On the supposed existence of efferent fibers from the diabetic center to the liver

To explain the causation of those forms of glycosuria which follow stimulation of the central end of sensory nerves and piqÛre of the medulla, it is commonly believed that there is a diabetic center in the medulla from which efferent impulses are transmitted to the liver causing the glycogen in this organ to become so rapidly converted into dextrose that hyperglycemia and glycosuria follow. Since section of the vagi does not prevent these forms of glycosuria, it is thought that the efferent impulses travel by the upper portion of the spinal cord and the greater splanchnic nerves.

That increased production of dextrose by the liver is the immediate cause of the glycosuria, there is no doubt, but the evidence that it is by nervous impulses transmitted from the medulla to the liver along the above path that this hyperglycogenesis occurs is very meager.

The evidence in favor of such a view is as follows:

1. Puncture of the floor of the fourth ventricle does not cause glycosuria if the splanchnic (greater) nerves, or the upper thoracic spinal nerves, or the spinal cord above the first thoracic nerves be cut (Eckhard, Marc Laffont, etc.).

2. Irritation of the cervical spinal cord, or of the upper thoracic sympathetic ganglia causes glycosuria (Pavy, Schifi).

Against such a view stands the fact that stimulation of the splanchnic nerves does not cause glycosuria (Cf. Pflüger).

As has been shown by us, and by other workers, the reducing power of the urine of dogs is, within certain limits, 110 index of the amount of sugar in the blood. Now, very little of the above evidence is based on observations of the amount of sugar in the blood, this being assumed to be increased whenever the urine strongly reduces.