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GLYCOSURIAS. 403
tain. Under all circumstances the sugar puncture glycosuria stands in
close relation to the adrenals and is generally considered as an adrenalin-
glycosuria. The same is true for the glycosuria after splanchnic stimula-
tion and probably for several other forms of glycosuria. In the gly-
cosuria produced by stimulation of the central vagus, according to
Bang, Ljungdahl and Bohm,1
the hyperglycemia (in rabbits) depends
upon an increased destruction of the glycogen of the muscles and not of
the liver.
Many investigators consider the glycosuria appearing after the occur-
rence of dyspncc,2
produced in various ways, and also after certain poisons
such as carbon monoxide, curare, ether, chloroform, strychnine, morphine,
piperidin and others as adrenalin glycosurias. That also in many of
such cases the glycosuria is brought about by an increased glycogen
destruction is not doubted. In certain cases, as in carbon monoxide
poisoning, a formation of sugar has been claimed from protein, because
Straub and Rosenstein 3
found that this glycosuria only occurred in
those animals that had a sufficient quantity of protein at their disposal.
Protein starvation and simultaneous abundant carbohydrate supply cause a
disappearance of this glycosuria.
A hyperglycemia and glycosuria may also be caused by a decreased
ability of the animal to consume or to utilize the sugar or to transform
it into glycogen. In this case the sugar must accumulate in the blood,
and the formation of severe cases of diabetes mellitus is now generally
explained by this process.
The inability of diabetics to destroy .or consume the sugar does not
seem to be connected with any decrease in the oxidative energy of the
cells. The oxidative processes are not generally diminished in diabetes
(Schultzen, Nencki and Sieber), and this has recently been sub-
stantiated by Baumgarten.4 This latter investigator made experiments
with several bodies which on account of their aldehyde nature were
closely related to sugar or were cleavage or oxidation products of it,
namely, glucuronic acid, d-gluconic acid, d-saccharic acid, glucosamine,
1
Hofmeister’s Bietrage, 10.
2
On the importance of the oxygen and the carbon dioxide content of the blood
for the non-appearance or appearance of glycosuria see Underhill, Journ. of biol. Chem.,
1; Penzoldt and Fleischer, Virchow’s Arch., 87; Sauer, Pfluger’s Arch., 49, 425, 426;
Macleod, Amer. Journ. of Physiol., 19, with Briggs, Cleveland Med. Journ., 1907;
Eddie, Bioch. Journ., 1, with Moore and Roaf, ibid., 5; Henderson and Underhill,
Amer. Journ. of Physiol., 28.
3
Straub, Arch. f. exp. Path. u. Pharm., 38; Rosenstein, ibid., 40.
4
Schultzen, Berl. klin. Wochenschr., 1872; Nencki and Sieber, Journ. f. prakt.
Chem. (N. F.), 26, 35; Baumgarten, " Ein Beitrag zur Zenntniss des Diabetes mel-
litus," Habilitationschrift, also Zeitschr. f. exp. Path. u. Therap., 2, 1905.
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