According to the oldest views, acetone is formed in the intestinal tract from the decomposition of the carbohydrates. The so-called intestinal form of acetonuria and the fact that so-called acetone autointoxication is often accompanied or preceded by gastro-intestinal disorders seem to favor this view. It is true that several investigators have succeeded in finding acetone in the stomach and the intestinal secretions of such patients and that quite recently Magnus-Levy even succeeded in finding B-oxybutyric acid in the gastric contents. The quantities found in the gastro-intestinal tract are, however, so small in comparison with the quantities found circulating in the blood that one is hardly justified in postulating that the acetone bodies are formed in the stomach and intestines. It is much more feasible to assume that per contra these bodies are excreted into the intestine from the blood. The fact, in addition, that thorough cleansing of the gastro-intestinal tract by laxatives, does not decrease the acetonuria (F. Müller-Lüthge) and that this procedure occasionally even increases the amount of acetone in the urine of diabetics (von Noorden) militates against the enterogenous origin of this substance. Very recently, J. Müller has again pointed to the gastrointestinal tract as the source of the acetone bodies.

He based his view on the discovery that sugar given by mouth reduces the amount of acetone, whereas sugar administered as a clysma or subcutaneously, does not exercise this effect. In addition he demonstrated that fatty acids introduced subcutaneously did not increase the acetonuria, and this too he considers an argument in favor of his view. Neither of these arguments, however, is altogether correct. The amounts of sugar introduced subcutaneously or per rectum are altogether too small. Although J. Müller has undoubtedly proceeded with the greatest care, one can nevertheless imagine that less carbohydrate enters the circulation than is necessary to produce a reduction of the acetonuria. We know from recent respiration experiments (by Reach) that the absorption of carbohydrates is less complete from the intestine than from the stomach, and that consequently the body receives less carbohydrate through the former channel.

The same applies to sugar that is introduced subcutaneously or the fatty acids that are introduced in the same way. Of the latter we do not even know whether they are at all burnt up or whether they are excreted unchanged. At all events, both substances are absorbed into the circulation much too slowly, and much too little of them, moreover, is present in the circulation during each time unit to allow us to conclude that they could be capable, when introduced subcutaneously, of exercising any appreciable effect upon the formation of acetone. The fact, moreover, that such enormous quantities of acetone bodies are excreted in the former case speaks decidedly against the enterogenous origin of this body. All the facts of the case, therefore, particularly when combined with the arguments given above, point definitely to intra-cellular processes. It is of course impossible to determine for the present whether or not all the organs of the body participate in this process. Magnus-Levy, however, discovered that B-oxybutyric acid was a product of the autolysis of the liver, and his observation may, therefore, possibly be considered an argument in favor of the view that the liver has something to do with the formation of acetone bodies.