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Docosahexaenoate is usually considered to be the principal endpoint of a-linolenate metabolism in mammals. Nevertheless, several studies over the past 30 y have shown that more carbon from a-linolenate is recycled into newly synthesized lipids than is used to make docosahexaenoate. Our objective in this study was to assess carbon recycling from a-linolenate in suckling rats made deficient in n-3 polyunsaturated fatty acids (PUFA). Female Long-Evans rats were given a diet deficient in n-3 PUFA at weaning and then bred 8 wk later. Pups from the second generation were nursed by their respective dams and gavaged with 1 mg [U-13C]-a-linolenate at 10 d old. Brain and liver were obtained 24 h later, and the fatty acid profiles and 13C enrichment analyzed. Docosahexaenoate was markedly depleted in brain (-82%) and liver (-97%) of the n-3 PUFA–deficient rats. In the controls, 13C enrichment in products of carbon recycling (cholesterol and fatty acids other than n-3 PUFA) exceeded that in docosahexaenoate by 2.4-fold (liver) and 7.5-fold (brain). n-3 PUFA deficiency reduced the ratio of 13C enrichment in products of carbon recycling compared with 13C incorporated into docosahexaenoate by 63% in the brain but not in the liver. Despite severe n-3 PUFA deficiency, carbon recycling still consumed 50% more 13C from a-linolenate than went into docosahexaenoate in the liver and 2.8-fold more in the brain. We conclude that carbon recycling is an integral part of neonatal metabolism of a-linolenate and is not simply an overflow pathway arising from excess availability of preformed docosahexaenoate.

Docosahexaenoic acid (DHA), a 22-carbon, highly unsaturated, n-3 fatty acid, is important for optimal nervous system function. In this study, designed to quantify how preformed dietary DHA regulates metabolic pathways in vivo, 8-d-old rat pups were divided into four groups and fed artificial rat milk diets. One group was fed formula with deuterium-labeled LNA (d5-LNA) as the only source of n-3 fatty acids, and a second group was fed formula that contained d5-LNA and unlabeled DHA. Two additional groups were dam-reared to permit analysis of fatty acyl pool sizes at postnatal days 8 and 28. The dams were fed a diet that contained 3% unlabeled LNA. DHA in brain and liver was analyzed. Our study demonstrated that preformed DHA in the diet markedly decreased the amount of biosynthesized DHA that accumulated in the brain and the liver. Surprisingly, ~40% of the DHA that was newly acquired during this period in the “LNA” group was unlabeled. Because there were no unlabeled n-3 fatty acids in this diet, this DHA must have been derived from body stores of n-3 fatty acids. Thus, body stores can be a significant source of brain DHA in animals that are fed LNA as the only source of n-3 fatty acids.