THE EFFECT OF TRYPSIN-INHIBITOR ON THE PANCREAS AND SMALL-INTESTINE OF MICE

Pancreatic and intestinal growth rates were measured in mice fed on raw soya-bean flour (RSF) for up to 24 weeks. Control animals were fed on standard chow. The effects of RSF on the mouse pancreas resembled that seen in rats, showing hypertrophy with some hyperplasia. A marked increase in small intestinal weight was also found in mice fed on RSF but not in rats fed on this diet. Histological studies showed an increase in both villous and crypt thicknesses in the small intestine from these mice, and DNA, RNA and protein measurements indicated that the increase in intestinal weight was due to hypertrophy and hyperplasia of the mucosal layer. To determine whether the intestinal growth in mice fed on RSF was purely a response to the trypsin inhibitor (TI) component of the diet, pancreatic and intestinal growth rates were also determined in mice fed on the synthetic trypsin inhibitor camostate, at levels of 0.5 or 2 g/kg in rat chow, for periods of 1-8 weeks. Control animals were fed on standard chow. RSF and 0.5 g camostate/kg had similar trypsin inhibitor activities (measured against bovine trypsin), and both caused similar increases in pancreatic weight, DNA, RNA and protein content. However, 0.5 g camostate/kg did not affect small intestinal weight. Chow containing 2 g camostate/kg contained twice as much TI activity as the RSF diet but produced only a small increase in small intestinal weight at 2 and 8 weeks. This intestinal growth was significantly less than that seen with RSF. The present study shows that, in the mouse, RSF or a diet containing camostate in the appropriate dose produces pancreatic growth comparable to that seen in the rat. RSF also causes intestinal growth, but camostate-containing diets have little or no effect on the growth of the intestine.