6-46 DI ABET EH 



H H H H on OH Oil 



I I I I I I I 

 IT— C— OH C=0 0=0 H— C— OH C=0 C=0 0=0 



II I I I I I 

 H— C— on H— C— OH HO— ( — H C'=0 H— C— OH H— C— OH HO— C-H 



II I i I I I 



H— C— Oil H— C— OH H— C— OH H— C— OH H— C— OH H— C— H IT— C— H 



I I I I I I I 



H TT II H H H H 



Glycerol dglycerio l-glyceric dihydroxy d-glyceric d-lactic acid. 1-lactic acid. 



aldehyde aldehyde acetone acid ' ■: ' 



(alcohol) (aldose) (aldose) (ketose) 3-carbon saccharinic 



acid. 



Neuberg fed animals and men considerable doses of impure d,l- 

 o-lycerie aldehyde (glycerose) and saw its apparently complete util- 

 ization. Parnas demonstrated increased glycogen in tortoise livers 

 perfused witli d,l-glyceric aldehyde. Smedley noted the rapid dis- 

 appearance of glyceric aldehyde added to liver emulsions. Sansum 

 and AVoodyatt fed pure crystalline d,l-glyceric aldehyde to rabbits 

 and guinea pigs in doses as high as 2.8 gm. per kg. with no apparent 

 ill effects. A dose of 5 gm. per kg. in a rabbit caused diarrhea with 

 unchanged triose in the passages. There was marked diminution of 

 urine with albuminuria, which then persisted for 10 days. A dose 

 of 6.8 gm. per kg. killed in 4 hours. In no case was there an alimen- 

 tary triosuria. The average lethal dose hj the subcutaneous route was 

 2.2 gm. per kg. as compared with 18 gm. of glucose per kg. in the 

 same set of animals. Suppression of urine is a regular manifestation, 

 but the visceral changes at autopsy are slight. AVhen d,l-glyeeric 

 aldehyde is injected intravenously at the rate of only 0.15 gm. per kg. 

 per hour, and possibly at slower rates, unchanged glyceric aldehyde 

 appears in the urine, but no glucose. ( It will be recalled that glucose 

 may be injected continuously at the rate of 0.8 gm. to 0.9 gm. per kg. 

 per hour without causing glycosuria.) When administered to diabetic 

 individuals d,l-glyceric aldehyde may increase glycosuria. AVhen 

 given to completely phlorhizinized and glycogen-free dogs it is pos- 

 sible to demonstrate a quantitative conversion of the triose into glucose, 

 the increase in glycosuria corresponding exactly with the weight of 

 glyceric aldehyde given. However, owing to the toxic effects of gly- 

 ceric aldehyde on the kidneys there may be an incomplete excretion 

 of all the sugar formed. The suppression of urine has in the past 

 been mistaken for a beneficial effect, since it may lead to diminished 

 excretions of sugar, acetone, aceto-acetic and /J-hydroxybutyric acids. 



Einbden and his coworkers demonstrated the formation of lactic 

 acid from glyceric aldehyde added to washed blood corpuscles. The 

 keto-triose, dihydroxyacetone, was observed to produce less lactic acid, 

 but otherwise it is not improbable that the behavior of the ketotriose 

 is analogous to that of the aldo foi-ms. Thus AFostowski found dihy- 

 droxyacetone to be a glycogen forinei-. and Kingei- "'' reported its com- 



iiKingcr and Fraiikol, Jour. V,\o\. ( licm., \\n\ (18), 233. 



