Suckling rats actively recycle carbon from a-linolenate into newly synthesized lipids even during extreme dietary deficiency of n-3 polyunsaturates

Docosahexaenoate is usually considered to be the principal endpoint of alpha-linolenate metabolism in mammals. Nevertheless, several studies over the past 30 y have shown that more carbon from cc-linolenate is recycled into newly synthesized lipids than is used to make docosahexacnoate. 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-C-13]-alpha- linolenate at 10 d old. Brain and liver were obtained 24 h later, and the fatty acid profiles and C-13 enrichment analyzed. Docosahexaenoate was markedly depleted in brain (-82%) and liver (-97%) of the n-3 PUFA-deficient rats. In the controls, C-13 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 C-13 enrichment in products of carbon recycling compared with C-13 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 C-13 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 front excess availability of preformed docosahexaenoate.