NERVOUS GLYCOSURIA 519 



defect may lie in the nervous system, in some cases in the pan- 

 creas, the relation of which organs to glycosuria will be con- 

 sidered later ; but in any case of alimentary glycosuria the 

 difficulty lies, either primarily or secondarily, with the liver, 

 which, for one reason or another, cannot convert all the glucose 

 into glycogen. If the liver is primarily affected, it is usually 

 found that assimilation of levulose is more affected than 

 assimilation of glucose, and hence levulose is more useful in 

 determining " hepatic insufficiency " than is glucose. 



Why the kidney should retain the amount of sugar present 

 normally in the blood, yet excrete that which is in excess, is an 

 unsettled question. What seems to be the most simple explan- 

 ation is that the normal 0.1 per cent, of sugar in the blood does 

 not exist free, but is combined partly with lecithin as jecorin, 

 partly with proteids. It is certain that at least part of the 

 sugar is so combined, but we do not know how much. If it is 

 practically all combined, as many believe, we can readily under- 

 stand how the sugar combined with large colloidal molecules 

 could be retained by the glomerular membranes, while the exces- 

 sive uncombined sugar diffused through into the urine. How- 

 ever, recent work by Asher and Rosenfeld 1 throws considerable 

 doubt on the existence of blood-sugar in a non-diffusible com- 

 bination. 



2. NERVOUS GLYCOSURIA 



The classical example of glycosuria due to nervous impulses 

 is that discovered by Claude Bernard, who found that a minute 

 puncture of the floor of the fourth ventricle, between the roots 

 of origin of the eighth and tenth pairs of nerves, causes glyco- 

 suria. This glycosuria begins in about an hour after the punc- 

 ture (piqdre) is made, and lasts only as long as glycogen remains 

 in the liver, for this form of diabetes depends upon the rapid 

 conversion of the glycogen of the liver into sugar. Because of 

 this excessive liberation of sugar, the blood contains more than 

 the normal amount (hyperglycemia), and the excess escapes 

 through the kidneys. If the animal has been starved and exer- 

 cised, so that the glycogen in the liver is reduced to a minimum, 

 no glycosuria is produced. All of the excess of sugar comes 

 from the liver, for if the hepatic vessels are first ligated, no gly- 

 cosuria results from puncture. 



This "diabetic" or " glycogenic center" seems to exist in all 

 varieties of animals, and in man chronic glycosuria has been 

 observed as a result of tumors or other lesions involving this 

 1 Cent. f. Physiol., 1905 (19), 449. 



