FATTY METAMORPHOSIS 411 



tion of fat by the lipase will go on uncontrolled. The result will be 

 a disintegrated cell containing many fat-droplets, i. e., fatty degen- 

 eration.^^ In cloudy swelling there also appear droplets stained with 

 osmic acid but not by sudan 111, which Hess and Sa.xl"' have shown 

 to result from intravitam cell autolysis, and to be a precursor of true 

 fatty degeneration. 



Work with cells in tissue cultures indicates that fatty changes of 

 all types may occur independently of the circulation. Lamberf^ 

 states that the amount of fat in the culture cells is roughly propor- 

 tional to the amount in the culture medium, and cells rich in fat may 

 move actively and undergo normal mitosis. Lewis, however, observed 

 fatty changes in cells growing in fat-free media, and made the espe- 

 ciall}'' interesting observation that cells grown in 2.5-3 per cent, alco- 

 hol will show a rich fat accumulation. Also, an accumulation of fats 

 and lipoids in cells grown in the presence of such steatogenetic poi- 

 sons as phosphorus and Oleu7n pulegii has been observed by others, "'^ 

 which indicates that free cells behave the same under the influence 

 of such poisons as the cells of the fixed tissues. 



The process of unmasking the masked fats is explained by M. H. 

 Fischer^'' on a physical basis, as follows: The fats of the cells are 

 distributed as an emulsion in a hydration compound of water with 

 hydrophilic colloids, notably proteins and soaps. Such an emulsion 

 breaks down whenever the hydrophilic colloid is either dehydrated or 

 diluted beyond certain ranges. As the usual conditions that cause 

 fatty degeneration, such as poisoning with phosphorus, arsenic, etc., 

 or local circulatory disturbances with local acidosis, all tend to de- 

 hydrate some of the cell colloids and to dilute others, it would seem 

 probable that the appearance of the fat droplets in the cells is the 

 result of such changes in the colloids that previously held them in an 

 emulsion too fine to exhibit readily visible fat particles. The relation 

 of cloudy swelling to fatty degeneration is readily explained on this 



^^ Interference with oxidation does not necessarily irnply 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. Duccheschi 

 and Aluiagia (Arch. Ital. Biol., 1903 (39), 29) found the normal amount of lipase 

 in phosphorus-livers, but also observed no decrease in ability to oxidize salicylic 

 aldehyde, which, however, does not prove a normal power to oxidize fats. Gierke's 

 observation (Ziegler's Beitr., 1905 (37), 502) that glycogen and fat accumulate 

 under identical conditions might be cited as indicating decreased oxidative power. 

 Wells (Jour. Exper. Med., 1910 (12), 607) found that the power of liver tissue to 

 oxidize purines was not decreased by the maximum degree of fatty degeneration, 

 but Waldvogel (Deut. Arch. klin. Med., 1907 (89), 342) found that obese persons 

 can burn fatty acids which arise in metabolism less readily than normal; and Quinan 

 (.Jour. Med. Res., 1915 (32), 73) found the ester-splitting lipolytic enzymes of the 

 liver much reduced in the liver of chloroform necrosis, but the relation of these 

 esterases to true lipases is not known. 



^« Virchow's Arch., 1910 (202), 149. 



*' Trans. Assoc. Amer. Phys., 1913 (9), 93; Jour. Exp. Med., 1914 (19), 398. 



" Krontowski and Poteff, Beitr. path. Anat., 1914 (58), 407. 



^^ Fischer and Hooker, Science, 1910 (43), 468; Fischer, Fats and Fatty Degen- 

 eration, Wiley, New York, 1917. 



