Pancreatic polypeptide release by intraluminal fatty acids

The question of whether the response of pancreatic polypeptide to intestinal fatty acids is influenced by the site of intestinal perfusion or the chain length of the fatty acid was investigated. Six dogs with chronic gastric, pancreatic, and intestinal fistulas were studied. Proximal perfusates were administered at the pylorus and diverted via a Foley catheter in the orad stoma of an intestinal fistula placed 45 cm beyond the pancreatic cannula. Distal perfusates were administered into the caudal stoma of the intestinal cannula. Three experimental protocols were used: proximal fatty acid perfusion (20, 40, or 80 mmol/L) combined with distal saline perfusion; distal fatty acid perfusion (20, 40, or 80 mmol/L) combined with proximal saline perfusion; or distal fatty acid perfusion combined with proximal fatty acid perfusion of 80 mmol/L. Each dose of fatty acid was given in random order and the two fatty acids (dodecanoate and oleate) were tested on different days. Blood samples were drawn for pancreatic polypeptide radioimmunoassay, and pancreatic secretion was collected for determination of bicarbonate and protein outputs. Pancreatic polypeptide responses to perfusion of both proximal and distal segments with oleate exceeded (P < 0.05) those evoked by dodecanoate. The responses of pancreatic polypeptide to dodecanoate administration into either the proximal segment or the distal intestine were not significantly different. In contrast, perfusion of the proximal intestinal segment with oleate released significantly (P < 0.05) less pancreatic polypeptide than did distal intestinal perfusion with oleate. It is concluded that oleate is a more potent stimulus of canine pancreatic polypeptide release than is dodecanoate and that maximal pancreatic polypeptide release in response to intestinal oleate can be achieved even if the proximal 45 cm segment of intestine is excluded.