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A more recent version of this article appeared on November 1, 2007

Papers In Press, published online ahead of print August 22, 2007
J. Lipid Res., doi:10.1194/jlr.M700315-JLR200
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Submitted on July 11, 2007
Revised on August 17, 2007
Accepted on August 20, 2007

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

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

BPMS/NIA/NIH, Bethesda, MD 20892

Corresponding Author: mikii{at}mail.nih.gov

Fifteen weeks of dietary n-3 polyunsaturated fatty acid (PUFA) deprivation increases coefficients of conversion of circulating a-linolenic acid (a-LNA, 18:3n-3) to docosahexaenoic acid (DHA, 22:6n-3) in rat liver but not brain. To see if these increases reflect organ differences in enzymatic activities, we examined brain and liver expression of converting enzymes and of two of their transcription factors, PPARa and SREBP-1, in rats fed an n-3 PUFA “adequate” (4.6% a-LNA of total fatty acid, no DHA) or “deficient” diet (0.2% a-LNA, no DHA) for 15 weeks post-weaning. In rats fed the “deficient” compared with “adequate” diet, mRNA and activity levels of 5 and 6 desaturases and elongases 2 and 5 were upregulated in liver but not brain, but liver PPARa 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 a-LNA than does the brain in animals on an “adequate” n-3 PUFA diet, and why liver synthesis capacity is increased by dietary deprivation. The data support liver n-3 PUFA metabolism determining DHA availability to the brain when DHA is absent from the diet.


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