METABOLISM. 351 



when very large amounts of sugar are taken by the mouth. The in- 

 gestion of starch, even in large quantities, does not lead to glycosuria, 

 since its digestion and absorption are sufficiently slow to enable the 

 liver to convert the sugar 'into glycogen. 



(2) Adrenalin Glycosuria. The injection of a small quantity of 

 adrenalin into the circulation is followed by the appearance of dextrose 

 in the urine ; at the same time, glycogen disappears from the liver, and 

 the percentage of sugar in the blood, is increased. Evidently the 

 adrenalin causes the liver to discharge its glycogen into the blood as 

 sugar, which is excreted by the kidneys. Glycosuria may also occur 

 under any conditions in which adrenalin is set free into the blood 

 stream in larger amount from the suprarenal glands. 



(3) Diabetic Puncture. Claude Bernard was the first to show that 

 puncture of the floor of the fourth ventricle in rabbits is followed by 

 hyperglycaemia, glycosuria, and the disappearance of glycogen from the 

 liver; if the animal has been previously starved to rid its liver of 

 glycogen, glycosuria does not follow the puncture. This experiment 

 was regarded by Bernard as a further proof of his theory as to the 

 function of glycogen in the body. The diabetic puncture fails to pro- 

 duce glycosuria after division of the splanchnic nerves or removal of 

 the suprarenal glands, and in all probability the puncture stimulates 

 the medulla oblongata in such a way that adrenalin is set free into the 

 circulation and causes glycosuria. 



(4) Phloridzin Glycosuria. Phloridzin is a glucoside, which on 

 hydrolysis yields glucose and phloretin. A small amount of phloridzin 

 or phloretin, when injected into an animal, produces glycosuria and 

 the disappearance of glycogen from the liver ; but phloridzin glycosuria 

 differs from that just described in that the percentage of sugar in the 

 blood is not increased, but tends rather to be diminished. Phloridzin 

 acts upon the cells of the renal tubules, causing the kidneys to excrete 

 dextrose, even when the percentage of the latter in the blood is not raised. 

 That it acts upon the kidneys may be shown by collecting the urine 

 separately from the two kidneys, and injecting a small dose of phloridzin 

 into one, e.g. the right, renal artery ; the urine flowing from the right 

 kidney is then found to contain sugar some time before it appears in 

 the urine from the opposite kidney. Phloridzin appears to act directly 

 upon the cells of the renal tubules, stimulating them to secrete sugar 

 from the blood, and this view is supported by the observation that the 

 repeated administration of phloridzin produces definite histological 

 changes in the cells of the renal tubules. 



When repeated doses of phloridzin are given tb an animal, the 

 glycosuria persists after the glycogen has disappeared from the liver, 



