v INTERNAL RESTITUTIVE SECRETIONS 305 



These results were subsequently confirmed by Musculus, v. 

 Mering, Kiilz, Pregl, and others. 



Theoretically the amylolytic enzyme of the liver may be 

 derived from a special zymogen contained in the protoplasm of the 

 hepatic cell, which is destroyed along with the enzyme when a 

 freshly excised liver is thrown into boiling water. 



Noel Paton (1893) observed that chloroform or sodium fluoride 

 retarded the first phase of sugar- formation in the excised liver, 

 during the period in which it is most active owing to survival 

 of the hepatic cells. Since Pavy and Salkowski show r ed that 

 chloroform does not modify the activity of the amylolytic enzyme 

 extracted from the liver, it appears to us that the delay in 

 glycogenesis observed by Paton must be due to alteration of the 

 protoplasm of the hepatic cells. This would retard the formation 

 of the zymogen on which the development of diastase in the 

 excised liver depends. 



In a recent series of experiments E. Cavazzani brings forward 

 the following facts : 



(a) Formation of glucose in the liver is increased by stimula- 

 tion of the caeliac plexus, but the amount arid activity of the 

 haemodiastase in the blood circulating through the liver is not 

 increased. Equal quantities of hepatic blood collected before and 

 after stimulation of the caeliac plexus convert an equal quantity 

 of starch into sugar in the time unit and under the same 

 experimental conditions. 



(6) In a mixture of blood and glycogen solution the conversion 

 of the glycogen into sugar by the haemodiastase is very slow, 

 whereas post-mortem glycogenesis is a very rapid process. 



(c) Methyl violet, which does not affect the saccharifying 

 action of haemodiastase, when injected into the circulation, be- 

 comes mainly fixed in the liver, and in suitable doses checks the 

 hyperglycaemia of asphyxia, and greatly reduces post-mortem 

 glycogenesis. Methyl violet (as was previously known, and 

 confirmed by Cavazzani) exerts a markedly paralysing action on 

 protoplasm. 



(d~) Sulphate of quinine, again, which is indifferent to enzymes 

 and toxic for protoplasm, acts like methyl violet on the formation 

 of sugar in the liver. 



Cavazzani's observations do not, however, prove that hepatic 

 glycogenesis is not due to an amylolytic enzyme formed by the 

 liver. At most they support the thesis that the diastase of the 

 blood does not depend on that of the liver, and that methyl violet 

 and salts of quinine reduce post-mortem glycogenesis because, by 

 paralysing the protoplasm of the hepatic cells, they obstruct the 

 formation of the zymogen, and its conversion into the diastatic 

 enzyme. 



Cl. Bernard regards hepatic glycogenesis as a process of 



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