Effects of Total Parenteral Nutrition on the Exocrine and Endocrine Pancreas. An Experimental Study

Sammanfattning: During total parenteral nutrition (TPN) adequate nutrition is provided intravenously and the enteral route is bypassed. The integrity of the gastrointestinal (GI) tract, however, is dependent on the passage of food through it. This thesis deals with the effects of TPN on the pancreas and the parotid glands. TPN induced hypotrophy of the exocrine pancreas and the parotid glands. The amylase concentration in the pancreas was unaffected, while the concentrations of trypsin and chymotrypsin increased. The atrophy and changes in enzyme concentrations were not related to the amount of fat infused. Cholecystokinin (CCK) is believed to be the greatest stimulator of pancreatic growth, but hyperCCKemia, induced by PBD operation or by infusion of CCK, caused less growth of the pancreas during TPN than in fed control rats. Therefore food passage through the digestive tract must induce the release of other growth promoting factors. The basal insulin concentration was reduced and the insulin secretory response to glucose infusion was impaired during TPN. The basal glucose concentrations and the plasma glucose curves on intravenous glucose tolerance testing were not affected by TPN. Studies on isolated pancreatic cell islets revealed no signs of glucotoxicity. The activities of the glycogen hydrolyzing enzyme glucan-1,4-a-glucosidase and several other lysosomal enzymes were reduced during TPN, probably due to the hyperlipidemia it causes. In conclusion, TPN induces atrophy of the exocrine pancreas and an impairment in insulin secretion. We suggest that the atrophy is due to the loss of several intestinal growth factors, whose release is usually induced by food passage through the digestive tract, and that the impairment in insulin secretion is due to hyperlipidemia.