Intestinal,Pancreatic,and Hepatic Effects of Gastrointestinal Hormones in a Total Parenteral Nutrition Rat Model

The adverse effects of long-term total parenteral nutrition (TPN) are well documented. Lack of gastrointestinal (GI) stimulation from oral feeding, reduction of GI hormone secretion, and interruption of enterohepatic circulation of bile may be found. TPN results in atrophy of the digestive system, intestinal bacterial overgrowth and translocation, liver cell damage, and gallstone formation. In addition, the increase incidence of sepsis of gut origin may lead to an increase in mortality. In some studies, results of the administration of GI hormones to patients receiving prolonged TPN suggest the possibility of reducing some of the adverse effects of long-term TPN. To evaluate the role of GI hormone in the prevention of adverse effects of TPN, we designed the following study: 50 young adult male Wistar rats, weighing approximately 200 g, were divided into five equal groups. All animals received identical TPN infusate for 7 days. GI hormone was added to the TPN infusate as follows: Group A (control) received no GI hormone, group B was given glucagon at a dosage of 330 μg/kg per day, group C was administered cholecystokinin 2 Ivy dog units twice a day, group D received secretin 2 clinical units twice a day, and group E was given both cholecystokinin and secretin at the dosages stated for groups C and D. Maintenance of mucosal brush-border hydrolase activity was found in group B. Neither atrophy of the pancreas nor hypoplasia of intestinal villi was observed in groups C and D. Group C showed improvement of liver function-associated tests, better weight gain, and acceleration of enterohepatic circulation of bile. Mucosal weight and DNA contents were increased in group D, and acceleration of cholesterol catabolism was found in group E. We concluded that cholecystokinin seems capable of preventing some adverse effects of 7-day TPN treatment on the GI system. The benefit of glucagon or secretin administration was limited. (Journal of Parenteral and Enteral Nutrition 17:364-369, 1993)