X. EFFECTS OF DEFICIENCY 93 



A most extensive study of the urinary excretion of choline in rats and 

 in man has been carried out by Borghn.^^^ The output in the urine of rats 

 varied with the intake and amounted to 0.27 to 0.44% of the chohne in 

 the food. The dietary chohne was the principal factor governing excretion, 

 the presence or absence of other sources of methyl, of protein, and of fat 

 having relatively little effect. 



The oxidation of methyl groups of choline to carbon dioxide has been 

 noted previously, and it is reasonable to assume that the nitrogen of the 

 demethylated choline or betaine is excreted as urea. There is some (luestion 

 regarding the fate of administered trimethylamine. Davies reported the 

 quantitative excretion of this compound and of its oxide as the oxide in the 

 cow.-^" Langley, however, recovered only 20 % of the trimethylamine given 

 to rabbits; the remainder of the nitrogen was believed to be excreted as 

 urea.^"" 



C. AVIAN SPECIES 



WENDELL H. GRIFFITH and JOSEPH F. NYC 



The primary effects of a deficiency of choline in chicks are interference 

 with growth and the appearance of perosis or "slipped tendon disease." 

 This characteristic abnormality is influenced by multiple factors but, if 

 caused by a lack of choline, is prevented readily by supplements of choline 

 or of compounds with specific choline activity. There is gross enlargement 

 of the tibial-metatarsal joint, twisting or bending of the distal portion of 

 the tibia and of the proximal end of the metatarsus, and slipping of the 

 gastrocnemius tendon from its condyles. If this occurs in severe form, the 

 chick is incapacitated. Until 1940 a lack of manganese was considered the 

 principal cause of perosis.^°^ In this year Jukes demonstrated that in cer- 

 tain diets, adequate in manganese, choline was an effective antiperotic and 

 growth-stimulating agent.^"- This unexpected finding was soon confirmed 

 in a number of laboratories. ^''^"^''^ 



An understanding of the relation of choline to the prevention of perosis 

 is complicated V)y the fact that the abnormality is aggravated by creatine,^"*' 



299 N. E. Borglin, Ado Pharmacol. Toxicol. 3 Suppl. 1 (1947). 



3o« W. D. Langlej', ./. Biol. Chem. 84, 561 (1929). 



30' H. S. Wilgus, L. C. Norris, and G. F. Heuser, /. Nutrition 14, 155 (1937). 



302 T. H. Jukes, /. Nutrition 20, 445 (1940). 



SO' A. G. Hogan, L. R. Richardson, H. Patrick, and H. L. Kempster, J. Nutrition 21, 



327 (1941). 

 3»4 D. M. Hegsted, R. C. Mills, C. A. Elvehjem, and E. B. Hart, J. Biol. Chem. 138, 



459 (1941). 

 3" P. R. Record and R. M. Bethke, Poultnj Sci. 21, 271 (1942). 

 306 T. H. Jukes, Proc. Soc. Exptl. Biol. Med. 46, 155 (1941). 



