5i8 TEXT-BOOK OF PHYSIOLOGY 



nerve impulses become more efficient. These facts do not decide the ques 

 tion, however, as to the character of the nerves involved, that is, whether the} 

 are purely vaso-motor or secretory in character. The evidence for the exist 

 ence of glycogenolytic nerves is not decisive. 



Glycosuria. The mechanism by which the sugar is stored in the livei 

 as glycogen, and subsequently transformed into glucose, and discharged int< 

 the blood in amounts just sufficient to meet the needs of the tissues withou 

 giving rise to hyperglycemia and glycosuria, as well as the mechanism b] 

 which it is oxidized is apparently very delicate and easily disturbed as indi 

 cated by the ease with which a glycosuria more or less pronounced and o 

 longer or shorter duration can be established. The causes of glycosuria ar< 

 many and their mode of action often obscure. 



Alimentary Glycosuria. When carbohydrate food, sugar more especiall] 

 is consumed in amounts beyond what constitutes the assimilation or storagi 

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

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

 an assimilation capacity of approximately 150 grams of glucose. Shoulc 

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

 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 { 

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

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

 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 subcutaneou; 

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

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

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

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

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

 of adrenalin into the blood. The increased transformation of glycogen t< 

 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. Ii 

 either case the adrenalin excites an increased transformation of glycogen t( 

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

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

 page 504.) 



Pancreatic Glycosuria. It has been known for some years that if the 

 pancreas be extirpated and the animal survive the operation, glycosuria is 

 promptly established, followed by a series of symptoms which gradually, in- 

 creasing in severity, and lead to the death of the animal in from two to foui 

 weeks. In addition to the presence of sugar, acetone, aceto-acetic, /3-oxybu- 

 tyric acid, and an excess of urea have been found in the urine. The 

 quantity of sugar excreted and the gravity of the attendant symptoms maj 

 be much diminished, if not entirely prevented by allowing a portion of the 

 gland to remain even though its capacity for the production of pancreatic 

 juice is entirely abolished. Transplantation of various portions of the pan- 

 creas into the subcutaneous tissue, in the walls of the abdomen, will alsc 



