omais OF THE acetone bodies 555 



The studies of Knoop,'" and his associates have indicated that 

 ill the catabolisni of fatty acids, the chains are bi'okeii (hjwn by 

 oxidation of the cafboii atom lliii'd ffoiii tlic ciid, tliat is, the 

 ^-position, and the two end carbon atoms are tlien split off. Tliere- 

 fore, two carbon atoms are always split off at a time, and hence every 

 fatty acid wliich contains an even numl)er of carl)ou atoms can l^e 

 oxidized into oxybntyric acid, which includes the ordinary fatty acids 

 (oleic, palmitic and stearic) of fat tissue, which have each an even 

 number of carbon atoms (16 or 18), and also butyric, caproie and sim- 

 ilar acids. Normal fatty acids which contain an odd number of car- 

 bon atoms cannot yield oxybutyric acid. However, according to A. 

 Loeb,*' aceto-acetic acid may be built up from acetic acid in the 

 liver, and the urine in diabetes may contain acetic acid. "The for- 

 mation of oxybutyric acid and of diaeetic acid in all these cases may 

 be said to be due to the fact that the diabetic oroanism is not able 

 quite to finish the attack on the beta-carbon atom of butyric acid" 

 (Folin). 



From the results of tliese studies it seems that the acetone bodies 

 can, theoretically be formed from any of the three classes of food- 

 stuffs, but that ordinarily they come chiefly from the fats, and in 

 severe diabetes also to considerable extent from fatty acids formed 

 hy deaminization of amino-acids. Although it is probable that the 

 acetone bodies are formed in many if not all tissues, yet there is 

 abundant evidence that the liver plays an important part in ketogene- 

 sis, as shown by the decrease in acetone bodies in Eck fistula dogs, and 

 their great increase when the blood supply of the liver is augmented.*^ 



In addition to the sources of acidosis substances from metabolic proc- 

 esses, as outlined above, it is also possible that they may be derived 

 from organic acids formed by bacterial action in the alimentary canal, 

 as emphasized by Palacios.^*'' 



Sarcolactic Acid often is found in the urine, but in origin and sig- 

 nificance it is entirely different from the acetone bodies, and it prob- 

 ably is never present in sufficient amounts to cause an acid intoxica- 

 tion by abstraction of alkalies from the blood. //( vitro, we obtain 

 sarcolactic acid whenever sugar is placed in an alkaline solution, 

 provided the supply of oxygen to the solution is deficient: but if the 

 oxygen supply is adequate, sugar will not yield lactic acid with alka- 

 lies (Nef). Similarl}', an isolated surviving muscle, when asphyxi- 

 ated by any means, shows a rapid accumulation of lactic acid, which 

 fails to occur when sufficient oxygen is supplied. This lactic acid 

 comes chiefly from sugar, but about 25 to ;30 per cent, of it can have 

 it:; origin in protein (or fat?) (Woodyatt). If an organism as a 



40 Full bibliofirraphy and discussion by Porges. Frsjcbnisse Physiol.. 1010 (10), 

 G. See also Rinfrer, Jour. Piol. (hem., 1!)1.3, Vol. 14. 

 4V Biochem. Zeit., 1012 (47), US. 



48 Fischer and Kossow. Dent. Arch. klin. INfed.. 101.3 (101). 470. 

 48aAmer. Jour. Med. Sci., 1015 (149), 267; Med. Eecord. starch 25, 1916. 



