272 IV. DIGESTION OF LIPIDS OTHER THAN FATS 



have demonstrated that cholestanol cannot be absorbed from the in- 

 testine. 



A second transformation of cholesterol in the intestinal tract is its 

 conversion to coprostanol. Coprostanol has been known since 1862, 

 when Austin Flint 139 separated it from human feces and showed that it 

 differed from cholesterol. It was originally called stercorine, 140 and later 

 koprosterin, by Bondzyriski, 141 who rediscovered it in human feces. In 

 the more recent literature it is referred to as coprosterol. The term co- 

 prostanol, which is gaining favor as the designation for this compound, 

 is probably to be preferred, inasmuch as it connotes that the alcohol is 

 saturated, and is isomeric with cholestanol. It has the same empirical 

 formula as cholestanol, namely C 2 7H 48 0, but it differs widely from the 

 latter compound. 



The most important evidence of the transformation of cholesterol into 

 coprostanol is the demonstration that the amount of coprostanol in the 

 feces is increased after the administration of cholesterol or cholesten- 

 one 95,142-144 j£ was fij,^ believed that a direct reduction was mediated 

 by intestinal bacteria, but this direct reaction was open to objection, since 

 only cholestanol could be shown to originate. 143 Although Dam 98 recog- 

 nized the importance of intestinal bacteria in coprostanol formation, he 

 suggested that they act, not on cholesterol, but on an intermediate of this 

 sterol. 



An alternate pathway for the conversion of cholesterol to coprostanol 

 has been postulated by Rosenheim and Webster, 145 and by Anchel and 

 Schoenheimer. 146 This involves a conversion to cholestenone, which is 

 reduced to coprostanone. Coprostanone can be reduced either to co- 

 prostanol or to epicoprostanol. These transformations are illustrated in 

 the accompanying equations. 



There are two pathways by which coprostanol can be synthesized in 

 the laboratory. If coprostenol is reduced, equal amounts of coprostanol 

 and cholestanol are formed. 147 Since no traces of coprostenol were re- 

 ported in the organism by Schoenheimer et a/., 124 it is believed that this 

 route must be excluded in the animal. 



139 A. Flint, Am. J. Med. Scl, 44, 305-365 (1862). 



140 A. Flint, Z. physiol. Chem., 28, 363-367 (1897). 



141 S. Bondzynski, Ber., 29, 476-478 (1896). 



142 R. Schoenheimer, D. Rittenberg, and M. Graff, /. Biol. Chem., Ill, 183-192 (1935). 



143 G. Bischoff, Biochem. Z., 227, 230-236 (1930). 



144 C. Dor^e and J. A. Gardner, Proc. Roy. Soc. (London), B80, 227-239 (1908). 

 146 O. Rosenheim and T. A. Webster, Nature, 186, 474 (1935). 



146 M. Anchel and R. Schoenheimer, ./. Biol. Chem., 125, 23-31 (1938). 



147 A. Windaus, Ann., 458, 101-112 (1927). 



