818 XIII. ESSENTIAL FATTY ACIDS 



that the fat deficiency reduces the secretion of luteinizing hormone from the 

 acidophil cells, and that the consequent reduction in ovarian stimulation 

 results in a diminished estrogen secretion, with consequent disturbance of 

 the estrus cycle. The increased percentage of basophils can be attributed 

 to the reduction in estrogen secretion. 



The activity of the cytochrome oxidase system in the liver is markedly 

 increased in rats deficient in essential fatty acids, according to Kunkel and 

 Williams.'** These workers noted a slight decrease in choline oxidase 

 acti\'ity, but no alteration was observed in that of succinic oxidase, during 

 the fat-deficiency syndrome. Succinic dehydrogenase and butyric dehy- 

 ch'ogenase in the liver were found by Tulpule and Patwardhan'*^ to be signifi- 

 cantly reduced in EFA deficiency. Glutamic dehj'drogenase, also, was 

 present in a lower concentration when fats were excluded from the diet.^^^ 



The lipolytic enzymes of the liver were considered by Saka and Sipahio- 

 glu^^" to be related to the content of unsaturated fatty acids in the diet. 

 It was observed that arachidonic acid was more effective in furthering the 

 reestablishment of liver lipases after the ingestion of a fat-free diet than 

 were other unsaturated acids. It was reported'"- that a minimiun intake 

 of arachidonate is re(|uired before the cell depots are loaded with fat. Sub- 

 sequently, during the true growth process, comparatively large amounts 

 of arachidonate disappear from the tissues. However, the EFA are not 

 concerned with the synthesis of lecithin. Hevesy and Smedley-MacLean'^^ 

 reported that the uptake of radioactive phosphorus w^as surprisingly con- 

 stant on a fat-free diet, or on one containing arachidonate. In the case of 

 the rats on a fat-free regimen, the phosphorus uptake in the muscle was one- 

 third as great as in rats on a diet containing EFA. 



It is suggested that the increased activity of the cytochrome oxidase 

 system may largely account for the augmented level of metabolism in fat 

 deficiency. It will be recalled that Wesson and Burr,'^- as early as 1931, 

 and also Wesson alone, '^^ reported that high metabolic rates and high 

 respiratory quotients regularly accompanied the fat-deficiency syndrome. 

 Engel'^^ postulated that, in the absence of the essential fatty acids, choline 

 fails to exert its normal lipotropica ction. Smed ley-Mac Lean and Nnnn'^^ 



188 H. O. Kunkel and J. N. Williams, Jr., J. Biol. Chem., 189, 755-761 (1951). 



18" P. G. Tulpule and V. N. Patwardhan, Arch. Biochem. Biophi/s., 3.9, 450-456 (1952). 



'™ M. O. Saka and tj. Sipahioglu, Am. J. Phi/siol., 174, 49-50 (1953). 



1" G. C. Hevesv and I. Smedlev-MacLeau, Biochem. ./., 34, 903- 905 (1940). 



192 L. G. Wesson and G. O. Burr, ./. Biol. Chem., 91, 525-539 (1931). 



193 L. G. Wesson, J. Biol. Chem., 100, 365-371 (1933). 

 19^ R. W. Engel, ./. Nutrition, 24, 175-185 (1942). 



195 1. Smedley-MacLean and L. C. A. Nunn, Biochem. J., 35, 983-989 (1941). 



