50 II. DIGESTION AND ABSORPTION OF PATS 



cholinesterase levels and hemoglobin, serum carotene, degree of under- 

 weight, physical signs indicative of malnutrition, or general appearance 

 from a nutritional standpoint. 



In studies of liver diseases in man, Faber 284 found s-cholinesterase low in 

 the blood; the enzyme content rises after recovery. Wescoe and co- 

 workers 285 also reported that serum cholinesterase in patients with liver 

 disease was subnormal. Moreover, the regeneration rate of serum cholin- 

 esterase was significantly lower than the normal after the administration 

 of DFP to patients with liver disease. These facts led Wescoe et at. to 

 conclude that the liver is the primary site of formation of serum cholin- 

 esterase. Benard et al. m noted that, in the case of livers damaged experi- 

 mentally with carbon tetrachloride, serum tributyrinesterase (s-cholin- 

 esterase?) first increases, and then drops back to a value lower than the 

 original level, while cholinesterase (e-type?) remains relatively unchanged. 

 Brauer and Root 274 likewise reported an increased plasma cholinesterase in 

 male dogs poisoned with carbon tetrachloride, while a decrease in the level 

 followed transfusion. In the presence of a functioning liver, but not after 

 hepatectomy, the serum cholinesterase returned to the normal level. The 

 liver is considered to be a storehouse of cholinesterase ; the total quantity is 

 5 to 7 times that in the blood. Brauer and Root 274 reported a significant 

 degree of correlation between the liver and plasma cholinesterase. These 

 experimental data are to be interpreted as further evidence of the hepatic 

 origin of serum cholinesterase. 



There is no definite conclusion as to what role folic acid plays in main- 

 taining cholinesterase levels. Davis and Hamilton 287 presented evidence 

 that folic acid (pteroylglutamic acid) increases the cholinesterase activity 

 of the plasma of dogs and human subjects. Moreover, Davis 288 reported 

 that folic acid caused a remission of hyperchromic anemias (induced by 

 acetylcholine) in dogs; this was accompanied by reticulocyte responses. 

 An analogous effect was produced by liver extract. In the latter case, 

 serum cholinesterase was increased twelve-fold. Likewise, in some in- 

 stances, incubation of sera with liver extract or with folic acid increased 

 their cholinesterase activity. It is concluded that the important action of 



284 M. Faber, Acta Med. Scand., 114, 59-71, 72-91 (1943). 



28S W. C. Wescoe, C. C. Hunt, W. F. Riker, and I. C. Litt, Am. J. Physiol., 149, 549- 

 551 (1947). 



286 H. Benard, A. Gajdos, and M. Gajdos-Torok, Compt. rend. soc. biol, 142, 1372-1374 

 (1948). 



287 J. E. Davis, Proc. Soc. Exptl. Biol. Med., b'.-i, 287-290 (1946); and W. M. Hamilton, 

 Federation Proc, 6, 95 (1947). 



288 J. E. Davis, Am. J. Physiol, 147, 404-411 (194(5). 



