no 



CHOLINE 



and so leave the liver. Cell remnants of disrupted cysts may survive for 

 some time, as their nuclei are not often damaged. Condensation of these 

 atrophic parenchymal cells (along with their reticular stroma) produces 

 the so-called "fibrous" trabeculae of the cirrhotic lesion (Fig. 9). The con- 

 densation is responsible for the annular surface depressions, while paren- 

 chymal hyperplasia (compensatory in nature) in the portal regions produces 

 the nodular, raised areas. 



Fig. 9. The cells in the wall of this fatty cyst ;iro thinned and stretched. The sur- 

 rounding stroma is condensed, and the c.yst is enmeshed in a trabecula. A portion of 

 a radicle of an hepatic vein is shown in the upper left corner. Liver of a rat fed a 

 choline-deficient diet for 6 months; paraffin section; hematoxylin and eosin stain; 

 X800. 



The fact that the natural sequence of events is the formation, rupture, 

 and dissolution of fatty cysts^^'' with consequent escape of their contents 

 from the liver explains why the amount of fat in the liver decreases as the 

 fibrosis increases. For, with the rupture of each additional cyst, more fat 

 escapes from the liver and condensation of the cellular and stromal elements 

 of the torn cyst adds to the growth of trabeculae. The loss of parenchyma 

 incident to the eventual destruction of each cyst (a large one may con- 

 sist of as many as 60 cells) stimulates compensatory hyperplasia in portal 

 areas. This region commonly exhibits only a moderate degree of fat storage 

 which is almost entirely intracellular in nature. Intracellular fat is very 

 rapidly mobilized when the deficiency in lipotropic factors is corrected. This 



