Till METABOLISM OP Till CARBOHYDRATES <i71 



with a sustentacular material. By <1 irrupt inv this combination and thus 

 exposing the glycogen to the action of glycogenase, glycogen \ ill 



occur. We may call this the mechanical hypothesis and it d< 

 serious consideration, for it lias been shown thai very little postmortem 

 glycogenolysis occurs in tin- intact liver of Progs in winter, though 



at this time the organ contains an excess of glycogen,- hut becomes 

 marked when the liver is broken down by mechanical means. 



The third view depends on the well-known fad thai enzyme activities 

 become mosl markedly altered by slight changes in the <-li«-m i«-;il nal 

 of the environment in which they art. Diastatic enzymes are partic- 

 ularly susceptible i<> the reaction ■:<',,, of their environment, a very 

 slighl degree of acidity favoring and a trace of alkalinity markedly 

 depressing their activities. That a tendency to increasing acidity in 

 the liver cells may accelerate the breakdown of glycogen is suggested by 

 the depressing effect produced on the assimilation limit i sugars by 

 administering acids, and by the observation that postmortem crl ; 

 olysis becomes marked in proportion as the dying liver becomi 1 in 



reaction. It mighl ho thought then that glycogenolysis in the 1 i \ • 

 could he set up by the local production of a certain amount of acid. 

 Such a liberation of free acid could he brought aboul by a curtailment 

 in the arterial blood supply of the hepatic cell, producing a local ac 

 mulation either of carbonic or of other less completely oxidize.] adds 

 g., lactic'. It may he that asphyxia causes hyperglycemia by such 

 a mechanism. Vasoconstriction and consequent curtailment of arterial 



hi 1 supply occurs in the liver when the hepatic nerves are stimulated, 



and it i^ possible that the glycogenolysis which is also s.-t up by such 

 stimulation is due to the appearance of acids. The accelerate [ 

 of epinephrine on glycogenolysis mighl also he explained as due to 

 limitation of blood supply on account of vasoconstriction and local 



asphyxia. 



THE REGULATION OF THE BLOOD SUGAR LEVEL 

 Tin' level at which the concentration of BUgar in the dc blood 



is maintained represents the balance between two opposing factoi>: 1 



the consumption of glucose bv the tissues, and 2 the production 

 glucose by the liver, since this is the most readily oxidizable of all 



the proximate principles ( >f f l pi j . muscular activity 



large quantities of it to he consumed hat its concentration in the 



blood tends to fall below the physiological level, a tendency which is 

 immediately met by an increased discharge of glucose from the 1; 

 The question therefore arises as to how tin 

 transmit their requirements for glucosi i<> //<< liver. There are two 



