CHAP, v.] NUTRITION. 423 



suppose that under certain circumstances, as in the absence of 

 adequate food, the carbohydrate material thus formed is at once 

 discharged into the hepatic blood, for the general use of the body, 

 but that under other circumstances as when an amylaceous meal 

 has been taken, the immediate wants of the economy being covered 

 by the carbohydrates of the meal, the carbohydrate products of the 

 hepatic metabolism are stored up as glycogen. Under such a view 

 the sugar of the meal is used up somewhere in the body and the 

 glycogen to which it gives rise comes direct from the hepatic 

 protoplasm. An argument against such a view is afforded by the 

 behaviour of the substance glycerine. This substance when taken 

 into the alimentary canal, or when injected into the portal vein, 

 gives rise to an increase of glycogen in the liver, but when it is 

 injected into the general venous system no such increase is ob- 

 served. But if the formation of glycogen were due to the glycerine 

 covering in some way or other the carbohydrate expenditure 

 of the body and thus sparing the products of hepatic metabolism, 

 we should expect to find an increase of glycogen in the latter case 

 as well as in the two former cases. From this not taking place 

 we infer that glycerine gives rise to glycogen by being in some 

 way or other transformed into glycogen by the agency of the 

 hepatic cell, or at all events by the glycerine producing changes in 

 the hepatic cell. And the small quantity of glycogen which 

 results from proteid food is probably in a similar way the product 

 of the direct action of the proteid on the hepatic protoplasm. 

 From these and similar cases we may conclude that sugar also and 

 the other carbohydrates give rise to glycogen, not by covering the 

 general carbohydrate expenditure, but by producing changes in the 

 liver itself. How far the sugar reaching the hepatic cell by the 

 portal capillaries enters into the upward and downward series of 

 the protoplasm of the cell, whether it is actually built up into the 

 protoplasm before its elements reappear in the course of the 

 destructive metabolism of the complex protoplasm as glycogen, 

 formed so to speak afresh, or whether the protoplasm simply 

 dehydrates the sugar as we just now suggested, while it is still 

 outside itself, we have not at present sufficient evidence to decide. 

 Though the former method seems to entail an unnecessary labour 

 there may be reasons why it should be adopted. 



We have said that glycogen is readily converted by ferments 

 into sugar, and that, after death, a conversion into sugar goes on in 

 most cases with considerable rapidity and energy. An amylolytic 

 ferment may be extracted from the hepatic tissue and it seems pro- 

 bable that the post-mortem appearance of sugar in the liver is due to 

 the uncontrolled action of such a ferment. If this be the case, 

 the question may be asked, How is it possible for the glycogen 

 to remain as glycogen and become stored up in larger quantities 

 in the presence of such a ferment ? We can only answer that the 

 solution of this problem is of the same kind as that of the 



