METABOLISM, NUTRITION AND DIETETICS 519 



nervous stimulation of the liver-cells, or to withdrawal of such 

 stimulation or control (see also p. 470). There is some evidence 

 that excitation of the uncut great splanchnic nerve (on the left 

 side) in dogs may cause an increase in the hyperglycaemia, 

 diuresis, and glycosuria, even under conditions in which as far 

 as possible circulatory effects are eliminated. But absolute proof 

 of the existence of glycogenolytic nerve fibres has not yet been 

 brought forward (Macleod). 



In the natural diabetes of man, as in all the forms of glycosuria 

 mentioned, the immediate cause of the glycosuria is the increase 

 of sugar in the blood. Instead of the i part per 1,000, or a little 

 more or less, which constitutes the normal proportion in a healthy 

 man, in diabetes 3 or 4 parts, and in exceptional cases even 

 7 to 10 parts per 1,000 may be present. The riddle of diabetes 

 is the explanation of this persistent hyperglycaemia. It is 

 possible that in some cases the sugar coming from the alimentary 

 canal passes entirely or in too large amount through the liver, 

 owing to a deficiency in its power of forming glycogen. But 

 although in certain cases of diabetes specimens of the hepatic 

 cells, obtained by plunging a trocar into the liver, have been 

 found free from glycogen, in others glycogen has been present. 

 The muscles also are usually much poorer in glycogen than 

 normal muscles. The cause of this defect in glycogen-forming 

 power has been supposed by some to be the absence of a glycogen- 

 forming ferment, or its production in too small an amount. But 

 this has not been proved. In addition to an interference with 

 the due and regulated storage of the surplus sugar as glycogen, 

 it is necessary for a rational explanation of many of the facts of 

 diabetes to assume that from some change in the tissues sugar 

 has ceased to be a food for them, or is used up in smaller amount 

 than in the healthy body. The change may be the loss or diminu- 

 tion of a glycolytic ferment or a substance necessary for the 

 activation of such a ferment. And although the sugar-destroying 

 power of blood from diabetic patients, or from animals in which 

 glycosuria has been caused by phloridzin, is not at all inferior to 

 that of healthy blood, it may be that the intracellular glycolytic 

 ferments, if such really exist, are much less active, especially in 

 the more severe forms of the disease. The actual primary pro- 

 duction of sugar may be no greater than in a normal person with 

 the same diet. And there is no reason to suppose that an over- 

 production of dextrose is ever in pathological diabetes the proxi- 

 mate cause of the hyperglycaemia and glycosuria. But a secon- 

 dary overproduction of sugar unquestionably occurs in many 

 cases. The tissues, bathed as they are in liquids rich in dex- 

 trose, are nevertheless starving for sugar, since they cannot use 

 what is offered to them, and the body labours to avert the famine 



