CAUSES OF FATTY METAMORPHOSIS 341 



areas the intracellular oxidases cannot destroy these substances 

 as they normally do, because of lack of oxygen. The accumu- 

 lation of fat in dead areas depends, therefore, on the fact that 

 the constituents of fat can diffuse into the dead tissue, whereas 

 the oxygen, being held in the corpuscles, cannot enter the 

 anemic area. 



It is to be supposed that poisons also cause fatty degenera- 

 tion in a similar way by interfering with oxidation. We have 

 much evidence that in phosphorus, chloroform, and other poison- 

 ing associated with fatty degeneration of the liver, oxidation is 

 impaired. 1 If we imagine for a moment, a cell in which oxida- 

 tion is checked by any means, we shall have in this cell the 

 lipase and the proteolytic enzymes not balanced, as they nor- 

 mally are by the action of the oxidases, and hence the processes 

 of cell autolysis and of the accumulation of fat by the lipase 

 will go on uncontrolled. The result will be a disintegrated 

 cell containing many fat-droplets, i. e., fatty degeneration. 2 



Summary. Fatty metamorphosis involves changes of two 

 kinds. First, infiltration of fat, which occurs when the oxi- 

 dative power of the cells is decreased, so that fat is not des- 

 troyed, but is accumulated from the blood under the influence 

 of the lipase of the cells ; if there is not any serious injury to 

 the cells, the histological changes consist in the accumulation of 

 one or a few large droplets of fat in each cell, constituting the 

 condition kno^yll anatomically as "fatty infiltration." This 

 occurs, pathologically, chiefly in the liver. If at the same 

 time the cytoplasm is disintegrated through autolytic changes, 

 the fat-droplets do not fuse, but remain as small, more or less 

 discrete, fat granules among the granules of cell debris, consti- 

 tuting the microscopic picture of " fatty degeneration " ; this 

 condition occurs particularly in the heart and liver. 



Second, each cell contains a large amount of fat (5-25 per 

 cent, of its dry weight), which is so combined that it cannot be 

 detected microscopically ; this fat may be liberated during the 

 autolytic processes of cell disintegration and become visible, 



1 See Welsch, Arch. int. de pharm. et therap., 1905 (14), 211. 



2 Interference with oxidation does not necessarily imply destruction of the 

 oxidases. As yet we know practically nothing concerning the oxidases of the 

 cells in disease, and the above hypothesis has yet to be demonstrated. Duc- 

 cheschi and Almagia (Arch. Ital. Biol., 1903 (39), 29) found the normal amount 

 of lipase in phosphorus-livers, but also observed no decrease in ability to oxi- 

 dize salicylic aldehyde, which, however, does not prove a normal power to 

 oxidize fats. Gierke's observation (Ziegler's Beitr., 1905 (37), 502) that glyco- 

 gen and fat accumulate under identical conditions might be cited as indicating 

 decreased oxidative power, were it not in direct contradiction to the results 

 obtained by Kosenfeld. 



