X. EFFECTS OF DEFICIENCY 91 



acid and B12, or by additional choline or betaine with supplements of folic 

 acid and Bi2.'^^° Later it was shown that leukemic mice excreted larger 

 quantities of creatine and allantoin than normal animals^^^ and that this was 

 the result of increased synthesis of creatine.-" Kelley et al. caused marked 

 leucocytosis in rats by feeding excessive levels of glycine (10 %) and choline 

 (2%). Riboflavin and folic acid were essential for this effect."^ 



Chevremont concluded that choline was responsible for spontaneous trans- 

 formation of cells of cultures of skeletal muscle or of subcutaneous connec- 

 tive tissue into histiocytes. ^^^ The change of muscle cells into histiocytes, 

 believed to be caused by high concentration of choline, was observed also 

 by Firket and Cornil."^ 



Abdon and Borglin observed bradycardia in choline-deficient rats, which 

 disappeared quickly following intravenous administrations of choline .-^^ 

 Choline restored to normal an increased level of pseudocholinesterase in 

 male rats and a decreased level in female rats.^^'' 



Guggenheim and Olson determined the specific activity of tissue fatty 

 acids after administration of carboxyl-labeled acetate and were unable to 

 find evidence of impaired lipogenesis in choline-deficient rats.-^^ Deuel et al. 

 showed that the lipotropic activity of choline was not due to an increased 

 rate of oxidation of fat."^ The deposition of vitamin A in the livers of de- 

 pleted rats was not affected by choline deficiency or by the presence of a 

 fatty liver.-^" Impaired metabolism of carbohydrate and of fat, as well as 

 functional damage to liver cells, decreased the hepatic synthesis of choline.^^^ 

 Elevated environmental temperature increased the choline requirement of 

 rats.-^- The report that choline deficiency resulted in a loss of contractility of 

 the uterus and partial atrophy of both uterus and ovaries in rats-^^ has not 



"0 J. S. Dinning, L. D. Payne, and P. L. Day, Arch. Biochem. 27, 467 (1950) ; J. Nutri- 

 tion ^Z, 525 (1951). 



"1 J. S. Dinning and L. D. Seager, Science 114, 2967 (1951). 



"2 J. S. Dinning, L. D. Seager, L. D. Payne, and J. R. Totter, Science 116, 121 (1952). 



"3 B. Kelley, M. Northrup, and P. D. Hurley, Proc. Soc. Exptl. Biol. Med. 76, 804 

 (1951). 



"* M. Chevremont, J. Morphol. 76, 139 (1945). 



"5 J. Firket and A. Cornil, Compt. rend. soc. biol. 139, 51 (1945). 



"« N. O. Abdon and N. E. Borglin, Acta Pharmacol. Toxicol. 2, 247 (1946). 



2" R. D. Hawkins and M. T. Nishikawara, Biochem. J. 48, 276 (1951). 



"8 K. Guggenheim and R. E. Olson, J. Nutrition 48, 345 (1952). 



"9 H. J. Deuel, Jr., S. Murray, L. F. Hallman, and D. B. Tjder, J. Biol. Chem. 120, 

 277 (1937). 



"« L. S. Bentley and A. F. Morgan, ./. Nutrition 31, 333 (1946). 



28' H. K. Barrenscheen and D. Papadopoulou, Hople-Seyler's Z. physiol. Chem. 284, 

 236 (1949). 



282 C. A. Mills, Proc. Soc. Exptl. Biol. Med. 54, 265 (1943). 



28' M. Peet and M. M. Sampson, Science 107, 548 (1948). 



