Abstract
We quantified incorporation rates of plasma-derived alpha-linolenic acid (alpha-LNA, 18:3n-3) into "stable" liver lipids and the conversion rate of alpha-LNA to docosahexaenoic acid (DHA, 22:6n-3) in male rats fed, after weaning, an n-3 PUFA-adequate diet (4.6% alpha-LNA, no DHA) or an n-3 PUFA-deficient diet (0.2% alpha-LNA, no DHA) for 15 weeks. Unanesthetized rats were infused intravenously with [1-14C]alpha-LNA, and arterial plasma was sampled until the liver was microwaved at 5 min. Unlabeled alpha-LNA and DHA concentrations in arterial plasma and liver were reduced >90% by deprivation, whereas unlabeled arachidonic acid (20:4n-6) and docosapentaenoic acid (22:5n-6) concentrations were increased. Deprivation did not change alpha-LNA incorporation coefficients into stable liver lipids but increased synthesis-incorporation coefficients of DHA from alpha-LNA by 6.6-, 8.4-, and 2.3-fold in triacylglycerol, phospholipid, and cholesteryl ester, respectively. Assuming that synthesized-incorporated DHA eventually would be secreted within lipoproteins, calculated liver DHA secretion rates equaled 2.19 and 0.82 micromol/day in the n-3 PUFA-adequate and -deprived rats, respectively. These rates exceed the published rates of brain DHA consumption by 6- and 10-fold, respectively, and should be sufficient to maintain normal and reduced brain DHA concentrations, respectively, in the two dietary conditions.
Highlights
We quantified incorporation rates of plasmaderived a-linolenic acid (a-LNA, 18:3n-3) into “stable” liver lipids and the conversion rate of a-LNA to docosahexaenoic acid (DHA, 22:6n-3) in male rats fed, after weaning, an n-3 PUFA-adequate diet (4.6% a-LNA, no DHA) or an n-3 PUFAdeficient diet (0.2% a-LNA, no DHA) for 15 weeks
Based on evidence that high amounts of dietary DHA or a-LNA suppress the expression in rat liver of D5 and D6 desaturases and elongases that catalyze DHA synthesis from a-LNA [1,2,3,4, 11] and that DHA synthesis from a-LNA is reduced in rat astrocytes incubated with DHA [12], we hypothesized that conversion would be upregulated in rats fed a diet with low compared with adequate n-3 PUFA content
Rats fed the deficient compared with the adequate diet had significant reductions in n-3 PUFA concentrations in the plasma and liver unesterified and esterified fatty acid pools (Tables 1, 2) and increased liver concentrations of cholesterol and cholesteryl ester but decreased concentrations of phosphatidylinositol and sphingomyelin
Summary
We quantified incorporation rates of plasmaderived a-linolenic acid (a-LNA, 18:3n-3) into “stable” liver lipids and the conversion rate of a-LNA to docosahexaenoic acid (DHA, 22:6n-3) in male rats fed, after weaning, an n-3 PUFA-adequate diet (4.6% a-LNA, no DHA) or an n-3 PUFAdeficient diet (0.2% a-LNA, no DHA) for 15 weeks. Assuming that synthesized-incorporated DHA even tually would be secreted within lipoproteins, calculated liver DHA secretion rates equaled 2.19 and 0.82 mmol/day in the n-3 PUFA-adequate and -deprived rats, respectively. These rates exceed the published rates of brain DHA consumption by 6- and 10-fold, respectively, and should be sufficient to maintain normal and reduced brain DHA concentrations, respectively, in the two dietary conditions.— Igarashi, M., J. On a per gram basis, in rats fed a high-DHA diet (2.3% of total fatty acids), conversion rates of plasma a-LNA to DHA were 0.24 and 6.6 nmol/s/g tissue 3 1024 in brain and liver, respectively [7, 9, 10]. The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of three tables
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