Functional Disorders of the Liver. 425 



metamorphosis is imperfect they pass out of the system in the 

 urine, producing a temporary glycosuria. As shown above gly- 

 cogen is produced in the liver cells, and stored up there, in great- 

 est abundance during digestion of starchy and saccharine food, 

 but it is also formed in animals kept on a purely albuminous diet, 

 (flesh), and in the fcetal calf and unhatched chick to which 

 neither starch nor sugar has been furnished as food. It is pro- 

 duced during the decomposition of albuminoids, along with the 

 other end products, leucin, tyrosin and urea. None of these last 

 three is found in the portal vein nor bile ducts, but all four are 

 found in the liver cells, and in the hepatic veins. 



In health a physiological balance is maintained by the oxida- 

 tion of the glucose, mainly in the lungs, so that in the blood of 

 the pulmonary veins no sugar is found. There is an exception 

 to ■ this observable after a full meal, rich in starch and sugar, 

 which produces such an excess of glycogen that a portion is car- 

 ried to the kidneys and expelled by them causing temporary 

 glycosuria. 



A small amount of glycogen is also produced habitually by the 

 white blood cells and stored up in them, but this is insufficient to 

 determine its appreciable elimination by the kidneys. 



In cases of persistent glycosuria the fault may be held to con- 

 sist in one of three functional derangements : 



1 st. The failure of the liver to transform the alimentary sugar 

 into glycogen. 



or 2d. The excessive production of glycogen in the liver. 



or 3d. The arrest of the destructive oxidation of sugar in the 

 lungs and tissues. 



In a diabetic patient who died suddenly of apoplexy Bernard 

 found that the liver was enlarged, comparing with the average as 

 25:14 while the contained sugar bore the ratio of 37.5:22. This 

 enlargement coming from malaria or other poison, such as 

 alcohol, ether (Harley), arsenic, quinia (Aitken), ammonia, 

 chloroform, or phosphoric acid (Murchison), is an established 

 condition of glycosuria. A rich and abundant food (starchy and 

 saccharine especially), or an unusually active hepatic circulation 

 acts in the same way. 



Bernard as early as 1849 showed that the glycogenic function 

 of the liver was greatly increased and glycosuria determined by 



