| Dietary n-6 polyunsaturated fatty acid deprivation increases docosahexaenoic acid metabolism in rat brain. | |
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MedLine Citation:
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PMID: 22117540 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Dietary n-6 polyunsaturated fatty acid (PUFA) deprivation in rodents reduces brain arachidonic acid (20:4n-6) concentration and 20:4n-6-preferring cytosolic phospholipase A(2) (cPLA(2) -IVA) and cyclooxygenase (COX)-2 expression, while increasing brain docosahexaenoic acid (DHA, 22:6n-3) concentration and DHA-selective calcium-independent phospholipase A(2) (iPLA(2) )-VIA expression. We hypothesized that these changes are accompanied by up-regulated brain DHA metabolic rates. Using a fatty acid model, brain DHA concentrations and kinetics were measured in unanesthetized male rats fed, for 15 weeks post-weaning, an n-6 PUFA 'adequate' (31.4 wt% linoleic acid) or 'deficient' (2.7 wt% linoleic acid) diet, each lacking 20:4n-6 and DHA. [1-(14) C]DHA was infused intravenously, arterial blood was sampled, and the brain was microwaved at 5 min and analyzed. Rats fed the n-6 PUFA deficient compared with adequate diet had significantly reduced n-6 PUFA concentrations in brain phospholipids but increased eicosapentaenoic acid (EPA, 20:5n-3), docosapentaenoic acid n-3 (DPAn-3, 22:5n-3), and DHA (by 9.4%) concentrations, particularly in ethanolamine glycerophospholipid (EtnGpl). Incorporation rates of unesterified DHA from plasma, which represent DHA metabolic loss from brain, were increased 45% in brain phospholipids, as was DHA turnover. Increased DHA metabolism following dietary n-6 PUFA deprivation may increase brain concentrations of antiinflammatory DHA metabolites, which with a reduced brain n-6 PUFA content, likely promotes neuroprotection and alters neurotransmission. |
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Authors:
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Miki Igarashi; Hyung-Wook Kim; Lisa Chang; Kaizong Ma; Stanley I Rapoport |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Intramural Date: 2012-01-23 |
Journal Detail:
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Title: Journal of neurochemistry Volume: 120 ISSN: 1471-4159 ISO Abbreviation: J. Neurochem. Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-03-07 Completed Date: 2012-06-01 Revised Date: 2013-04-15 |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: England |
Other Details:
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Languages: eng Pagination: 985-97 Citation Subset: IM |
Copyright Information:
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Published 2011. This article is a US Government work and is in the public domain in the USA. |
Affiliation:
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Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA. miki.i@uci.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acyl Coenzyme A
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metabolism Animals Animals, Newborn Body Weight Brain / metabolism* Carbon Isotopes / pharmacokinetics Chromatography, Gas Chromatography, High Pressure Liquid / methods Dietary Fats / administration & dosage*, metabolism Docosahexaenoic Acids / metabolism*, pharmacokinetics Fatty Acids, Omega-6 / deficiency* Gene Expression Regulation / drug effects, physiology* Lipids / blood Rats Rats, Inbred F344 |
| Grant Support | |
ID/Acronym/Agency:
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ZIA AG000399-05/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acyl Coenzyme A; 0/Carbon Isotopes; 0/Dietary Fats; 0/Fatty Acids, Omega-6; 0/Lipids; 25167-62-8/Docosahexaenoic Acids |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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