220 IV. CONVERSION OF FAT TO CARBOHYDRATE 



oleic acids, or the methyl ester of lauric acid,^^ were given. Geelmuyden^" 

 likewise found that caproic acid was ineffective as a source of extra glucose 

 in the phlorhizinized dog, but was actually ketogenic. Some investigators 

 reported the formation of glycogen when neutral fats were the principal 

 components of the diet, while the majority failed to find this metabolite. 

 Thus, on the one hand, Takao,^^ Burn and Ling,^^ and Magnusson^^ all re- 

 ported high values for liver glycogen following fat feeding. However, 

 Takao does not consider that his results furnished any conclusive proof of 

 the conversion of fat to carbohydrate, inasmuch as the glycerol contained 

 in the bacon which was fed may have accounted for the high glycogen level. 

 In the experiments of Burn and Ling,^- values as high as 4.6% were re- 

 corded for liver glycogen following the feeding of fat to rats over a period of 

 ninety-six hours. On the other hand, negative results were noted by 

 Qj.ggg 27 i^y Bodey et al.,''* and by Greisheimer.''^ Krantz and Carr^^ found 

 that the glycogen storage in the liver of rats fed dried powdered root of bur- 

 dock (Arctium lappa), in addition to the basal diet of cacao butter, was five 

 or six times that of rats on the basal diet alone (9.79:0.14%). The bur- 

 dock root contains 50 to 70% carbohydrate. 



Although Gregg" did note some increase in liver glycogen following the 

 administration of butterfat, he ascribes this finding to the glycerol moiety. 

 Gemmill and Holmes^^ also found that, when butter was fed to rats on a 

 fast, the liver glycogen was first reduced to zero, but that after the first 

 day it gradually increased mitil it had reached a level of approximately 1% 

 in the rats sacrificed after four or five days. It is possible to account for 

 such quantities of glycogen after the administration of butterfat without the 

 necessity of a gluconeogenesis. Since tributyrin cannot be stored as such in 

 the animal body, it is probable that the butyrate moiety is oxidized; this 

 leaves the glycerol free for glycogenesis. The occurrence of such a course in 

 the rat is indicated by the demonstration of increased glycogen following 

 the administration of tributyrin to normal fasting rats.-^ Deuel et al^"^ were 

 not able to demonstrate glycogen deposition in rats after trilaurin and 

 natural fats such as Wesson oil, cottonseed oil, peanut oil, or linseed oil had 

 been given, although butterfat and coconut oil were glycogenic. Another 

 possible explanation for the results obtained by Gemmill and Holmes-* 

 is that liver glycogen may have arisen from protein. During fasting, condi- 



" T. Takao, Biochem. Z., 172, 272-279 (1926). 



" J, H. Burn and H. W. Ling, Quart. J. Pharm. and Pharmacol., 2, 1-16 (1929). 



" R. Magnusson, Skand. Arch. Physiol., 55, 278-279 (1929). 



''* M. G. Bodey, H. B. Lewis, and J. F. Huber, /. Biol. Chem., 76, 715-723 (1927). 



" E. M. Greisheimer, /. Nutrition, 4, 411-418 (1931). 



^8 J. C. Krantz, Jr., and C. J. Carr, J. Pharmacol, 41, 83-87 (1931). 



