METABOLISM OF CARBO-HYDRATES GLYCOSURI AS 547 



left (p. 636). Diabetes in man is known to be frequently associated 

 with pancreatic lesions. Although much still remains obscure, the 

 study of this pathological form of glycosuria and of the experimental 

 glycosurias has thrown light upon the normal metabolism of carbo- 

 hydrates and upon those regulative mechanisms whose breakdown 

 is responsible for the excretion of sugar. It will be best to discuss 

 the experimental glycosurias first, and to begin with the form which 

 probably is better understood than any other, the so-called punc- 

 ture glycosuria. 



Puncture Glycosuria Sugar-Regulating Mechanism. An arti- 

 ficial and temporary glycosuria, in which the sugar in the urine un- 

 doubtedly arises from the hepatic glycogen, can be caused by punc- 

 turing the medulla oblongata in a rabbit for example, at a level 

 between the origins of the auditory nerves and the vagi. It is stated 

 that a puncture of the thalamencephalon, or 'tween-brain (p. 850), 

 produces the same effect. If the animal has been previously fed with 

 a diet rich in carbo-hydrates that is, if it has been put under con- 

 ditions in which the liver contains much glycogen the quantity of 

 sugar excreted by the kidneys will be large. The immediate cause 

 of the glycosuria is an increase in the sugar content of the blood 

 (hyperglycaemia), an increase which is most pronounced in the blood 

 of the hepatic vein. If, on the other hand, the animal has been 

 starved before the operation, so that the liver is free, or almost free, 

 from glycogen, the puncture will cause little or no sugar to appear 

 in the urine, and the proportion of sugar in the blood will remain 

 normal. That nervous influences are in some way involved in the 

 mobilization of the glycogen reserve of the liver is shown by the 

 absence of glycosuria if the splanchnic nerves, or the spinal cord 

 above the third or fourth dorsal vertebra, be cut before the puncture 

 is made. But sometimes these operations are themselves followed 

 by temporary glycosuria, due, it is believed, to irritation of the 

 same efferent nervous path whose elimination when the splanchnics 

 are divided prevents the glycosuria. The simplest explanation of 

 the phenomena is that a ' sugar centre ' that is to say, a centre 

 which has the important office of regulating the sugar content of the 

 blood by governing the rate at which glycogen is built up and de- 

 composed in the liver, as the salivary centre regulates the rate at 

 which the constituents of saliva are formed and discharged has 

 been injured or irritated by the puncture. If a nervous centre does 

 in fact preside over this internal secretion of the liver, it will, of 

 course, be connected with efferent and afferent nerves. The former, 

 as defined by the experiments alluded to, seem to be confined to 

 the splanchnic nerves; the latter are believed to run especially, 

 though not exclusively, in the vagus. Section of the vagi has no 

 effect either in causing glycosuria of itself or in preventing the 

 ' puncture ' glycosuria, but stimulation of the central ends of these 



