A patient deficient in trypsin inhibitor has primary abnormality that involves the
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Feedback regulation of pancreatic enzyme secretion as a mechanism for trypsin inhibitor-induced hypersecretion in rats
Gary M Green, RL Lyman
Proceedings of the Society for Experimental Biology and Medicine 140 (1), 6-12, 1972
The mechanism by which dietary trypsin inhibitor induces excessive pancreatic secretion was investigated in rats with bile-pancreatic duct fistulas. It was found that removal of bile-pancreatic juice from the intestine resulted in a large increase in pancreatic enzyme secretion. Infusion of trypsin or chymotrypsin as well as bile-pancreatic juice suppressed the secretion of pancreatic enzymes. When trypsin was present in the intestine, a large pancreatic enzyme response was obtained by infusion of trypsin inhibitors. A similar increase in pancreatic enzyme output was evoked when trypsin infusion was stopped. The results indicated that pancreatic enzyme secretion in the rat is subject to feedback inhibition from intestinal trypsin and chymotrypsin, and that trypsin inhibitors stimulate pancreatic enzyme secretion indirectly, by binding or neutralizing trypsin and thereby removing its feedback inhibition.