Antifatty Liver Activity of Crystalline Trypsin

The fatty liver that develops in insulin-treated, depancreatized dogs and in dogs subjected to ligation of their pancreatic ducts has been the subject of considerable study (1). Soon after its discovery it was shown to be prevented by the feeding of raw pancreas (2), while later findings revealed that it could also be prevented by the feeding of pancreatic juice and certain fractions derived from raw pancreas (1). In understanding this type of fatty liver, it is important to recognize that the condition develops in completely depancreatized dogs fed abundant amounts of choline and methionine in the form of lean meat (1,3,4). But the feeding of extra choline or extra methionine, in their free forms, did prevent the development of a fatty liver (4). This difference in the action of free and bound methionine suggested that, in dogs deprived of the external secretion of their pancreases, there is some disturbance in the gastrointestinal tract whereby the methionine of ingested protein is not made available for lipotropic purposes. The subsequent observation that hydrolyzed casein prevented the development of fatty livers, whereas unhydrolyzed casein had no such effect, lent further support to such a view (5). On the basis of the above findings it W~ZJ proposed as a working hypothesis that the proteolytic enzymes contained in pancreas accounted for its antifatty liver activity. Evidence for this hypothesis is presented here. It is’ shown that the feeding of crystalline trypsin effectively prevents the development of fatty livers in completely depancreatized dogs maintained with insulin.