Protein- and fat-rich test meals elicit a strong stimulatory effect on postprandial somatostatin (SLI) and pancreatic polypeptide (PP) release, whereas carbohydraterich meals rather attenuate the response of both hormones. Since there is evidence that intestinal hormones might contribute to the postprandial SLI and PP response, it was the aim of the present study to determine in dogs the effect of low-dose cholecystokinin octapeptide (CCK-8) on basal hormone levels and also during a background infusion of amino acids or glucose. In a group of six conscious dogs, sulfated CCK-8 was infused intravenously (i.v.) via a hindleg vein at stepwise increasing infusion rates of 10, 30, and 50 pmol · kg−1 · h. The infusion of CCK was applied during a background infusion of saline (2 ml/min), glucose (0.2 g/min), or an amino acid mixture (8.5%, 2 ml/min). CCK-8 had no effect on plasma insulin and glucagon. levels under all experimental conditions. Plasma SLI levels were significantly stimulated by all doses of CCK. This stimulatory effect was similar during background infusions of either saline, glucose, or amino acids, respectively.
Pancreatic polypeptide (PP) levels rose 200–300 pg/ml during CCK plus saline. This was slightly attenuated by glucose. During CCK plus amino acids, the PP response was augmented to 600–800 pg/ml. Since secretin is also released after the ingestion of a meal and intraduodenal acidification is a potent stimulus not only of secretin but also of gastric and pancreatic SLI release, the effect of secretin was examined additionally. The infusion of secretin (0.03 CU · kg−1 · h) had no effect on basal levels of SLI, PP, insulin, or glucagon and abolished the stimulatory effect of CCK-8 on SLI and PP levels. Interestingly, the concomitant infusion of glucose or amino acids together with secretin restored the stimulatory effect of CCK-8 to those levels observed in the absence of secretin. In conclusion: (1) Postprandial SLI and PP release might in part be due to the stimulatory effect of CCK-8. (2) CCK-induced PP release is attenuated by elevated plasma glucose levels and augmented by elevated levels of circulating amino acids. CCK-induced SLI release remains unaffected by either glucose or amino acids. (3) Low-dose secretin abolishes CCK-8-induced SLI and PP release. Interestingly, circulating nutrients can restore the CCK effect via as yet unknown mechanisms. (4) CCK-8 at the low doses employed has no effect on insulin and glucagon release, suggesting that its primary target cells are the pancreatic PP cells and the gastric and pancreatic D-cells rather than A- and B-cells.