PANCREAS AND CARBOHYDRATE METABOLISM. 929 
stances, its amount, as in the case of phloridziu glycosuria, rises and 
falls with the amounl of uitrogen in the urine (see p. 921), it may 
be assumed that it is derived in these cases also from the splitting of 
proteids. 
The exact amount of the pancreas which it is necessary to leave in 
order to prevent the occurrence of glycosuria cannot he exactly given, 
but a comparatively small amount is sufficient. If somewhat less than 
this minimum be removed, diabetes of a less severe type than that 
following complete removal may occur. There is, however, a tendency 
for it to become more severe in process of time, probably from a certain 
amount of atrophy occurring in the pancreatic tissue which has been 
left. 1 
Cause of pancreatic diabetes. — It appears probable that the pancreas 
exerts its influence upon carbohydrate metabolism, either by promoting 
the formation of glycogen in the liver from the dextrose taken to it by 
the portal blood, or by furthering the oxidation of dextrose in the tissues 
generally. In either case the effect would be the prevention of the 
accumulation of dextrose in the blood, so that the percentage of sugar 
in this fluid would be kept down to its normal, small amount. Whether 
this is brought about by the direct action of the organ upon dextrose 
which reaches it with the blood, or whether it acts indirectly in promot- 
ing the metabolism of dextrose by an internally secreted material, which 
passes out from the organ into the blood and tissues, is a question which 
it is impossible at present to give an answer to. Diabetes which results 
from removal of the pancreas, is not necessarily due to an increased 
glycogenosis from transformation of glycogen (although this is the cause 
of the glycosuria which first makes its appearance), for it will continue 
after the glycogen has completely disappeared from the liver and muscles. 
Moreover, the amount of sugar which is passed is altogether too great 
to be accounted for by the amount of glycogen present in the body. 
Nor is it due to a diminished consumption of sugar by the tissues. 2 
It has been suggested that it is caused by the absence of the glyco- 
lytic ferment, which is described as being usually present in the blood. 
Lepine 3 has supposed that the pancreas forms such a glycolytic ferment, 
which effects the splitting of sugar prior to its oxidation in the tissues. 
But Minkowski 4 has shown that the blood of an animal deprived of its 
pancreas still possesses just as much power of glycolysis as a normal 
animal. Kausch, 5 who succeeded in producing diabetes in ducks and 
geese by pancreatic extirpation, also found that, after removal of the 
liver in the diabetic animal, moderate amounts of sugar were still con- 
sumed in the tissues. Pancreatic glycosuria diminishes or disappears 
during fever. 6 
The symptoms are not allayed by giving raw pancreas with the 
food, as those of thyroidectomy are by feeding with raw thyroid. Nor 
1 Cf. Hedon, Compt. rend. Acad. d. sc, Paris, 1893, tome clvi. p. 649 ; and Thiroloix, 
Arch, dc physiol. norm, etjpath., Paris, 1892. 
2 Kaufmanrj, Compt. rend. Acad. d. sc, Paris, 1894, tome cxviii. p. 656; Arch, de physiol. 
norm, ebpath., Paris, 1896, p. 151. 
3 " Le ferment glycolytique et la pathogenie du diabete, " Paris, 1891. Lepine's theory 
is supported by Vangban Harley (Brit. Med. Jov/rn., London, 27th August 1892), and 
has been criticised by, amongst others, Spitzer (Berl. Mm. Wchnschr., 1894, S. 949). 
4 Arch. f. exper. Path. u. PharmakoL, Leipzig, 1893, Bd. xxxi. 
5 Ibid., 1896, Bd. xxxvii. S. 274 ; and 1897, Bd. xxxix. S. 219. 
6 Kaufmann, Compt. rend. Soc. de biol., Paris, 1896, p. 227. Fever was fcmnd by Poore 
to diminish sugar in natural diabetes (Trans. Clin. Soc. London, 1894). 
VOL. I.— 59 
