In the case of glycosuria through stimulation of the sympathetic nerve or its ganglia the action may be concluded to be direct. Strangely enough, irritation of the sympathetic between the tenth and twelfth ribs or the splanchnic nerves fails to produce glycosuria, though the hepatic branches of the sympathetic pass through them.
In ordinary cases of reflex glycosuria it may be assumed that the existence of irritation at the peripheral ends of the vagus and of some other nerves, leads to an apparent glycogenic influence passing through these to the brain, and of the distribution of the efferent impulse through the upper portion of the spinal cord, as far as the fourth dorsal vertebra in the rabbit (Cyon, Aladoff, Schiff), and through the sympathetic nerve to the liver. This may account for the appearance of the disorder as a sequel of disease in any part to which the vagus in particular is distributed, and notably in the lungs. A number of poisons (malarial, alcoholic, ether, carbon monoxide, amyl nitrate, curare, or the nitro-propionic acid, methyl delphinin, morphia, chloral hydrate, arsenic, quinia, ammonia, chloroform, phosphoric acid, and phlorizin) produce glycosuria.
The intravenous injection of dilute saline solutions, or frequent blood letting materially increases the sugar, probably by causing solution of the red globules. Phlorizin is the most potent of all these agents. Whether given hypodermically or by the stomach it causes in three hours a marked production of glucose which continues to be eliminated for a period of thirty-six hours. The urine may become charged with glucose to the extent of from 6 to 13 per cent., and without any rise in the body temperature. This artificial glycosuria may be kept up indefinitely by the continued administration of phlorizin, and even in the fasting animal, or one on an exclusively albuminous diet, as well as in those on an aliment rich in saccharine or hydro-carbonaceous matter. In the frog it produces diabetes even after the extirpation of the liver showing that it stimulates other sources of sugar production beside the hepatic or that it inhibits the transformation of sugar derived from the alimentary canal and other sources.
Another suggestive source of mellituria is disease of the lungs, or any condition which interferes with the due æration of the blood and oxidation of the alimentary or hepatic sugar. But it cannot be assumed that the rôle is altogether or mainly chemical. The thoracic organs being supplied by branches of the vagus and sympathetic nerves there is the obvious suggestion of a reflex action through the diabetic centers in the brain. The frequent complication of diabetes with lung diseases (inflammatory, tubercular, syphilitic, and otherwise) is abundantly proved, whether it is to be explained on the above hypothesis or through other unknown changes in the blood.
Diabetes has been repeatedly found in connection with disease of the pancreas, and the complete extirpation of the pancreas in dogs gives rise to glycosuria (Mering and Minkowski, Thiroloix, Lancereaux, Lepine). If a small portion of the pancreas remains glycosuria does not supervene. It has been suggested that the pancreas has a double function, and beside its secretion, produces a glycolytic ferment which passing into the portal blood determines the formation of glycogen in the liver. Arrest of the pancreatic secretions does not cause glycosuria, so it has been suggested that the glycogenic enzyme is a product of the connective tissue cells of the pancreas. Functional as well as structural disease of the pancreas can be conceived of as inhibiting the production of this ferment and the consequent elaboration of glycogen. Chauveau and Kauffmann deduce from their observations that the action is a reflex one established through the glycogenic centres in the medulla. Pancreatic glycosuria is especially fatal (Harley).
Finally extirpation of the thyroid body in dogs has been followed by glycosuria (Falkenberg). This suggests a systematic examination of the urine in all cases of goitre, with extensive glandular changes.
Apart from experimental cases diabetes in the lower animals has been observed to be nearly always associated with diseased liver. Fatty degeneration has been the most frequent lesion, but cirrhosis, hypertrophy and congestion were present in other cases. In a number of cases as the fatty degeneration reached an extreme degree, the sugar disappeared from the urine, the hepatic cells being no longer functionally active, and death speedily followed. The same has been observed in the fatty degeneration attendant on poisoning by arsenic or phosphorus.
GLYCOSURIA IN SOLIPEDS.
Heiss records two cases of this disease in heavy Belgian horses ten and eleven years old, the urine of which showed a percentage of 3.75 of grape sugar, and which died in two months in a state of marasmus. The liver was enlarged and of a clay yellow color. Dieckerhoff reports one fatal case in which there were also yellow discoloration, congestion and hypertrophy of the liver. No lesion could be found in the pancreas nor nervous system. Perosino records a case in a horse suffering from contagious adenitis, which may be supposed to have been connected with the action of the toxins or the imperfectly oxidized albuminoids on the nerve centres or liver. Delprato relates six cases in the same stable in overworked, half starved and emaciated horses. Rueff and Mouquet each contributes a case occurring in paraplegia attendant on hæmoglobinuria and in which the amounts of sugar were respectively 5.85 and 1.01 per cent. These latter cases are manifestly complicated ones in which the reflex irritation (or inhibition of glycogenesis) is transmitted from the diseased or poisoned brain to the already disordered liver.
Symptoms. There is a profound interference with nutrition, a rapid loss of flesh and weight, of spirit and energy and an extreme muscular weakness in spite of an excessive appetite. The subject is fatigued and breathless under the slightest exertion, the flanks are retracted and hollow, and the hair dry, rigid and lifeless. Appetite is poor and fastidious, but an intense and consuming thirst is usually present, the animal drinking deeply at every opportunity, and passing urine with corresponding frequency and abundance. The urine is clear, yellow, neutral, and saccharine, the sugar varying from 1 to 12 per cent. (3.6 on an average). Notwithstanding the amount passed (55 litres per day, Cadeac) the density usually exceeds the normal (1052 and upward), normal being 1040 to 1050. There may or may not be hyperthermia, and in exceptional cases appetite has been retained to the last. Cataract and corneal ulceration are sometimes observed as in man.