title: Physiological response of the human pancreas to enteral and parenteral feeding.
abstract: OBJECTIVE
  Normal digestive physiology is a highly orchestrated process, integrating the mechanical breakdown of food, the secretion of digestive juices, the control of motility, and the efficient absorption of nutrients. As enteral and parenteral feeding techniques bypass many of these control mechanisms, nutritional utilization can be expected to be disturbed. This review examines recent publications that have investigated this question in clinical practice.
  
  
  RESULTS
  Studies in healthy volunteers have shown that all forms of oral and enteral tube feeds commonly used, including proximal jejunal elemental diets, stimulate pancreatic secretion. Avoidance of the cephalic phase with duodenal feeding does not reduce the secretory response. 'Pancreatic rest' can, however, be achieved if feeding is delivered 40-60 cm past the ligament of Treitz by activating the ileal brake, or if it is given intravenously by avoiding intestinal cholecystokinin stimulation and the cholinergic reflex. These forms of feeding, however, can cause complications as they will result in malabsorption unless elemental formulae are used, and hyperglycemia as the metabolic utilization of intravenous nutrients is impaired.
  
  
  CONCLUSIONS
  An understanding of normal pancreatic physiology and how interventional feeding techniques affect it will help prevent complications and improve outcome in hospitalized patients.
authors.affiliation: Division of Gastroenterology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. sjokeefe@pitt.edu
authors.forename: Steven J D
authors.initials: SJ
authors.lastname: O'Keefe
mesh_terms: D002766:Cholecystokinin / Q000097:blood; D004750:Enteral Nutrition; D006760:Hospitalization; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology; D008286:Malabsorption Syndromes / Q000209:etiology; D010179:Pancreas / Q000378:metabolism / Q000502:physiology*; D010288:Parenteral Nutrition
chemical_list: D002766:Cholecystokinin