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plt'tc 1 1'aiist'oi'iiiat ion into glucose in tlic i'ull\- plilorliizini/.cd (1(»<j:. 

 The complete conversion of d,l-glyceric aldehyde into glucose in 

 phlorhizinized dogs — its transformation into glycogen in the perfused 

 liver, its disappearance as such when added to liver emulsions, all 

 indicate that glyceric aldehyde (like diose and other sugars in gen- 

 eral) is converted into glucose in the body as a preliminary step in 

 utilization. The fact that large doses may be given by the alimentary 

 route without causing melituria or death, whereas much smaller doses 

 given subcutaneously may prove lethal, together with the very low 

 rate at which glyceric aldehyde has to be given by vein in order not to 

 produce melituria, all point to the liver (and bowel wall) as the chief 

 sites of its conversion. Glj-ceric aldehyde has figured prominently in 

 theories of the normal catabolism of glucose, and on the basis of his 

 observations concerning the formation of lactic acid from this triose 

 by blood corpuscles Embden regards it as a chief normal intermediate 

 substance in the oxidation of glucose in the cells. Now glucose may 

 be oxidized in the body at the rate of 0.6 gm. per kg. per hour under 

 suitable circumstances, and if eveiy molecule of glucose oxidized were 

 first split to give two molecules of glyceric aldehyde, as the Embden 

 hypothesis would demand, then glyceric aldehyde would be formed 

 in the body at the rate of 0.6 gm. per kg. per hour, and the place of 

 formation would be within the cells of the body at large, the muscles 

 representing the most important sites of oxidation. However, if 

 glyceric aldehyde is introduced into the systemic blood at only one- 

 fourth of this rate, unchanged triose appears in the urine and may be 

 demonstrated in the blood. But glyceric aldehyde has never been 

 found in the blood, urine or tissues under any other circumstances. 

 Olyceric aldehyde may of course enter the body via the portal route 

 at faster rates without causing triosuria, but then, as stated, it would 

 appear not to be oxidized directly but first assimilated, i.e., trans- 

 formed into glucose. Recently, for other reasons, von Flirth ^" has 

 also questioned the tenability of Embden 's hypothesis. 



Lactic acid from triose: \\'lien alkali acts on (rlncose (or licxoscs in srcTieraH 

 in the absence of oxycren, lactic acid is formed in amounts as hipli as 40 to 60 

 per cent, of the weifrlit of the sugar used, provided the conditions are propcrlv 

 controlled. Hut in tlie y)resence of sufficient oxyiren no lactic acid is formed. 

 Still, ]n-cformed lactic acid will not be destroyed if it is added to this latter 

 mixture. So it is clear that lactic acid is not an intermediate in the oxidative 

 breakdown of su<iars in the alkaline solution. Meisenlicinicr accord<nurly sutr- 

 gested the obvious prol)ability that there was some labile i)rccursor i>f lactic 

 acid which burned in the presence of oxy<ren : in the absence of oxyfren, rearranged 

 to give lactic acid. He proposed glyceric aldehyde as such a body. Xef. how- 

 ever, holds that the immediate precursor of lactic acid is methyl glyoxal 

 (CH3 — CO — COH). which forms lactic acid bv undergoing what is known to 

 chemists as a "henzilic acid rearranuenient."' These phenomena are remarkably 

 similar to those that occur in tlie body. 



One other important point should be emphasized in this place. The trioses 

 condense in the i)resence of alkali to yield among other things certain hexoses. 



iTBiochem. Zeit.. 1916 (69), 199. 



