Hepatic Glycogenesis. 



93 («S7) 



The stimulating influence of alkali on hepatic glycogenesis. 



By J. J. R. Macleod. 



[From the Physiological Laboratory, Western Reserve Medical 

 School, Cleveland, 0.\ 



The pronounced influence which acids and alkalies exert on the 

 rate at which glycogenase converts glycogen into reducing sugar 

 has suggested the possibility that variations in the activity of this 

 enzyme in the liver cells may depend primarily on changes oc- 

 curring in the reaction (H-ion concentration) of the immediate 

 environment in which the enzyme is acting. 1 Although there are 

 now many facts which indicate that a condition of hyperglycemia 

 (and glycosuria) usually develops when acids gain entry to the 

 blood and that the opposite condition of hypoglycemia is readily 

 induced with alkalies, yet there is no direct evidence that these 

 changes in the reducing power of the blood are immediately de- 

 pendent upon corresponding alterations in the rate of hepatic 

 glycogenolysis in warm blooded animals. 



A direct method for testing the influence of changes in reaction 

 in the liver cells on the glycogenolytic process is offered in the 

 experimental procedure which has recently been described by 

 Pearce and Macleod. 2 Briefly, this consists in an estimation of 

 the reducing power of the blood removed at short intervals (2-3 

 minutes) from the portal vein and vena cava inferior (opposite 

 the entry of the hepatic veins), several consecutive estimations 

 being made before, during and after the injection of a dextrose 

 solution under constant pressure, into a branch of the mesenteric 

 vein. When the percentage reducing power is equal in the 

 two bloods, the glycogenolytic process in the liver is presumably 

 dormant; when the percentage is higher in the vena cava than in 

 the portal vein, glycogenolysis must be active; and when lower, 



1 Cf. Pavy and Bywaters. Journ. Physiol., 1910, LXI, p. 168; Elias, Biochem. 

 Zlschr., 1913, XLVIII, p. 120; Elias and Kolb, ibid., 1913, LII, p. 331; Macleod. 

 "Diabetes, etc.," 1913, p. 150; Murlin and Kramer, Jour. Biol. Chem., 1913, XV, 

 p. 365; and Proc. Soc. Biol. Chcm., 1915, III, p. 25, and Kramer and Marker, ibid., 

 p. 24. 



1 Macleod and Pearce, Am. Journ. Physiol., 1915, XXXVI II, p. 425. 



