This shows that in diabetics acetonuria occupies a peculiar position, although on the other hand it is true that in many diabetics the same factors seem to influence the excretion of acetone as in healthy subjects. Wherever we find these peculiarities in diabetic subjeets it is not so much the quantity of carbohydrate that is disassimilated as the manner in which the carbohydrates or the fats are disassimilated that determine the special features. If we understood what phase of carbohydrate metabolism determines the oxidation of acetone, we would understand the abnormalities better. Unfortunately, however, we know nothing about this. We know, however, that in diabetics the perversion of the carbohydrate metabolism may be manifold, for there may be, first, interference with the oxidation of the carbohydrates; secondly interference with the power of the body to form fat from carbohydrates; third, interference with the power of the organism to form glycogen from the carbohydrates and to store it. We are not justified in assuming that in all cases of diabetes these three perversions of metabolism are developed to the same degree. On the contrary, there is much evidence to show that these three anomalies of function, any one of which may lead to glycosuria, are more or less indepen dent of one another (see the hypothesis of VonNoorden on diabetogenous obesity). The question now arises, which one of these functions is concerned with the oxidation of the acetone bodies. This question we cannot answer. We can very well imagine, however, that the degree of acetonuria varies if one or the other or all of these functions are perverted. This view would explain the fact that certain diabetics, although they are living on the same diet and are excreting the same amount of sugar, still produce different quantities of acetone, and that many diabetics, even though they do not excrete any sugar, nevertheless excrete much more acetone than a healthy subject living on the same diet.

One other possibility must be considered in this connection, viz.: - the tendency of diabetics to produce quantities of the acetone bodies that are much greater than those excreted by healthy subjects or by patients suffering from any other pathological condition, may also be due to abnormalities of the fat me tabolism. We do not refer to the increased disintegration of fats that is so common in diabetes, for this factor, according to universal experience, could only explain the excretion of moderate quantities of acetone but not the excretion of the enormous quantities of acetone bodies that severe cases of diabetes frequently eliminate. We refer, moreover, to those qualitative differences in the catabolism of the fats, that von Noorden first mentioned. For we have much clinical evidence to show that in severe cases of diabetes carbohydrates can be formed from fatty acids; the chemical formula for this conversion, it is true, is still lacking.

This leads us to the question of intermediary metabolisma field that is obscure and more or less hypothetical.

Generally speaking, the following statements can be made in regard to diabetic acetonuria (the excretion of acetone bodies).

Diabetic acetonuria in general follows the same laws as acetonuria in non-diabetic subjects, i. e., it may be attributed to insufficient utilization of the carbohydrates. Whereas, however, the relation between the carbohydrate metabolism and acetonuria in healthy subjects (a few peculiarities excepted) is due to quantitative disturbances, it is due in diabetics to qualitative changes in the metabolism of the fats and carbohydrates.