A fat‐deficient diet was initiated in mice before birth and at different ages during development and maturation. The induction of an essential fatty acid deficiency in brain was most effective when the deficient diet was initiated prenatally. With increasing time on the deficient diet, there was an increase in 20∶3(n−9) and a decrease in 20∶4(n−6) in the phosphoglycerides of subcellular brain fractions. The highest ratio of 20∶3(n−9) to 20∶4(n−6) observed was 1.5 for both diacyl and alkenylacyl glycerophosphorylethanolamines in the synaptosome‐rich fraction from mice on the deficient diet from before birth to 7 months of age. The acyl groups of brain ethanolamine plasmalogens are quite susceptible to alteration by the fat‐deficient diet. Elongated products of 20∶3(n−9), tentatively identified as 22∶3(n−9) and 22∶5(n−9), also were present in brain during essential fatty acid deficiency. These fatty acids were preferentially linked to the alkenylacyl glycerophosphorylethanolamines. It further was observed that, even when the deficient diet was initiated after maturation, similar changes in fatty acid composition occurred in both myelin and synaptosomerich fractions, but at a slower rate. For mice on the deficient diet from 12–18 months of age, the highest ratio of 20∶3(n−9) to 20∶4(n−6) was 0.6 for the alkenylacyl glycerophosphorylethanolamines from the myelin.
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Sun et al. (1974) studied this question.