METABOLISM 153 



in this respect was the earliest to be discovered and may be 

 appropriately considered first. 



When dextrose is being freely resorbed from the digestive 

 tract, it undergoes dehydration and polymerization in the liver, 

 yielding the polysaccharid glycogen (25), which is stored up 

 in the liver cells. If, on the other hand, the resorption of dex- 

 trose from the intestines is insufficient to maintain the supply 

 in the blood, glycogen previously formed may undergo the 

 reverse process of hydration and cleavage, giving rise to a pro- 

 duction of dextrose. This regulatory activity, discovered by 

 Claude Bernard in 1853, by which carbohydrates are held back 

 or released according to the demands of the body, is called the 

 glycogenic function of the liver. While this function has other 

 aspects, as will appear later, as respects the digested carbohy- 

 drates the liver may be likened to a storage reservoir by which 

 the flow of a stream is controlled. 



214. Mechanism of regulation. It is of interest to note 

 that this phase of carbohydrate metabolism illustrates two of 

 the general conceptions formulated on preceding pages. 



First, the formation of glycogen is a synthetic reaction. The 

 comparatively simple molecules of dextrose are built up tem- 

 porarily into the more complex molecules of the polysaccharid. 

 In other words, almost the first step in carbohydrate metabolism 

 is an anabolic change (203). 



Second, the process of the formation and destruction of gly- 

 cogen is susceptible of explanation as a reversible enzym re- 

 action (212). It is known that the conversion of glycogen into 

 dextrose is effected by an enzym or enzyms which may be ex- 

 tracted from the liver and which, it would seem, must be similar 

 to those of the digestive tract. The action of one of the latter, 

 maltase, however, is claimed to be reversible (211), and one is 

 naturally tempted to infer that the synthesis of the liver gly- 

 cogen is effected by the same enzym which brings about its cleav- 

 age, although experimental proof that such is the case is lacking. 

 According to this hypothesis, the changes taking place in the 

 liver would be represented by the equation 



(C 6 H 12 6 ) $ C 6n H 10w 5 n + n(H 2 0) 



An excess of dextrose in the blood would have the effect of 

 displacing the point of equilibrium in the direction of the for- 



