Blood Sugar Studies. 



411 



Wesselow. They gave fifty grams of glucose which caused the 

 blood sugar to rise and fall sharply. Then, when the curve had 

 returned to normal, they gave a second dose of fifty grams which 

 produced a response almost identical with the first. We find that 

 the second dose may cause little or no response, depending upon 

 the time at which it is taken (Table III). If the second dose is 



TABLE III. 

 Effect of Repeated Doses of Glucose. 

 Two doses of 100 gm. each at interval as noted by asterisk. 



Blood Sugar. Mg. per 100 c.c. Whole Blood. 



Time. 



Exp. 21. 



• 



Exp. 24. 



Exp. 27. 



Exp. 4. 



Before first dose 



95 



99 



100 



109 



15 min. after first dose . . 



171 



139 



166 





30 " " 



140 



81 



ii5 



150 1 



45 " " " " • • 



102 









60 " 



105 1 . 



62 1 



84 1 



156 



75 ' • • 



IOI 



57 



85 





90 " " " " . . 



95 



63 



88 



99 



105 " 



86 



57 



89 





120 " " " " . . 









78 



Second dose swallowed immediately after this blood sample was taken. 



taken when the rise is near its peak it produces only a slight 

 "bump" in the curve, which we interpret as meaning that the 

 mechanism (glycogen formation?) has nearly attained the same 

 speed as the inflow of sugar from the gut. However, if the second 

 dose be taken soon after the curve has returned to normal or 

 below, it has no detectable effect on the sugar content of the venous 

 blood (i.e., the mechanism is now at top speed and can handle 

 any quantity of sugar pouring in from the intestine). McLean 

 worked with "finger blood" (arterial and capillary) while we used 

 venous. We cannot yet say whether or not this is the cause of the 

 apparent discrepancy. 



Finally, the epinephrine hyperglycemias are not to be recon- 

 ciled with Folin and Berglund's hypothesis. Here absorption by 

 the tissues is normal (Palmer) 1 but nevertheless the hyperglycemia 

 is excessive and prolonged. We are led to the conclusion that the 

 chief factor in preventing hyperglycemia is glycogen formation, 

 since this is presumably the only carbohydrate function which is 



1 Palmer, W. W., Jour. Biol. Chem., 191 7, xxx, 79. 



