Diabetologisk disputation
academic dissertation - Effects of total Parenteral Nutrition on the Exocrine and Endocrine Pancreas - an experimental study5 november 1997
EFFECTS OF TOTAL PARENTERAL NUTRITION ON THE EXOCRINE AND ENDOCRINE PANCREAS - an experimental study
5 nov 1997 kl 09.00 Universietssjukhuset, Lund
Author:
Bo-Guang Fan, M.D.,
Department of Surgery
S221 85 Lund, SwedenABSTRACT
During total parenteral nutrition TPN adequate nutrition is provided intravenously and the enteral route is passed. 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 (CKK) is believed to be the greatest stimulator of pancreatic growth, but hyper CCKemia, 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 glucose toxicity. The actitivities of the glycogen hydrolyzing enzyme glucan-1,4-alfa-glucosidas 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.
Key words: cholecystokinin, exocrine pancreas, endocrine pancreas, food passage, hyperlidemia, hypotrphy, insulin, lysosomal enzymes, parotid gland, TPN
Fakultetsopponent
Docent Johan Permerth,
Kirurgiska kliniken,
Huddinge
