EFFECTS OF CERTAIN DRUGS AND POISONS 749 



has shown in frogs that there is an actual loss of total body fat, that of 

 the phosphorus-poisoned animals when killed being 22 per cent less than 

 that of the controls. There was some increase in the gross weight of the 

 poisoned frogs which Taylor ascribed to edema. 



Shibata confirmed in mammals the diminution of total body fat after 

 phosphorus. 



Rosenfeld(a) (&) confirmed Lebedeff s results and found the blood con- 

 tent in fat increased under phosphorus, thus detecting the material in the 

 stage of transportation to the liver. Leathes(fr) showed that the liver alters 

 the depot fats in certain respects, regarding this as a necessary preliminary 

 to the utilization of the fats in metabolism. Fatty infiltration of the liver 

 would represent an excessive attempt at such a conversion ; it is found in 

 all conditions in which there is a high need for fat (starvation, etc.). If 

 such animals are freely fed, the fatty infiltration of the liver may disap- 

 pear within a day (Mottram(fr)). Rettig has shown that a carbohydrate- 

 rich diet tends to prevent the fatty infiltration. 



Carbohydrate Metabolism. The finding by numerous of the earlier 

 observers that glycogen soon disappears from the liver in phosphorus in- 

 toxication was confirmed by Welsch, Notwithstanding this, glycosuria is 

 a comparatively rare feature; for example, Walko detected sugar in the 

 urine of only 6 out of 141 patients. In these cases it was not associated 

 with -any special degree of severity or other definite feature. The blood 

 sugar as Neubauer, as well as Frank and Isaak, found is, if anything, 

 somewhat decreased. Thus phosphorus poisoning is differentiated from 

 typical asphyxial conditions where glycogen disappearance is regularly 

 associated with hyperglycemia and glycosuria. 



Frank and Isaak regarded interference with the synthesis of 

 glycogen as the primary action of phosphorus. They attributed the in- 

 creased protein destruction to the need of compensation for a low energy 

 production from carbohydrates. 



The lactic acid which accumulates in phosphorus poisoning arises from 

 glucose, as shown by Lusk and Mandel. For lactic acid disappears from 

 the urine as soon as the phosphorus-poisoned dog is treated with phlor- 

 hizin; the glucose is hurried away before the lactic acid can be split off 

 from it. In accord with this Fuerth has shown that the quantity of lactic 

 acid elimination in phosphorus poisoning may be increased by feeding 

 an excess of sugar. 



Increased autolysis, especially in the liver, is regarded as the funda- 

 mental disturbance in phosphorus poisoning by Jacoby, as well as Forges 

 and Pribram. The latter authors attribute this to oxygen deprivation. 

 In this connection, Duncker and lodbauer, as well as Burge, maintain 

 that catalytic activity is somewhat decreased. 



Ishikawa produced alimentary glycosuria early in phosphorus-poisoned 

 rabbits but obtained no hyperglycemia, which fact he attributed to dam- 



