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Rats were fed various levels of either ethyl linoleate, ethyl arachidonate, or ethyl linolenate. Weight gain, fat-deficiency status, and fatty acid composition of the liver lipids were determined. Dietary linoleate, fed in excess of 1% of calories, maintained good growth and cured fat deficiency. Increasing amounts of dietary linoleate were stored in the liver lipids and converted into fatty acids of the linoleate family—20:4 and 22:4. The concentration of 20:3 was decreased. Dietary arachidonate cured fat deficiency three times more effectively than linoleate. Increasing amounts of dietary arachidonate were stored in liver lipids and converted to 22:5ω6. The level of 20:3 was lowered three times more effectively than when linoleate was fed. No fatty acids of the linolenate family were synthesized from linoleate or arachidonate. Dietary linolenate did not support weight gain as efficiently as did linoleate or arachidonate. Fat-deficiency symptoms could not be cured completely. Increasing amounts of dietary linolenate increased the levels of fatty acids of the linolenate family; linolenic acid was stored, and 20:5, 22:5ω3, and 22:6 were synthesized from linolenate. The level of 20:3 was lowered in the same fashion as when linoleate or arachidonate was fed. Thr level of 20:4 was decreased with increasing amounts of dietary linolenate.

The fatty acid Composition of lipids from erythrocytes and depot fat of rats whose diet was supplemented with various levels of linoleate, arachidonate, or linolenate has been investigated. Dietary linoleate and linolenate are incorporated into the depot fat. The ratio of eicosatrienoic acid to eicosatetraenoic acid, derived from the analysis of depot fat, decreases with increasing amounts of all three dietary essential fatty acids (EFA) in the same manner as observed in organ lipids. The composition of the unsaturated fatty acids of erythrocyte lipids is altered readily by increasing amounts of dietary EFA. The concentration of 20: 3 is lowered extensively by all three EFA. The synthesis of arachidonate is inhibited by dietary linolenate and 20:5 and 22:5ω3 (double bond between third and fourth carbow from ω end) can be detected only in animals given linolenate.

Linoleate, linolenate, arachidonate, docosahexenoate and six other fatty acids were major components of 24 ester preparations fed as 5% of the diet for 60 days to groups of male white rats. The experiment was designed so as to provide that all major fatty acid components were independent of each other in the sense that the intake of each was poorly correlated with the intake of any of the others. Fatty acid compositions of liver lipids were determined and were related to the composition of the diet lipids. Linolenate and docosahexaenoate contents of diet and tissue revealed the same relationships reported previously from experiments in which individual pure acid esters were added to a fat-free diet. Linoleate, when fed in lipid mixtures, was more effective in raising the linoleate concentration in liver lipids than when fed alone, but this increase did not change the shape of the dose-response curve or the estimated nutritional requirement. Large amounts of fish oil in the diet tended to depress the arachidonate concentration in tissue lipids.

Malonyl coenzyme A is synthesized by transacylating S-malonyl-N-decanoyl cysteamine with coenzyme A. A simplified procedure for the preparation of S-malonyl-N-decanoyl cysteamine, using cysteamine as starting material, is described.

Fifteen groups of rats were maintained on diets free of fat or supplemented with different levels of linoleate, arachidonate or linolenate. After 100 days on the diets the rats were sacrificed and liver slices were incubated with acetate-1-14C. The individual fatty acids were separated by gas chromatography and their radioactivity was determined by liquid scintillation counting. The C20 esters were separated by GLC, collected, and the structures of the components were determined by ozonolysis. The acetate incorporation into the various polyunsaturated fatty acids was influenced by the previous dietary conditioning. The distributions of radioactivity indicated that metabolic reactions taking place in the rat liver are modified by dietary supply of essential fatty acids.

Weanling rats were fed a fat-free diet supplemented with various ratios of corn and linseed oils to furnish a constant dietary level of linolenate at 1% of calories and levels of linoleate from 0.3 to 17.3% of calories. The fatty acid composition of the total liver lipids was analyzed by gas chromatography. Increasing amounts of dietary linoleate suppressed the levels of the 20:5, 22:5 and 22:6 metabo lites of linolenic acid in the liver lipids. The level of dietary vitamin E had no effect upon this phenomenon. When the level of dietary linoleate was increased, the level of 22:4 in the liver lipids, as well as the other metabolites of linoleate, was shown to increase.

Linoleic acid-1-14C was incubated with subcellular fractions of rat liver to study the mechanism of polyunsaturated fatty acid synthesis. The most effective system for the chain elongation of linoleic acid to eicosadienoic acid was liver microsomes plus malonyl coenzyme A with cofactors, NADPH, and ATP. Under anaerobic conditions, the chain elongation reaction could be separated quantitatively from the dehydrogenation reaction which otherwise required the same system. The chain elongation of linoleic acid was inhibited by saturated fatty acids of which myristic and pentadecanoic acids were most effective. Mono-unsaturated and polyunsaturated fatty acids also act as inhibitors. From consideration of reaction kinetics and inhibition by other fatty acids, the conversion of linoleic acid to γ-linolenic acid seems preferred over the conversion of linoleic acid to homolinoleic acid.