During the last decade the iodine supply in Germany has increased significantly, but there is still a high frequency of goitre. Therefore the question of iodine bioavailability has arisen. In a two-period study 12 women were given a mixed diet of ordinary foods with milk and milk products of different batches. None of the volunteers suffered from an iodine deficiency according to WHO-criteria. Each period ended with a 9-day balance-study protocol in which all foods were provided. Food and fluid intake were registered, and urine and faeces were quantitatively collected. The iodine content was determined by ICP-MS. The mean intake in the form of solid food amounted to 175 +/- 10 micrograms I/d and to 27 +/- 15 micrograms I/d in fluid form. Milk and dairy products represented the main source of iodine (37%). Iodine was predominantly excreted in the urine (89%, 171 +/- 45 micrograms I/d) and the faeces 11% (20 +/- 11 micrograms I/d). The resulting iodine balance was approximately . In one case an iodine-rich erythrosine preparation with a low iodine bioavailability was used. Between the two periods of consuming different batches of milk and milk products no differences were observed concerning the high bioavailability of iodine.
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.
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