METABOLISM 527 



nals or ligation of the adrenal veins, by which the secretion is prevented from 

 entering the venous blood, the removal of the pancreas is not followed as 

 usual by glycosuria. The simultaneous injection of an extract of pancreas 

 and an injection of that amount of adrenalin ordinarily necessary to produce 

 glycosuria prevents its development. 



Assuming the former view to be more nearly correct and based on 

 experimental data, it is permissible to assume that the muscle ferment, 

 in association with, or by being activated by, the pancreatic hormone, 

 leads during muscle activity to the disruption and oxidation of sugar 

 whereby its contained energy is liberated for the most part as heat and 

 mechanical motion. 



Glycosuria. From the foregoing statements it is apparent that the 

 mechanism regulating carbohydrate metabolism is quite complex. 

 Clinical observations show that is is easily disturbed, leading to a glyco- 

 suria more or less pronounced and of longer or shorter duration. The 

 causes of glycosuria are many and their mode of action often obscure. 



Alimentary Glycosuria. When carbohydrate food, sugar more especially 

 is consumed in amounts beyond what constitutes the assimilation or storage 

 limit, the excess soon appears in the urine. This limit varies somewhat in 

 different animals. The tissues collectively of a normal human being have 

 an assimilation capacity of approximately 150 grams of glucose. Should 

 an amount of sugar be consumed much beyond this at one time, the excess 

 will be eliminated in the urine. Inasmuch as carbohydrate material con- 

 sumed each day is represented mainly by starch, and as digestion and ab- 

 sorption proceed slowly and metabolism continually, a glycosuria due to a 

 large amount of aliment is not of frequent occurrence, under physiologic 

 conditions. The assimilation limit may be lowered or raised beyond the 

 normal in accordance with variations in the activity of the hypophysis. 

 (See chapter on Internal Secretion.) 



Adrenal Glycosuria. As stated in a previous paragraph the subcutaneous 

 injection of adrenalin chlorid or of the watery extract of the medulla of the 

 gland is very soon followed by a glycosuria and hyperglycemia as well. The 

 degree of the glycosuria will depend on the extent to which glycogen has 

 been stored in the liver. It will also be recalled that stimulation of the left 

 splanchnic nerve is followed by glycosuria by reason of a greater discharge 

 of adrenalin into the blood. The increased transformation of glycogen to 

 sugar has been attributed to an exaltation of the irritability of the nerve end- 

 ings of the hepatic plexus or to a direct action on the liver cells themselves. 

 As to which view is more probable, future experiments may decide. In 

 either case the adrenalin excites an increased transformation of glycogen to 

 sugar. Any factor therefore which would more or less permanently increase 

 adrenal activity would cause a more or less permanent glycosuria. (See 

 page 508.) 



Pancreatic Glycosuria. From the result of experimental investiga- 

 tions on the pancreas stated on a previous page it is apparent that de- 

 structive lesions of this organ or a defective production of its activating 

 hormone, will be followed by a glycosuria (see pages 509 and 526). 



Pharmacologic Glycosuria. It is well known that various pharmacologic 

 agents when introduced into the body frequently give rise to glycosuria, 

 though the manner in which they do so is not always clear. Thus, the ad- 



