772 URINE. 



In regard to the origin of these bodies it was formerly considered that 

 they were produced by an increased destruction of protein. One of the 

 various reasons for this was the increase in the elimination of acetone 

 and acetoacetic acid during inanition (v. JAKSCH, FR. MULLER*). 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 product 

 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, BLUM, BORCHARDT and 

 LANGE, 4 has shown that there can be no doubt that leucine in par- 

 ticular is a strong acetone former, and consequently that acetone can be 

 formed from protein. Prot amines and hist ones 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 



Stoffwechsels. Berlin, 1906, and for recent work, Magnus-Levy, Die Azetonkorper, 

 Ergbn. d. inn. Med. u. Kinderheilk., I. 



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

 iiber 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. 



1 Hofmeister's Beitrage, 8. 



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

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

 Hofmeister's Beitrage, 9. 



