41 6 Relation of Salts to Carbohydrate Metabolism 



the "salt and water" hormone of the adrenal cortex, provided an adequate 

 supply of Na and CI ions were available. In partially depancreatized rats 

 NaCl did not produce glycosuria as the hormone did. 



Pulver and Verzar" offer in support of the theory— that K is involved in the 

 phosphorylation process leading to the formation of a polysaccharide— the 

 observation that substances which retard phosphorylation inhibit the uptake 

 of both glucose and K. "From this point of view," says Lasnitzki,*' "there 

 appear to be at least two main possibilities regarding the explanation of the 

 effect of K on fermentation and oxidation of glucose. Either K activates phos- 

 phorylation and thereby the subsequent formation of the supposed poly- 

 saccharide, or it activates the breakdown of the latter. In the former case, K 

 might be bound chemically, while in the latter case it might be adsorbed by 

 the polysaccharide (probably having colloidal properties). In either case 

 K would be liberated with breakdown of the polysaccharide." Verzar and 

 Somogyi^"'^^'^* suggested that K is organically bound in phosphorylation of 

 sugar. The latter process they regard as being under the control of the adrenals 

 in mammals. The disturbance in glycogenesis resulting from adrenalectomy 

 accounts for there being no increase in output of K to the blood from muscle 

 stimulation in the adrenalectomized animal, comparable to that shown by 

 Fenn^^ to occur in the normal animal. 



As first shown by D'Silva,^"'^ the concentration of K in the serum of animals 

 is regularly increased for a few minutes after the intravenous injection of 

 adrenalin. Posterior pituitary extract (pitressin, P.D.) had a similar effect, but 

 the rise was more delayed. Both agents are known to increase blood sugar, 

 also. The rise in serum K after adrenalin was shown to be followed by a more 

 prolonged fall, which was attributed to stimulation of insulin production by 

 the hyperglycemia. This "after fall" of K was practically absent in depancre- 

 atized animals. Paralysis of the parasympathetic system with atropine likewise 

 prevented the fall. The temporary rise in serum K after adrenalin injec- 

 tions has been confirmed by subsequent work (Marenzi and Gerschman;''*-^ 

 Schwartz;*" Houssay and co-workers"). In the human subject, Keys'^ found a 

 more transient increase in serum K than reported for lower animals. Houssay, 

 Marenzi and Gerschman" showed that the K entering the blood, following 

 injection of adrenaline or direct stimulation of the sympathetic nerves to the 

 liver, comes from the liver. Snyder and Johnson*^ demonstrated that the output 

 of both K and glucose from the perfused liver of the turtle was decreased by 

 vagal stimulation. 



Fenn" points out that K and lactic acid appear to move together in re- 

 lationship to muscular activity just as K and glucose rise and fall together 

 under certain conditions apparently concerned with the movement of glucose 

 into or out of the liver. Lactic acid and K increase together in the venous blood 

 plasma when muscles contract as they do in asphyxia, after hemorrhage and 

 in histamine shock. In the light of these observations, Fenn states: "It is tempt- 

 ing to suggest that K leaves the liver or enters muscle in company with glucose 



