Cephalic phase of lipolysis is impaired in pancreatic insufficiency: Role of gastric lipase

Background: Gastric lipase contributes significantly to overall lipolysis a nd is regulated by interacting neuro-hormonal mechanisms. Patients with alc oholic chronic pancreatitis (ACP) have low, or even absent, activity of pan creatic lipases. In that state the secretion of gastric lipase could be ess ential and compensate for the pancreatic defect. However, conflicting studi es have nut resolved the order of magnitude of gastric lipase secretion in these patient. This could be explained by differences in regulatory mechani sms, gastric mucosal changes, and abdominal vagal tone. Methods: Nasogastri c intubation with modified sham feeding and upper endoscopy including biops ies for histologic classification and Helicobacter pylori infection status were performed in eight ACP patients, and eight healthy volunteers were stu died on separate occasions. Vagal nerve function was assessed by calculatio n of heart rate variability in ACP patients. Gastric lipase was measured in aspirates by means of enzyme-linked immunosorbent assay and an enryme kine tic assay. Plasma concentrations of gastrin, secretin, cholecystokinin, and pancreatic polypeptide were measured throughout the study. Results: Sham f eeding rapidly and significantly increased gastric lipase secretion in heal thy volunteers, whereas ACP patients did not respond to sham feeding. Two o f right patients were infected with H. pylori and had mucosal changes accor dingly. The lack of lipase response could not be ascribed to dysfunction of the abdominal vagus. Conclusions: The cephalic phase of gastric lipase sec retion is impaired in ACP patients. Although their fundic cells continue to secrete gastric: lipase. they are not subject to normal neuro-hormonal reg ulation.