Abstract
Background: Clinical and experimental data have revealed that parenteral nutrition (PN) can lead to hypotrophy and dysfunction in the morphology and physiology of the pancreas. These adverse alterations appear to be related to many different factors. One important factor is the absence of a gastrointestinal hormone, such as cholecystokinin, which is the most important stimulator for the integrity of the pancreas. The level of cholecystokinin is decreased during absent enteral feeding, and the stimulatory effect of cholecystokinin is significantly reduced during PN. Methods: Original and review articles, editorials, and case reports published primarily in English and listed in MEDLINE/ISI up to September 2006 or identified by a manual search have been reviewed in an attempt to provide a comprehensive overview of the effects of PN on the exocrine pancreas in response to cholecystokinin. Results: When hypercholecystokininemia, produced by endogenous and exogenous procedures, is present during PN, the morphology and functions of the pancreas are still unable to be fully reversed. Conclusions: Other growth factors besides cholecystokinin are probably involved in the pancreatic regulation, and enteral feeding seems to be important for the full expression of the trophic effects of cholecystokinin on the pancreas.
Cholecystokinin is a main stimulator of the pancreas, but its stimulatory effect on exocrine pancreas is decreased during long-term parenteral nutrition. This may be due to other factors besides cholecystokinin that are regulated in the exocrine pancreas during parenteral feeding.
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