J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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Originally published In Press as doi:10.1194/jlr.M700315-JLR200 on August 22, 2007

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Journal of Lipid Research, Vol. 48, 2463-2470, November 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Dietary n-3 PUFA deprivation for 15 weeks upregulates elongase and desaturase expression in rat liver but not brain

Miki Igarashi1, Kaizong Ma, Lisa Chang, Jane M. Bell and Stanley I. Rapoport

Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892

Published, JLR Papers in Press, August 22, 2007.

1 To whom correspondence should be addressed. e-mail: mikii{at}mail.nih.gov

Fifteen weeks of dietary n-3 PUFA deprivation increases coefficients of conversion of circulating {alpha}-linolenic acid ({alpha}-LNA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) in rat liver but not brain. To determine whether these increases reflect organ differences in enzymatic activities, we examined brain and liver expression of converting enzymes and of two of their transcription factors, peroxisome proliferator-activated receptor {alpha} (PPAR{alpha}) and sterol-regulatory element binding protein-1 (SREBP-1), in rats fed an n-3 PUFA "adequate" (4.6% {alpha}-LNA of total fatty acid, no DHA) or "deficient" (0.2% {alpha}-LNA, no DHA) diet for 15 weeks after weaning. In rats fed the deficient compared with the adequate diet, mRNA and activity levels of {Delta}5 and {Delta}6 desaturases and elongases 2 and 5 were upregulated in liver but not brain, but liver PPAR{alpha} and SREBP-1 mRNA levels were unchanged. In rats fed the adequate diet, enzyme activities generally were higher in liver than brain. Thus, differences in conversion enzyme expression explain why the liver has a greater capacity to synthesize DHA from circulating {alpha}-LNA than does the brain in animals on an adequate n-3 PUFA diet and why liver synthesis capacity is increased by dietary deprivation. These data suggest that liver n-3 PUFA metabolism determines DHA availability to the brain when DHA is absent from the diet.

Supplementary key words ß-oxidation • diet • docosahexaenoic acid • {alpha}-linolenic acid • polyunsaturated fatty acid

Abbreviations: AA, arachidonic acid (20:4n-6); CPT-1, carnitine palmitoyltransferase-1; DHA, docosahexaenoic acid (22:6n-3); DPA, docosapentaenoic acid (22:5n-6); DTA, docosatetraenoic acid (22:4n-6); EPA, eicosapentaenoic acid (20:5n-3); FAME, fatty acid methyl ester; KPB, potassium phosphate buffer; LA, linoleic acid (18:2n-6); {alpha}-LNA, {alpha}-linolenic acid (18:3n-3); PPAR, peroxisome proliferator-activated receptor; PUFA, polyunsaturated fatty acid; SREBP, sterol-regulatory element binding protein


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