A small amount of glycogen is also produced habitually by the white blood cells and stored up in them, but this is insufficient to determine its appreciable elimination by the kidneys.
In cases of persistent glycosuria the fault may be held to consist in one of three functional derangements:
1st. The failure of the liver to transform the alimentary sugar into glycogen.
or 2d. The excessive production of glycogen in the liver.
or 3d. The arrest of the destructive oxidation of sugar in the lungs and tissues.
In a diabetic patient who died suddenly of apoplexy Bernard found that the liver was enlarged, comparing with the average as 25:14 while the contained sugar bore the ratio of 37.5:22. This enlargement coming from malaria or other poison, such as alcohol, ether (Harley), arsenic, quinia (Aitken), ammonia, chloroform, or phosphoric acid (Murchison), is an established condition of glycosuria. A rich and abundant food (starchy and saccharine especially), or an unusually active hepatic circulation acts in the same way.
Bernard as early as 1849 showed that the glycogenic function of the liver was greatly increased and glycosuria determined by pricking the floor of the fourth ventricle in the median line just in front of the calamus scriptorius and near the root of the vagus nerve, or a few millimeters in front of this.
It follows that irritation of this part of the medulla however produced, whether from local disease, or by reflex action from some distant organ in a state of irritation, may serve as the starting point of diabetes in particular instances. That the cause may be a reflex stimulus is shown by the suspension of the glycogenic function after section of the vagus nerves, and its reappearance when the central end of the cut vagus is galvanized, or, the floor of the fourth ventricle is irritated, the direct or efferent excitation being transmitted through the sympathetic nerve (Bernard). I can cite a case of glycosuria in a man supervening on a severe blow on the head from a falling ledger. Brain injuries which suspend animal functions, but not the nutritive ones, such as apoplexy, concussion of the brain or curare poisoning are liable to induce diabetes.
Traumatic injuries to other parts of the nervous system induce glycosuria. Thus traumatism of the optic thalami; of the cerebral lobes or peduncles; of the pons; of the cerebellum or of its middle or posterior peduncles; transverse section of the medulla or of the spinal cord opposite the second dorsal vertebra; traumatism of the superior or inferior cervical ganglion or the first thoracic (Eckhard); of the sympathetic twig which accompanies the vertebral artery (Pavy); of the brachial plexus; of the solar plexus (Munck, Klebs); or of the sciatic nerve (Schiff).
The explanation of these facts may be sought in a reflex action established by the conveyances of irritation to the true glycogenic centres in the brain and the transference of the efferent nervous impulse through the sympathetic nerve to the liver. It will be borne in mind that in the case of section of the vagus nerve electric stimulation of its detached peripheral part has no glycogenic effect on the liver, while galvanizing the central portion determines glycosuria.