374 VIII. CHOLESTEROL AND RELATED STEROLS 



terol begins after the second month, and continues up to the thirtieth week, 

 after which it decreases again up to the time of dehvery. ^^^ 



The administration of fat itself has been reported by a number of in- 

 vestigators to cause a concomitant hypercholesterolemia, although there is 

 no unanimity of opinion on this point. Conversely, Anderson and Keys' ^'* 

 reported that the serum cholesterol of patients decreased 21 mg. % over a 

 four -week period during which the level of dietary fat was decreased from 

 140 to 70 g. daily; an equicaloric diet containing 0.7 g. of cholesterol was 

 given. 



In addition to the immediate effect of fat ingestion upon blood choles- 

 terol, there is also a prolonged effect following the ingestion of this food- 

 stuff which may persist over several days. Thus, Entenman and Chai- 

 kofT^^^ demonstrated that an increase in blood cholesterol occurred after a 

 single fat feeding, although the serum fatty acids and phospholipids were 

 only slightly increased. Tolstoi^^^ observed a continued hypercholesterol- 

 emia in two human subjects who lived on an exclusive meai-fat diet for 

 over a year. 



Although one might expect the ingestion of cholesterol itself to be the 

 most potent procedure for provoking an increased level of blood choles- 

 terol, this result cannot readily be demonstrated in man. Thus, no in- 

 crease in blood cholesterol values in man, after the administration of 

 cholesterol in doses as high as 20 g. daily, have been observed by Turner 

 and Steiner,^^^ Gardner and Gainsborough,''^ or by Keys.^^^ However, 

 increased serum cholesterol values were reported in man when cholesterol 

 was fed in the form of egg yolk. ^20,121 j^ jg possible that the hypercholes- 

 terolemia in the latter cases may be attributed to the increased absorption 

 resulting from the lecithin present in the egg yolk. On the other hand, the 

 feeding of cholesterol to animals other than man is invariably followed by 

 an increased blood cholesterol, together Avith the development of fatty 

 livers. This hypercholesterolemia occurs in the case of rats,'-'-' guinea 



13 J. A. Gardner and H. Gainsborough, Lancet, 1929, I, 603-606. 



1^ J. T. Anderson and A. Keys, Federation Proc, 12, 169 (1953). 



1^ C. Entenman and I. L. Chaikoff, J. Biol. Chem., I42, 129-139 (1942). 



i« E. Tolstoi, /. Biol. Chem., 83, 753-758 (1929). 



" K. B. Turner and A. Steiner, ./. Clin. Invest., 18, 45-49 (1939). 



18 J. A. Gardner and H. Gainsborough, Biochem. J., 22, 1048-1056 (1928). 



IS A. Keys, Science, 112, 79-81 (1950). 



2« R. Okey and D. Stewart, J. Biol. Chem., 99, 717-727 (1933). 



" A. Steiner and B. Domanski, Am. J. Med. Sci., 201, 820-824 (1941). 



22 C. H. Best, H. J. Channon, and J. H. Ridout, /. Physiol, 81, 409-421 (1934). 



" R. P. Cook, Biochem. J., 30, 1630-1636 (1936). 



