Minkowski1 noted that the livers of his depancreatized dogs were free from glycogen, and this fact has been confirmed by other observers. He also found that when fructose was given glycogen could be stored.

Verzar2 has reported that the dog does not completely lose its power to oxidize glucose until the fourth day after pancreatectomy. Intravenous injection of a 10 per cent, glucose solution sufficient in quantity to raise the blood-sugar from 0.3 to 0.9 per cent, did not thereafter affect the respiratory quotient. During the first seven days, however, injection of fructose was able to raise the respiratory quotient, though on the twelfth and twenty-first days the administration of fructose was also without effect on this quotient. One may interpret the work as indicating that on the fourth day the organism lost the power to split glucose, whereas the ability to break fructose into oxidizable trioses or methyl-glyoxal remained intact. Later, the power to oxidize the three carbon atom chains was also lost, though the power to produce them and reconstruct them into glucose was preserved. There is no evidence existing which proves that sugar in order to be oxidized must first be converted into glycogen. That the diabetic liver cannot form glycogen from glucose appears from the experiments of Epstein and Baehr,3 who performed pancreatectomy and double nephrectomy upon a cat which had fasted nine days. The blood-sugar, which before the operation had been 0.06 per cent., rose to 1.1 percent, forty-eight hours after the operation, at which time the animal was killed. The liver proved to be free of glycogen and the muscle contained only 0.06 per cent, of the substance.

Glycosuria which follows exposure to cold, as originally observed by Araki,1 is very likely due to the asphyxial element brought about by vasoconstriction.

1 Minkowski: hoc. cit.

2 Verzan "Biochemische Zeitschrift," 1914, lxvi, 75.

3Epstein and Baehr: "Journal of Biological Chemistry," 1916, xxiv, 1.

Bohm and Hoffmann2 report that a dog barking at a cat induces glycosuria in the cat. Cannon and de la Paz3 term this "emotional glycosuria," and have found that the cat's blood contains an increased quantity of epinephrin as a sequence to the fright. This increased amount of epinephrin becomes the exciting cause of dilatation of the pupil, inhibition of the movements of stomach and intestines, acceleration of the heart, erection of the hairs on the back and on the tail, and the discharge of glycogen.

Cannon has elaborated these results and presented them in the form of a popular book which holds that emotional impulses act upon the adrenals, causing them to discharge epinephrin, which, in turn, mobilizes the physical and chemical resources of the body for supreme mechanical effort in both attack and defense.

Tying down a frightened rabbit to a board results in psychic glycosuria, the blood-sugar rising to 0.4 or 0.5 per cent, and the urine containing as high as 7.8 per cent, of sugar.4

The urines of 34 men and of 36 women students were tested by Folin5 before and after college examinations: 6 men and 6 women showed small but unmistakable traces of glycosuria immediately after examination. This further illustrates the phenomenon of emotional glycosuria.

Alimentary glycosuria is seen in normal animals and in man when sugar is given in larger quantities than the glycogen regulatory function can care for. Moritz6 found 2 grams of glucose in the urine of a man after the ingestion of 200 grams. Such an alimentary glycosuria lasts between three and six hours.

1 Araki: "Zeitschrift fur physiologische Chemie," 1892, xvi, 454; see also Wacker: Ibid., 1910, lxvii, 197.

2 Bohm and Hoffmann: "Archiv fur exp. Path, und Pharm.," 1878, viii, 280.

3 Cannon, Shohl, and Wright: "American Journal of Physiology," 1911, xxix, 280.

4 Hirsch and Reinbach: "Zeitschrift fur physiologische Chemie," 1913, lxxxvii, 122.

5 Folin, Denis, and Smillie: "Journal of Biological Chemistry," 1914, xvii, 519.

6Moritz: "Verhandlungendes ioten Congresses fur innere Medizin," 1891, p. 492.

Moritz1 observed 0.2 to 0.3 per cent, of sugar in the urine of 4 out of 6 healthy people who had partaken of a quantity of sweets and champagne.

Evidently such conditions as these are not to be classed with diabetes mellitus, where there is a fundamental disturbance in the sugar-burning power in the organism. It would be of service to distinguish between glycosurias where the sugar-holding capacity of the organs has been diminished or overstrained, and the glycosuria of diabetes in which the sugar-burning capacity has been affected. For example, Kleiner and Meltzer2 injected intravenously 4 grams of glucose per kilogram of animal into both normal and depancreatized dogs. The blood-sugar rose greatly in both groups of animals, but in the normal animals there was a rapid readjustment through elimination by the kidney, glycogen retention, and oxidation of glucose, whereas in the depancreatized animals, though removal of the glucose by the kidney was active, the other two functions were in abeyance and the blood-sugar continued at a high level long after it had readjusted itself in the normal animals.

A special type of glycosuria is caused by phlorhizin3 injections, as was discovered by von Mering.4 Here the blood itself while passing through the kidney loses the power of retaining its normal sugar content and a hypoglycemia results. Sometimes when the kidney is altered in B right's disease phlorhizin is ineffective and no glycosuria follows its administration. The renal character of phlorhizin glycosuria was demonstrated by Zuntz,5 who placed cannulae in the upper portions of the two kidneys and injected phlorhizin into the renal artery of one. On the injected side sugar-containing urine appeared in two minutes, and three minutes later the kidney on the opposite side yielded sugar through its ureter. The delay was due to the lapse of time necessary for the transportation of the phlorhizin by the blood-stream from the injected kidney to the other one. In this form of glycosuria sugar ingested per os, or subcutaneously, or as formed in protein metabolism, is all eliminated in the urine.1

1Moritz: "Deutsches Archiv fur klinische Medizin," 1890, xlvi, 217.

2 Kleiner and Meltzer: "American Journal of Physiology," 1914-15, xxxvi, 361.

3 Lusk: "Phlorhizinglukosurie, Ergebnisse der Physiologie," 1912, xii, 372.

4 von Mering: "Verhandlungen des 5ten Congresses fur innere Medizin," 1886, p. 185.

5Zuntz: "Archiv fur Physiologie," 1895, p. 570.