J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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Journal of Lipid Research, Vol. 41, 1808-1811, November 2000
Copyright © 2000 by Lipid Research, Inc.

Original Article

Specific linoleate deficiency in the rat does not prevent substantial carbon recycling from [14C]linoleate into sterols

S. C. Cunnanea, D. Trottia, and M. A. Ryana
a Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Canada M5S 3E2

Correspondence to: S. C. Cunnane

Compared with classic essential fatty acid deficiency or the feeding of a fat-free diet, little is known about specific linoleate deficiency in the rat. Carbon recycling into de novo lipogenesis has been reported to be an obligatory feature of linoleate metabolism in the liver, even in extreme linoleate deficiency (LA-D). The present study had two objectives: 1) to report a brief summary of the tissue n-6 polyunsaturated fatty acid (PUFA) profiles in specific LA-D, and 2) to quantify whole body carbon recycling from [14C]linoleate in specific LA-D. Rats consumed a linoleate-deficient diet for 12 weeks and then received a bolus of [1-14C]linoleate by gavage. In linoleate-deficient rats, the triene/tetraene ratio in several organs increased by 18- to 100-fold. The amount of 14C appearing in organ sterols (dpm/g) of linoleate-deficient rats was 2- to 10-fold higher than in the controls and equaled 16.3% of the [14C]linoleate dose given, compared with 7.4% in the controls.

We conclude that a similar amount (about 10%) of the carbon skeleton of linoleate is normally recycled into lipids synthesized de novo, as remains in the whole body pool of n-6 polyunsaturates. — Cunnane, S. C., D. Trotti, and M. A. Ryan. Specific linoleate deficiency in the rat does not prevent substantial carbon recycling from [14C]linoleate into sterols. J. Lipid Res. 2000. 41: 1808;–1811.

Supplementary key words: arachidonate, carbon-14, essential fatty acid


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