540 METABOLISM, NUTRITION AND DIETETICS 



into dextrose in the liver, there is evidence that the amount of the 

 enzyme which hydrolyses the glycogen is increased. Whether the 

 action of the enzyme is favoured in some other way e.g., by the 

 production of a co-ferment or by some change in the condition of 

 the glycogen which renders it more open to attack is unknown. 

 / Certain facts have recently been brought forward which go to 

 snow that the action of the splanchnic fibres on the liver is not 

 a direct action, but that in some way or other the concomitant 

 activity of the adrenal glands is essential. For if the adrenals have 

 been previously extirpated, the puncture does not cause glycosuriaJ 

 It was at first thought that the reason for this was that the removal 

 of the adrenals is itself followed by the disappearance of glycogen 

 from the liver, and, as has been pointed out, the presence of glycogen 

 in the liver is essential to the success of the puncture experiment. 

 The matter, however, is not so simple. For although in certain 

 animals e.g., the dog the liver does lose all its glycogen when the 

 adrenals have been taken away, this is not the case in the rabbit, 

 and yet in the rabbit also the urine remains free from sugar after 

 puncture in the absence of the adrenal glands. In some way or 

 other, then, the adrenals do intervene in the production of puncture 

 glycosuria. The observation, which is easily confirmed, that^the 

 injection of adrenalin (or epinephrin) (p. 541) under the skin or into 

 the blood, or into one of the serous sacs, does cause a- pronounced 

 increase in the sugar content of the blood, and the appearance of 

 dextrose in the uriney seemed at first to supply the missing link in 

 the chain of evidence. What could be simpler than the assumptk n 

 that the splanchnic fibres stimulated in the puncture experiment 

 were fibres going not to the liver, but to the adrenals, which occa- 

 sioned an outpouring of adrenalin into the blood, and that puncture 

 glycosuria was therefore merely a particular case of adrenalin glyco- 

 suria ? It is known that excitation of the splanchnic nerves causes 

 the passage of adrenalin into the blood of the adrenal veins (p. 640). 

 It is known that puncture of the medulla oblongata diminishes tl e 

 epinephrin content of the adrenal glands. The argument seemed 

 straightforward, and the adrenal hypothesis of puncture glycosuria 

 triumphant. As soon, however, as the matter was put to the test 

 of quantitative experiments, the hypothesis began to crumble. . It 

 was shown, for example, that during a stimulation of the splanchnic 

 nerves sufficient to cause a decided increase in the dextrose content 

 of the blood, a quantity of adrenalin was given oft to the adrencl 

 veins, which, when mingled with the rest of the blood on its way 

 to the liver, could not possibly amount to more than one in a hundred 

 million parts of blood, a concentration in which adrenalin, when 

 introduced artificially into the blood-stream, produces no glycosuria 

 whatever, nor, indeed, any recognizable physiological effect. Stiil 

 more significant is the fac<- that, after destroying the hepatic plexus, 



