432 A TEXTBOOK OF PHYSIOLOGY 



by the ingest ion of too much starch (*' glycosuria e amylo "). Many 

 healthy members of a German garrison were found to have sugar in 

 the urine because too much starch was included in their dietary. 

 Alimentary glycosuria occurs more readily in some individuals than 

 others. Clinicians differ as to whether people in whom this glycosuria 

 occurs easily are to be regarded as physiological or pathological. 



2. Puncture (Neurogenous) Glyccsuria has been already men- 

 tioned . It results from the disturbance of the glycogenic centre in the 

 medulla oblongata which controls the conversion of hepatic glycogen 

 into sugar. Clinical experience shows that a similar condition arises 

 from meningitis (inflammation of the coverings of the brain), injuries 

 to the brain and upper part of spinal cord, tumours of the brain, 

 especially of the fourth ventricle, cerebellar haemorrhage, and possibly 

 from psychic shock, mental worry, and overwork. The increased 

 mobilization of sugar in the blood may be secondary to the passage 

 of adrenalin into the blood, and possibly the internal secretion of the 

 pituitary gland. It has been shown that fright increases the output 

 of adrenalin. 



It is possible that some of the drugs, such as caffein and strychnine, 

 which cause glycosuria, act on the glycogenic centre. Injection of 

 piperine and the giving of anaesthetics cause glycosuria, apparently 

 due to the dyspnoea thereby produced, for it is abolished if oxygen 

 be given simultaneously. The same holds true of the glycosuria 

 induced by the stimulation of the central end of the vagus nerve. 

 The results may be due to the effect partly upon the centre, and 

 partly upon the peripheral nervous mechanism. 



3. Pancreatic Glycosuria. The remarkable discovery was made at 

 the end of last century that total extirpation of the pancreas results 

 in a fatal glycosuria, while if a small piece of gland (one-fifth) be left 

 in situ, or transplanted, no glycosuria results. The glycosuria has 

 no relation, therefore, to the digestive secretory function of the pan- 

 creas. Considerable discussion has taken place as to the cause of 

 this glycosuria. Some have contended that it results from operative 

 damage done to the splanchnic nerves and sympathetic ganglia in 

 the neighbourhood of the pancreas. This view now finds little 

 acceptance. 



It has been suggested by others that after the extirpation of the 

 pancreas the liver more actively produces sugar. In an ordinary 

 fasting animal, the liver loses more weight than the rest of the body, 

 whereas in a depancreatized animal starving from glycosuria (the 

 gland was removed in part at first, followed by subsequent destruc- 

 tion of the remainder) the liver does not lose weight, although the 

 total weight of the animal diminishes rapidly. 



The view most generally accepted, however, in regard to pan- 

 creatic glycosuria is that there results a diminished utilization of 

 sugar by the tissues. Possibly the hepatic control of sugar is 

 also affected. As the simultaneous injection of a pancreatic extract 

 prevents that glycosuria which follows injection of adrenalin, it has 

 been suggested that the internal secretions of the suprarenals and 



