Gastric and cephalic stimulation of human pancreatic polypeptide release

Abstract

We studied the factors which contribute to the increase in circulating pancreatic polypeptide concentrations which occur when food is eaten. Homogenized food, infused directly into the stomach, led to a marked increase in serum pancreatic polypeptide concentrations which was of similar magnitude in both normal subjects and in patients with duodenal ulcer. This response is unlikely to be attributed to gastrin or cholecystokinin released by food because intravenous gastrin and cholecystokinin failed to release pancreatic polypeptide in significant amounts. Food-stimulated pancreatic polypeptide release was unaffected by a previous truncal vagotomy, duodenal acidification, or cimetidine. On the other hand, the pancreatic polypeptide response to food was markedly inhibited by propantheline (P < 0.005). Gastric distention with glucose and saline significantly increased serum pancreatic polypeptide levels, although, compared to food, pancreatic polypeptide responses were small. Likewise, cephalic-vagal stimulation induced by modified sham feeding led to small but significant pancreatic polypeptide rises in normal subjects. Unlike the response to intragastric food, the pancreatic polypeptide response to sham feeding was reduced in vagotomized patients. We conclude that, although gastric distention and cephalicvagal stimulation contribute to the over-all pancreatic polypeptide response to eating, the majority of the response is caused by the presence of food per se in the gastrointestinal tract. It is likely that food in the stomach or small intestine sends a message to the pancreas, either via a nonvagal neural reflex or through the bloodstream, resulting in pancreatic polypeptide release. Because the pancreatic polypeptide response to food is inhibited by propantheline, it appears that a cholinergic pathway is involved.