At different times the carbohydrates, the pro teids and the fats have all been considered the mother substances of the acetone bodies. The old view that acetone is a product of the fermentation of carbohydrates in the intestine must be considered invalid in the light of what we know nowadays in regard to the effect of the carbohydrates on the excretion of acetone bodies. Still another assumption is improbable a priori, namely that the excretion of acetone bodies is due to the abnormal disassimilation of body carbohydrates occurring whenever there is a deficiency of carbohydrates in the food. The chief arguments against this view are certain observations that have been made in diabetic subjects, for it is a well known fact that the latter, as soon as the tolerance for proteids and carbohydrates increases, not only excrete less sugar but also less of the acetone bodies; in other words, act in this respect exactly like healthy subjects who are living on a meat-fat diet and who receive carbohydrates in sufficient quantities.

Until very recently the idea was generally prevalent that the proteids were a source of the acetone bodies. The reason for this was the observation that acetonuria was common when there was much catabolism of proteids. A leading argument against this view, however, was the fact that acetone and B-oxybutyric acid were also frequently excreted when the metabolism of the proteids was normal or even abnormally low. Another idea, namely that acetonuria, etc., was the result of the degradation of the body proteids (Honigmann, von Noorden) was advanced at one time but had to be abandoned as soon as careful metabolic studies were made in diabetic subjects, in whom it was found that proteids might be retained and at the same time B-oxybutyric acid be continuously excreted in the urine. (Weintraud, Magnus-Levy, numerous observations by von Noorden.) Some time prior to this Minkowski advanced the theory that the acetone bodies might be due to some qualitative perversion of proteid metabolism, in the sense, namely, that the nitrogenous end products of this catabolism would be normal, but that the catabolism of those parts of the molecule that contained no nitrogen proceeded along abnormal paths so that B-oxybutyric acid, etc., were the result.