402 RETROGRESSIVE CHANGES 



in the postmortem change, adipocere. But it has now been well es- 

 tabhshed that there is no true conversion of protein into fat in the fatty- 

 degeneration produced experimentally by poisoning with phosphorus, 

 etc.,^ and the other supposed instances of fat-formation above cited' 

 have been discredited by various methods which it will not serve our 

 purpose to discuss here, beyond mentioning that one of the chief 

 sources of error Hes in the fact that many fungi and bacteria^ can 

 form fat from protein. 



It having been rendered probable that fat was not formed by dis- 

 integration of the protein of the degenerating cells, it remained to 

 determine what the source of the fat observed in the cells under patho- 

 logical conditions might be, and this part of the problem has been 

 largely cleared up by Rosenfeld. This investigator proceeded as fol- 

 lows: Animals were starved until they were extremely poor in fat, 

 then fed upon easily identified foreign fats, such as mutton tallow 

 (which has a liigh melting-point and can combine with httle iodin) 

 or linseed oil (which has a low melting-point and can combine with 

 much iodin). The animals under these conditions laid up in their 

 fat depots, including the liver as well as the subcutaneous tissues, 

 large quantities of these foreign fats. By starving again for a few 

 days the foreign fat was removed from the liver, leaving still a large 

 amount in the other storehouses, and the animals were then poisoned 

 with phosphorus or other poisons that cause a typical fatty degener- 

 ation of the liver and other viscera. When the fat was extracted from 

 the fatty hver of these animals, it was found that the new fat that 

 had appeared in the liver during the process was not normal dog fat 

 (which it should have been if formed by degeneration of the cell pro- 

 teins), but was, in part, of the same type as the foreign fat which 

 the animals had deposited in their subcutaneous tissues and other fat 

 storehouses. Furthermore, it was found that animals starved to an 

 extremely low fat content do not develop the typical fatty liver of 

 phosphorus-poisoning, a fact which Lebedeff had already noted in a 

 ease of phosphorus-poisoning in an emaciated patient. Of similar 

 significance is the fact that in fatty human livers the iodin number, 

 normally high, falls as the amount of fat increases until it is approxi- 

 mately that of adipose connective tissue.'^ Therefore, it seems evident 

 that the fat accumulating iii the liver during fatty degeneration is not 

 derived, as Virchow thought, through a tJ-ansformation of cell proteins into 

 fat, but rather is an infiltrated fat brought in the blood fro^n the fat deposits 

 of the body to the disintegrating organ. This work has since been corro- 

 borated and extended by many observers, and its correctness can now 



^See Taylor, Jour. Exp. Med., 1899 (4), 399; Shibata, Biochem. Zeit., 1911 

 (37), 345. 



" See Beebe and Buxton, Amer. Jour, of Physiol., 1905 (12j, 466; Slosse, Arch. 

 Internat. Physiol., 1904 (Ij, 348. 



^ Leathes, Lancet, Feb. 27, 1909; Hartley and Mavrogordato, Jour. Path, and 

 Bact., 1908 (12;, 371; Jackson and Pearce, Jour. Exp. Med., 1907 (9), 578. 



