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Research Article| Volume 85, ISSUE 6, P361-368, December 2011

Regulation of rat brain polyunsaturated fatty acid (PUFA) metabolism during graded dietary n-3 PUFA deprivation

  • Hyung-Wook Kim
    Correspondence
    Corresponding author. Current address: University of Washington, Seattle, Department of Environmental and Occupational Health Science, 1705 Pacific St., Seattle, WA 98195, BOX 357234, USA. Tel.: +1 206 616 3634; fax: +1 206 685 3990.
    Affiliations
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Room 1S126, Bethesda, MD 20892, USA
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  • Jagadeesh S. Rao
    Affiliations
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Room 1S126, Bethesda, MD 20892, USA
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  • Stanley I. Rapoport
    Affiliations
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Room 1S126, Bethesda, MD 20892, USA
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  • Author Footnotes
    1 Current address: University of California, Irvine, Neurobiology and Behavior, 2205 McGaugh Hall, Irvine, CA 92697-4550, USA.
    Miki Igarashi
    Footnotes
    1 Current address: University of California, Irvine, Neurobiology and Behavior, 2205 McGaugh Hall, Irvine, CA 92697-4550, USA.
    Affiliations
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Room 1S126, Bethesda, MD 20892, USA
    Search for articles by this author
  • Author Footnotes
    1 Current address: University of California, Irvine, Neurobiology and Behavior, 2205 McGaugh Hall, Irvine, CA 92697-4550, USA.
Published:August 31, 2011DOI:https://doi.org/10.1016/j.plefa.2011.08.002

      Abstract

      Knowing threshold changes in brain lipids and lipid enzymes during dietary n-3 polyunsaturated fatty acid deprivation may elucidate dietary regulation of brain lipid metabolism. To determine thresholds, rats were fed for 15 weeks DHA-free diets having graded reductions of α-linolenic acid (α-LNA). Compared with control diet (4.6% α-LNA), plasma DHA fell significantly at 1.7% dietary α-LNA while brain DHA remained unchanged down to 0.8% α-LNA, when plasma and brain docosapentaenoic acid (DPAn-6) were increased and DHA-selective iPLA2 and COX-1 activities were downregulated. Brain AA was unchanged by deprivation, but AA selective-cPLA2, sPLA2 and COX-2 activities were increased at or below 0.8% dietary α-LNA, possibly in response to elevated brain DPAn-6. In summary, homeostatic mechanisms appear to maintain a control brain DHA concentration down to 0.8% dietary DHA despite reduced plasma DHA, when DPAn-6 replaces DHA. At extreme deprivation, decreased brain iPLA2 and COX-1 activities may reduce brain DHA loss.

      Abbreviations:

      AA (arachidonic acid), BDNF (brain derived neurotrophic factor), COX (cyclooxygenase), DHA (docosahexaenoic acid), DPAn-6 (docosapentaenoic acid), LA (linoleic acid), α–LNA (α-linolenic acid), LOX (lipoxygenase), cPLA2 (cytosolic phospholipase A2), sPLA2 (secretory PLA2), iPLA2 (Ca2+-independent PLA2), PUFA (polyunsaturated fatty acid), sn (stereospecifically numbered)

      Keywords

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