666 VI. OCCURRENCE OF LIPIDS IN THE ANIMAL 



were required to prevent kidney degeneration, but 10 mg. were needed to 

 avoid fatty infiltration of the liver. Methionine as well as choline pre- 

 vented kidney injury. Moreover, when rats were fed on a choline-low diet 

 in which the protein was arachin (a protein low in methionine) , kidney le- 

 sions developed. 745 Cystine exaggerated the kidney injury. 744 



Griffith and Wade 746 suggest that the role of choline in preventing kidney 

 injury is a more fundamental one than is its function as a lipotropic agent. 

 Presumably, it is related to its function in cell structure, which is supported 

 by the widespread distribution and the constancy of phospholipids in 

 various tissues, 349 - 352 and especially in the liver. 747 This effect on the 

 kidney presumably reflects a generalized condition, since, in the above 

 experiments, hemorrhages were shown to develop not only in the kidneys 

 but also in the adrenal glands, lungs, and eyes. Total liver homorrhages 

 have likewise been reported in rats receiving diets deficient in methionine 

 and cystine. 748 These studies serve to emphasize the importance of choline 

 in maintaining the cellular structure intact. 



Marked variations in susceptibility to kidney injury due to choline de- 

 ficiency are related to the sex, weight, and age of the rats. 746,749 Only six to 

 ten days are required to produce the injury in male rats weighing 40 g., and 

 twenty to thirty days old, while it becomes progressively more difficult to 

 bring about the deficiency in older and heavier rats. In fact, Griffith 750 

 noted a spontaneous partial recovery from kidney damage in animals which 

 had survived the initial ten-day period of the choline-deficient diet. En- 

 gel, 751 however, stated that symptoms of choline deficiency can be produced 

 in the rat within seven to fourteen days, at any time during the growth 

 period. In the absence of choline, the severity of the kidney injury is aug- 

 mented by cystine, fat, or cholesterol. 752 The histologic changes have been 

 described by Christensen 753 and by Gyorgy and Goldblatt. 754 



Since transmethylation was early recognized to be an important function 

 of choline, it is only natural that Griffith et ^.624,713,755,756 offered the ex- 



748 R. W. Engel and W. D. Salmon, J. Nutrition, 22, 109-121 (1944). 



746 W. H. Griffith and N. J. Wade, J. Biol. Chem., 131, 567-577 (1939). 



747 P. L. MacLachlan and H. C. Hodge, J. Biol. Chem,, 127, 721-726 (1939). 



748 T. E. Weichselbaum, Quart. J. Exptl. Physiol, 25, 363-367 (1935). 



749 W. H. Griffith, /. Nutrition, 19, 437-448 (1940). 



750 W. H. Griffith, Biol. Symposia, 5, 193-212 (1941). 



761 R. W. Engel, Proc. Soc. Exptl. Biol. Med., 50, 193-196 (1942). 



762 W. H. Griffith, /. Biol. Chem., 132, 639-644 (1940). 



763 K. Christensen, J. Biol. Chem., 133, xx (1940). 



754 P. Gyorgy and H. Goldblatt, /. Exptl. Med., 72, 1-9 (1940). 



'» W. H. Griffith and N. J. Wade, J. Biol. Chem., 132, 627-637 (1940). 



756 W. H. Griffith and D. J. Mulford, Proc. Soc. Exptl. Biol. Med., 45, 657-658 (1940). 



