24 The Chemistry of the Injured Cell 



lipid, 8.9-33.5 g. per 100 g. wet weight and 4 cirrhotic fatty livers 

 14.8-30.1 g. per 100 g. wet weight. Total fatty acid figures parallelled 

 these, showing that an increased neutral fat content was responsible 

 for the fatty change. Phospholipids showed no significant deviation. 

 Some earlier information about fatty liver bears out these conclu- 

 sions. The average total fat (g./lOOg. wet wt.) for two human 

 normal livers was 3.25, and for two fatty livers 5.29. Phospholipid 

 percentages were 54.4 and 36 respectively (Theis, 1929) . 



Neutral fat steadily accumulates in the myocardium after 

 coronary occlusion and in the damaged renal tubule cells after oc- 

 clusion of the renal artery or exposure to cyanide. We badly need 

 quantitative information in such cases. 



THE SIGNIFICANCE OF FATTY CHANGE 



The key to the fatty change in the damaged cell lies in our under- 

 standing of the metabolism of fat in the normal cell. Fortunately, 

 progress has been impressive in this field of endeavour and we can 

 now apply knowledge about normal processes to the abnormal cell 

 with some confidence, even though important gaps in our know- 

 ledge have still to be filled. 



BIOSYNTHESIS OF PHOSPHOLIPIDS 



Fats are digested in the small intestine into glycerol and fatty 

 acids and these products are absorbed into the lymphatics and blood 

 vessels of the intestinal wall during which process certain syntheses 

 are initiated and perhaps completed. Glycerol, for instance, is phos- 

 phorylated through interaction with adenosine triphosphate (ATP) 

 in the presence of the enzyme glycerokinase to give L-d-glycerophos- 

 phate. Certain fatty acids are converted into thio esters with co- 

 enzyme A and then combine with glycerophosphate to form phos- 

 phatidic acid which is promptly reduced to the diglyceride. Mean- 

 while, choline absorbed from the alimentary canal is brought to the 

 liver where it is phosphorylated by ATP in the presence of a liver 

 kinase to form choline phosphate. From this compound is formed, 

 through interaction with cytidine triphosphate, itself a product 

 of nucleoprotein breakdown, in the presence of a transferase, cyti- 

 dine-diphospho-choline. Under normal conditions, a transferase 



