X. EFFECTS OF DEFICIENCY 



111 



may he effected in a variety of ways, as, for example, decreased growth of 

 the animal (thus sparing more methionine for lipotropic use), reduced food 

 intake, or the addition of choline to the diet. The result is a cirrhotic liver 

 without obvious fatty change (Fig. 10). This sequence has been observed 

 repeatedly in experimental animals. The clinical counterpart of this pre- 

 sumably occurs when a cirrhotic alcoholic in hospital is denied access to 

 his alcohol and is given a well-balanced diet (with or without therapeutic 



Fig. 10. Almost all the stain.ililc i,ii m this cirrhotic liver of a cliDlincdeficient 

 rat has disappeared. That which remains is chiefly contained within persistent fatty 

 cysts. This demonstrates the small amount of abnormal fat which may be present in 

 a liver in which fibrosis has become severe. Liver of a rat fed a choline-deficient diet 

 for over a year. Paraffin section; hematoxylin and eosin stain; XIOO. 



adjuvants of choline or methionine). If, in addition, the patient's caloric 

 intake drops sharply owing to terminal complications such as ascites or 

 ruptured esophageal varices, his death may be preceded by a significant 

 loss in weight (which may be masked by ascites or edema) . This should mo- 

 bilize all intracellular fat from his liver and even much of the extracellular 

 lipid. Experiments with rats have demonstrated^^^' *^^ that most of the 

 extracellular fat in cysts will be resorbed e\'entually if the deficiency of 

 lipotropes is relieved. The only evidences of previous fatty change that can 

 then be found in liver sections are occasional remnants of cysts within the 



"5 W. S. Hartroft and K. A. Sellers, Am. J. Pathol. 28, 387-399 (1952). 



«6 C. H. Best, W. S. Hartroft, and E. A. Sellers, Gastroenterology 20, 375-384 (1952). 



