and the brain was removed after microwaving. Within plasma lipids, >96% of radioactivity was in the form of unchanged [1-(14)C]LA, but [(14)C]AA was insignificant (<0.2%). Eighty-six percent of brain radioactivity at 5 min was present as beta-oxidation products, whereas the remainder was mainly in 'stable' phospholipid or triglyceride as LA or AA (11 and <1%, respectively). Unesterified unlabeled LA rapidly enters brain from plasma, but its incorporation into brain total phospholipid and triglyceride, in the form of synthesized AA, is <1% of the amount that enters the brain. Thus, in rats fed even a diet containing low amounts of AA, the LA that enters brain is largely beta-oxidized, and is not a major source of AA in brain.

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