FAT NECROSIS 385 



pancreatic juice was the active agent. Flexner ^^ supported this con- 

 tention by demonstratinfj: tlie presence of a fat-splitting enzyme in 

 foci of fat necrosis, wliich was corroborated by Opie.-^ The latter'*" 

 was also able to (lenioiistrate the presence of lipase in the urine of a 

 patient with fat necrosis,'" and the highest values for amylase in the 

 blood and urine are found in pancreatitis (Stocks).'*^'' 



In a study of the pathogenesis of fat necrosis, particularly with 

 reference to the question whether the lipase or the trypsin of the 

 pancreatic juice was responsible. Wells ^- found that typical fat 

 necrosis could be produced by injecting extracts of fresh pancreas 

 into animals, either of the same species as that from which the pan- 

 creas was obtained, or into a foreign species. Commercial "pan- 

 ereatins" were also quite effective, whether in weak acetic acid or 

 weak alkaline solutions. The power of these materials to cause fat 

 necrosis was reduced by heating to or above 60° for five minutes, 

 and completely destroyed at 71°, indicating that the active agent 

 is an enzyme. But, as in the same material trypsin was injured by 

 temperatures above 60°, and destro.yed at between 70° and 72°, and 

 lipase was weakened above 50°, and destroyed above 70°, it was im- 

 possible to determine, by heating pancreatic preparations, whether 

 the lipase or the trypsin was the essential factor. By permitting 

 pancreatic extracts to digest themselves it was found that the power 

 to produce fat necrosis decreased, pari passu, with the decrease in 

 lipolytic strength. Preparations strongly tryptic, but very weak in 

 lipase, produced no fat necrosis, and, on the other hand, extracts of 

 pig's liver or of cat's serum, both rich in lipase but devoid of tryp- 

 sin, were equally ineflPective. Furthermore, mixtures of liver or 

 serum lipase and trypsin were incapable of causing fat necrosis. 

 Fresh pancreatic extracts from fasting dogs, containing lipase but 

 almost no trypsin (which in fresh extracts is still in the form of 

 inactive trypsinogen), produced abundant fat necrosis, whereas after 

 the trypsinogen in such extracts was activated by enterokinase, no 

 fat necrosis could be produced. It therefore seems certain that 

 trypsin alone cannot produce fat necrosis, and that the decrease in 

 strength of lipase in a pancreatic extract is associated with a cor- 

 responding decrease in power to produce fat necrosis. But, on the 

 other hand, lipase of liver or blood-serum alone, or when mixed with 



88 Jour. Exper. Med., 1807 (2), 413. 



89Contrib. of pupils of W. IT. Welch, Baltimore. 1000, p. 850; .Tolnis Hopkins 

 Hosp. Rep., 1000 (0), 8.50. 



00 Opie, "Diseases of the Pancreas," Lippincott, 1003, p. ].")6: .Johns Ildiikins 

 Hosp. Bull., 1002 (13), 117. 



91 It yet remains to be seen if this is a constant occurrence: and also if tlie 

 lipase so excreted comes from the pancreas, for Zeri (II Policlinico. 100.5 (12), 

 "3.3) has found lipase in the urine in hcmorrhajric nepliritis and inihimiiiation of 

 the urinary tract: also Pribram and Loewv, Zeit. phvsiol. Chem., 1012 (76), 480 



9ia Quart. .lour. Med., 1016 (0), 216. 



92 Jour. Med. Research, 1003 (9), 70. 



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