CARBOHYDRATES. 99 



tonuria is explained by a decreased decomposition of fat. If large quan- 

 tities of albumin are fed to the organism, the elimination of the acetone 

 bodies is likewise abated. Conversely, if the diet is made to consist of 

 fat with exclusion of carbohydrates, more acetone is formed. Schwarz l 

 observed, moreover, that the blood of diabetics always contains an exces- 

 sive amount of fat. 



For the present, we must leave the question of the source, or, perhaps 

 more correctly speaking, the sources, of the acetone bodies as undecided. 

 We know just as little concerning their place of formation. 



The occurrence of acetone bodies in the blood has for a long time been 

 considered to have considerable significance concerning the course of 

 diabetes. It has been assumed that the presence of acids decreases the 

 alkalinity of the blood, and thus brings about severe disturbances. This, 

 is, in general, not the case, because the organism can form ammonia which 

 by combining with acids keeps the reaction of the blood, and thereby that 

 of the tissues, within normal limits. The fact that the interchange of 

 oxygen is not materially altered during the elimination of considerable 

 amounts of these aldehyde bodies, speaks in favor of this assumption. 

 Sometimes, however, there takes place a rapid formation of large 

 amounts of these acetone bodies, resulting in considerable injury to the 

 whole organism, namely in coma diabeticum. By this name is meant a 

 complex of symptoms which very often occurs, in case intercurrent disease, 

 has not carried off the patient, at the period near the death of the diabetic. 

 The condition is characterized by progressive dyspnoea, somnolence, and 

 sinking of the body-temperature. In many cases the patient recovers, 

 the acetone bodies are again eliminated in the urine, and the organism has 

 time to combat the acid by the formation of ammonia. After some time 

 the symptoms reoccur with increased severity, until finally the patient 

 dies as a result of such an attack. The first explanation of this was in 

 attributing a specific poisonous action to the acetone bodies. This is, 

 however, as direct experiments with the separate substances has shown, 

 not the case. 2 Obviously we have here a true instance of acid poisoning. 

 The blood and tissue react acid after a diabetic has died in coma. There 

 takes place, together with this change in the reaction of the blood, a diminu- 

 tion in the processes of oxidation. The /?-hydroxy-butyric acid is no longer 

 oxidized to acetoacetic acid, or at least only to a slight extent. Both of 

 these acids unite with the free alkali in the blood. This explains the fact 

 that the amount of carbonic acid in the blood sinks during the coma. The 

 fact that there is less oxidation in the organism during this period is proved 

 by the fact that various products of the hydrolysis of albumin are now 



1 Deut. Arch. klin. Med. 76 (1903). 



J F. T. Frerichs: Z. klin. Med. 6, 3 (1883). P. Albertoni: Arch, exper Path. 

 Pharm. 18, 218 (1884). Stadelmann: ibid. 17, 419 and 443 (1883). 



