Effect of pancreatic atrophy and hypertrophy on the small intestine.

Abstract

SUMMARY Intestinal enzyme activities were investigated in mice with spontaneously occurring exocrine pancreatic insufficiency (EPI), in rats after induction of pancreatic insufficiency by intraductal injection of oleic acid, and in rats after feeding a proteinase inhibitor (Camostate) which induced a marked pancreatic hypertrophy. An increase in saccharase activity and in vitro uptake of L-phenylalanine was found in EPI mice, while activities of alkaline phosphatase and lactase were not altered. In oleic acid induced pancreatic insufficiency and in pancreatic hypertrophy no alterations in enzyme activities were observed. Morphometric analysis revealed no alterations in mucosal surface of EPI mice. It was suggested that the small intestine adapts functionally to severe and long lasting pancreatic insufficiency, but not to pancreatic hypertrophy.In exocrine pancreatic insufficiency an increase in intestinal enzyme activities of disaccharidases have been described in man and in animals. -4 It was suggested that the loss of pancreatic enzymes decreased the turnover of brush border enzymes.' On the other side, after ligation of the pancreatic duct, exocrine insufficiency was paralleled by a decrease of the absorbing area of the intestine.6 The aim of the present study was to analyse whether changes in intestinal enzyme activities were correlated with alterations in intestinal cell mass and transport function. Additionally we investigated whether intestinal adaptive changes depend on the severity of pancreatic insufficiency, and occur in pancreatic hypertrophy. Methods ANIMALSIn 12 CBA/J mice the spontaneously occurring exocrine pancreatic insufficiency syndrome (EPI) was diagnosed on the basis of rapid weight loss and fatty yellow stools four weeks before the intestinal studies.7 Twelve healthy adult CBA/J mice served as controls.In 18 rats pancreatic insufficiency was induced by a single injection of 50,l oleic acid into the pancreatic duct.8 Intestinal studies were done after six weeks.

Effects on gut properties in exocrine pancreatic insufficient (EPI) pigs, being growth retarded due to pancreatic duct ligation at 7 weeks but not at 16 weeks of age

“…In rats, after surgical transposition of intestinal segments, it has been shown that intestinal growth and villi morphology was dependent on the direct contact with the pancreatic juice [11,12]. Furthermore, in hamsters with experimentally induced EPI by pancreatic duct ligation or in mice that spontaneously develop EPI, it has been demonstrated that the lack of pancreatic juice affected the intestinal morphology causing villi atrophy and an increased expression of brush-border enzymes [13][14][15]. However, in another rat study no morphological differences in the small intestine were observed between pancreatic duct-occluded animals and controls [16].…”

The effect of trypsin inhibitor on the pancreas and small intestine of mice

“…This intestinal growth was probably secondary to an increased luminal load, due in turn to maldigestion and malabsorption resulting from inhibition of proteolytic enzymes. Food residues may stimulate gut growth (Johnson, 1987), and intestinal growth and functional small intestinal hypertrophy have been shown in mice with spontaneous exocrine pancreatic insufficiency (although morphological evidence of hypertrophy was not found; Adler et al 1987).…”