(ILYCOdEX I\ I'ATIIOIAXIICAL J'h'OCES.SES 431 



Even the nuclei may contain granules of glycogen without evident 

 permanent injury. 



PATHOLOGICAL OCCURRENCE 



According to the results obtained by Fichera and Gierke, it seems 

 probable that glycogen accumulation is produced under the same 

 conditions as are fatty changes, i. e., when oxidation is locally or 

 generally impaired. Fat and glycogen are, therefore, often found 

 together in the margins of infarcts and of tubercles, in passive con- 

 gestion of the liver, and in heart muscle with fatty changes due to 

 severe anemia. The glycogen, being more labile, seems to disappear 

 early when the cells become necrotic, and hence glycogen is not pres- 

 ent in older necrotic areas where the fat still persists. (This proba- 

 bly accounts for the frequently repeated statement that glycogen and 

 fat do not occur together.) Whether the glycogen can be trans- 

 formed into fat, perhaps forming an intermediary stage in a trans- 

 formation of protein into fat, has not been determined, but there 

 seems to be little doubt that it is infiltrated from outside the cell, 

 and not formed directly from degenerated protein. It seems to be 

 deposited only in cells that are still living, although it can become 

 split up in dead cells. All cells, but especially muscle-cells and leu- 

 cocytes, seem able to lay up glycogen in visible amounts under cer- 

 tain conditions. In inflamed areas glycogen is found in both tissue- 

 cells and leucocytes, but not in cells showing nuclear degeneration 

 (Best, Gierke). In pneumonia the leucocytes of the exudate, and 

 to a less extent the alveolar epithelium, contain glycogen as well as 

 fat. In tubercles glycogen is found in the cells which contain ba- 

 cilli, and it is generally present in the epitheloid cells, rarely in giant 

 cells, not at all in lymphoid cells or in the necrotic elements (De- 

 vaux). Liver glycogen is altered most in poisoning, being reduced 

 by phosphorus, arsenic, chloroform, IlgCU, and many other poisons; 

 the amount is reduced when death from any cause is slow, or when 

 putrefaction has occurred, but it is increased in carbon monoxide 

 poisoning (Massari).^^ In rabbits, at least, it is deposited in the liver 

 first about the central vein, and in fasting animals it disappears first 

 from the periphery-."** 



Glycogen in Tumors. — Glycogen has been observed frequently in 

 tumors. Brault believed the quantity an index of rate of growth, on 

 the principle that glycogen appears most abundantly in embryonal 

 tissues, and therefore in tumors the amount of glycogen should agree 

 with the degree to which the cells have gone back to the embryonic 

 type. Lubarsch considered that only tissues normally containing 

 glycogen give rise to glycogen-containing tumors. Gierke could cor- 



(Cent. f. Bact., Abt. 1, 100,3 (34), 831) found that iiiulpr certain conditions gly- 

 cogen impedes hemolysis by normal serum. 



STGax. degli Ospedali, 1006 (27), .537. 



sslshimori, Biochem. Zeit., 1913 (48), 332. 



