20 The Chemistry of the Injured Cell 



recognised that are directly concerned in the reactions by which 

 phospholipids, especially lecithins, are built up. 



When young male rats are fed a low choline diet the fat in their 

 livers increases markedly within forty-eight hours and reaches a 

 maximum after four to six days. Lipid droplets are seen in the liver 

 cells surrounding the central veins within 24 hours and grow into 

 large cytoplasmic masses during the first week of feeding. At this 

 time haemorrhagic degeneration appears in the kidneys along with 

 involution of the thymus and ocular haemorrhage. Liver fat may 

 be increased ten times, but it disappears rapidly when choline is 

 restored to the diet. If the choline deficiency is continued for one 

 to two months, serious liver injury sets in. Cells may rupture and 

 large fatty masses form in the lobules. Eventually the organ becomes 

 cirrhotic, i.e. fibrosed. 



Though choline is an important factor in the turnover of lipids 

 and by its absence can induce fatty change in cells, we must not for- 

 get that many other causes of this serious disturbance are known 

 to exist. These cannot be prevented from exerting their action by 

 giving choline (Best et al, 1953) . However, many animal species 

 respond to choline restoration, including dog, pig and calf, but so 

 far no-one has given direct evidence of such an action in man. It has 

 been argued, largely from experiments with rats, that human 

 alcoholic cirrhosis is the same as the cirrhosis of choline-deficient 

 animals, albeit there are considerable differences in the micro- 

 scopical picture. We badly need quantitative data on the composi- 

 tion of organs in men exposed to abnormal diets before we can 

 confidently apply the animal results to human beings. 



The metabolic aspect of fat disturbance needs further comment. 

 The fat content of cells is, of course, largely influenced by physiolo- 

 gical variation in the animal's diet, not only in fat but in carbo- 

 hydrate and protein. No less important are the various hormones 

 and vitamins that occupy their apportioned places in the series of 

 metabolic changes that determine the fate of lipids after absorption 

 from the intestine until their final utilisation in the tissues. More 

 than a suspicion exists, at any rate in laboratory animals, of the role 

 of vitamins of the B and perhaps E group, hormones from the anter- 

 ior pituitary gland, adrenals, pancreas, sex glands (oestrogens) in 



