ACETONE BODIES. 819 



and acetoacetic acid during inanition (v. JAKSCH, FR. MuLLER 1 ). This 

 also stands in accord with the observations that a considerable increase 

 in the quantity of acetone and acetoacetic acid eliminated is observed 

 in such diseases as fevers, diabetes, digestive disturbances, mental dis- 

 eases with abstinence and cachexia, where the body protein is largely 

 destroyed. The formation of acetone bodies from protein is also indi- 

 cated by the fact that acetone has been obtained as an oxidation prod- 

 uct from gelatin and protein (BLUMENTHAL and NEUBERG, ORGLER 2 ) . 

 The investigations of EMBDEN and collaborators are more conclusive. 

 After EMBDEN and KALBERLAH showed that the liver is an organ where 

 acetone is formed, EMBDEN, SALOMON and SCHMIDT 3 showed by exper- 

 iments on extirpated livers, that butyric acid, oxybutyric acid, leucine, 

 tyrosine and in fact those aromatic bodies which, like tyrosine, phenyl- 

 alanine, phenyl-a-lactic acid and homogentisic acid contain a combustible 

 benzene nucleus, are transformed, in the liver, into acetone. Research, 

 which has been continued further by EMBDEN and his collaborators 

 and substantiated by others, such as BAER, and BLUM, BORCHARDT 

 and LANGE, NEUBAUER and GROSS, SCHMITZ and FR. SACHS 4 has shown 

 that there can be no doubt that certain amino-acids, especially leucine, 

 are strong acetone formers, and consequently that acetone can be formed 

 from protein. Protamines and histones can also increase the acetone 

 elimination (BORCHARDT) or, as we say, may have a " ketoplastic " 

 action, and it is therefore possible that acetone can be formed from 

 arginine with a-amino-valerianic acid as intermediary step (BORCHARDT 

 and LANGE). 



As we cannot deny the possibility of a formation of acetone from pro- 

 teins, on the other hand we have observations which are inconsistent with 

 the origin of the acetone bodies entirely from the proteins. Thus no par- 

 allelism exists between the acetone bodies and the nitrogen excretion 

 in diabetics, and the fact, that in man no certain relation exists between 

 the acetone elimination and the nitrogen and sulphur excretion, seems to 

 show that the acetone bodies are not entirely derived from the proteins. 

 In man the excretion of acetone does not increase with the rise in the 



1 v. Jaksch, Ueber Acetonurie und Diaceturie. Berlin, 1885; Fr. Miiller, Bericht 

 liber die Ergebnisse des an Cetti ausgefuhrten Hungerversuches. Berlin, klin. Wochen- 

 schr., 1887. 



2 Blumenthal and Neuberg, Deutsch. med. Wochenschr., 1901; Orgler, Hofmeis- 

 ter's Beitrage, 1. 



8 Hofmeister's Beitrage, 8. 



4 Embden, ibid., 11, with Marx, Engel, Lattes and Michaud, ibid., 11; Baer and 

 Blum, Arch. f. exp. Path. u. Pharm., 55, 56, and 62; Borchardt, ibid, 53, with Lange, 

 Hofmeister's Beitrage, 9; Neubauer and Gross, Zeitschr. f. physiol. Chem., 67; Schmitz, 

 Bioch. Zeitschr., 28; Fr. Sachs, ibid., 27. 



