550 METABOLISM, NUTRITION AND DIETETICS 



stimulation or control (see also p. 509). There is some evidence 

 that excitation of the uncut great splanchnic nerve (on the left side) 

 in dogs may cause hyperglycsemia, diuresis, and glycosuria, even 

 under conditions in which as far as possible circulatory effects are 

 eliminated. Contrariwise, when in the puncture experiment on an 

 unnarcotized animal the small instrument does not wound the 

 medulla oblongata in the right place, a rise of blood-pressure due 

 to excitation of the vaso-motor centre may occur without any 

 glycosuria. But absolute proof of the existence of glycogenolytic 

 nerve fibres going to the liver that is, fibres whose stimulation 

 accelerates the hydrolysis of glycogen into dextrose (Macleod) has 

 not yet been brought forward. 



Adrenalin Glycosuria. In adrenalin glycosuria the sugar-content 

 of the blood is increased. A given quantity of adrenalin introduced 

 subcutaneously produces a more marked hyperglycaemia and 

 glycosuria than the same amount injected into a vein or into muscle. 

 The best evidence is that the glycosuria is produced by some action 

 on the liver, possibly through the excitation of sympathetic fibres 

 controlling the production of dextrose from glycogen (Underbill and 

 Closson), or by a direct effect on the hepatic cells, which hastens the 

 normal transformation of glycogen into dextrose, or hinders the 

 normal transformation of dextrose into glycogen. It has been 

 stated that in the isolated surviving liver of the frog adrenalin causes 

 the glycogen to be rapidly converted into dextrose. While this 

 confirms the view that experimental adrenalin glycosuria is due to 

 an action on the liver which increases the sugar-content of the blood, 

 it does not necessarily show that the action is exerted directly on 

 the hepatic cells without the intervention of nerve fibres. For the 

 sympathetic nerve-endings may survive a considerable time. The 

 theory that epinephrin causes glycosuria by inhibiting the internal 

 secretion of the. pancreas, and that the condition is therefore a par- 

 ticular variety of pancreatic diabetes, is erroneous. Adrenalin 

 glycosuria does not seem to be in any way related to true 

 diabetes. The complete metabolism of dextrose is not interfered 

 with. Indeed, a much larger proportion of the total heat produced 

 comes from the destruction of sugar after the subcutaneous injection 

 of epinephrin into dogs than in the normal animals (Lusk and Riche). 

 If in spite of this glycosuria ensues, it is only because the carbo- 

 hydrate reserve of the body is mobilized so rapidly that it cannot 

 possibly be all consumed. Nor does epinephrin cause any increased 

 production of sugar from protein or from fat. For in dogs rendered 

 diabetic by phlorhizin and freed from glycogen by shivering, injec- 

 tion of epinephrin is not followed by an' increase of either sugar or 

 nitrogen in the urine (Ringer). After repeated injections of adren- 

 alin, a tolerance for it is established, and glycosuria is no longer 

 caused. 



