6io THE CHEMISTRY OF THE URINE. 
in the bowel, some may be absorbed, not by the ordinary path of the capil- 
laries and portal vessels, but by way of the lacteals and thoracic duct, thus 
escaping the influence of the liver. The percentage of sugar in the blood is 
thereby increased, and the excess is excreted by the kidneys. A distinction 
between such cases and those in which diabetes exists, is seen in the fact that 
the " alimentary glycosuria " is not produced by starchy foods, however large 
the quantity taken, but only by excess of ready-formed sugar in the diet. 1 
According to Moritz, dextrose, lsevulose, cane-sugar, and probably milk-sugar, 
may all appear unaltered in the urine when severally taken by the mouth in 
considerable quantity (e.g. 200 grins.). Such alimentary effects last from 
three to six hours. - 
Pathological glycosuria. — The great increase of dextrose in the urine 
of diabetes is a familiar phenomenon. Its excretion may range in this disease 
from quite small quantities up to 500 or 600 grins, per diem. The morning 
urine is apt to contain least sugar; that passed three or four hours after a 
meal generally contains most. 
In other diseased conditions, quite apart from diabetes, a special tendency 
has been observed to the occurrence of an alimentary glycosuria ; gout, 
exophthalmic goitre, and certain nervous diseases may be instanced. An 
increase of reducing substances, almost certainly consisting at least in part of 
dextrose, is said to be found in the urine of some pyaemic conditions. As the 
effect of certain drugs and toxic substances, such as chloral, chloral amide, 
morphine, hydrocj'anic acid, turpentine, and carbon monoxide, the urine 
commonly reduces copper solutions ; but in most of these cases the reduction 
is due to conjugated compounds of glycuronic acid, and not to dextrose 
(vide p. 613). 
The detection and estimation of dextrose, which, as we have seen, have 
proved difficult problems in the case of the minute amount normally present 
in urine, become easy when the increased amount excreted in disease is to be 
dealt with. The methods used depend upon the reducing power which the 
sugar exerts upon metallic salts, or upon certain coloured organic substances, 
and these may be checked by the fermentation of the suspected urine by 
means of yeast, by the indications of the phenylhydrazine test, and again by 
the use of the polariscope. Of reduction tests a great number have been 
proposed ; we shall here refer to two only. The well-known Fehling's test 
consists of a solution of copper sulphate of definite strength, mixed with caustic 
alkali and alkaline tartrates (Rochelle salt). The presence of the last pre- 
vents the precipitation of cupric oxide when the solution is boiled by itself, 
but allows the precipitation of yellow or cuprous oxide when reduction has 
occurred from the action of the sugar. The reduction may be observed, 
after boiling the liquid, if the urine contain not less than 0'2 per cent, of 
dextrose. If less than about 0'5 per cent, be present, no precipitation occurs 
until after cooling, when the liquid becomes opaque, and of a greenish colour. 
With larger amounts a definite precipitate of a yellow or red colour is seen, 
immediately after heating the test with a small proportion of the urine. 
Nylander's solution has some advantages over Fehling's, in that it is much less 
affected by creatinin, urates, and reducing bodies other than sugar (vide supra). 
It is a modification of the bismuth test, originally suggested by Botteher, and 
is prepared with the same reagents as Fehling's solution, but with the sub 
stitution of basic nitrate of bismuth for the copper sulphate. On boiling this 
solution with urine containing sugar, the liquid turns black. The reaction is 
easily seen if 0T per cent, or upwards of dextrose is present. 
Both solutions are reduced by lactose and by glycuronic acid ; but the 
former of these substances can only be present under special circumstances 
1 Of. jSTeumeister, " Lehrbucli der physiol. Chem.," Th. 2, S. 306. 
-Moritz, Centralbl. f. klin. Med.. Bonn, Bd. xii. No. 28. 
