Cholecystokinin is a negative regulator of gastric acid secretion and postprandial release of gastrin in humans

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men

“…Therefore the present findings suggest that circulating CCK is not responsible for the enterogastrone effect of MCT, since MCT did not stimulate CCK release into the circulation, Furthermore, it is not likely that the more potent inhibitory effect of LCT on gastrin stimulated gas tric acid secretion when compared to MCT is a result of the ability of LCT to release CCK. Absence of suppression of gastric acid secretion by CCK-33 infusion in the present study agrees with the observation that intravenous infusion of CCK-8, inducing plasma CCK increments within the physiological range, did not significantly alter gastrin stimulated gastric acid secretion [42]. Absence of acid suppression by CCK in our study was not related to lack of biological activity of CCK, since CCK infusion markedly stimulated the release of pancreatic polypeptide [43][44][45].…”

“…Several possibil ities have been suggested [7,[9][10][11][12]34]. Of old, one of the most important enterogastrone candidates is CCK [7], In previous studies, infusion of high, probably supraphysiological, doses of CCK inhibited gastric acid secretion [35], Recent studies with CCK receptor antagonists also support an inhibitory effect of endogenous CCK on gastric acid secretion, since specific type A CCK-receptor antagonists augmented basal as well as stimulated gastric acid output [36][37][38][39][40][41]. However, in the present study infusion of CCK did not inhibit gastric acid secretion, and medium chain triglycerides were able to inhibit gastric acid secretion without concomitant release of CCK.…”

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

“…In the oxyntic mucosa, CCK was shown to control histamine release (Chen et al 2004). This mechanism was also demonstrated in the rat (Woltman & Reidelberger, 1999;Lloyd et al 1992Lloyd et al , 2001, in sheep (Zavros & Shulkes, 1997) and in man (Schmidt et al 1994) via occupation of the CCK 2 receptors present on the ECL cells (Modlin & Tang, 1996).…”

Cellular and subcellular localization of cholecystokinin (CCK)-1 receptors in the pancreas, gallbladder, and stomach of mice

“…It is reported that CCK may act preferably on CCK1 receptors of D cells to trigger somatostatin release, resulting in the inhibition of gastric acid secretion in rats (Lloyd et al 1992a), dogs (Lloyd et al 1994), and humans (Buchan et al 1993;Schmidt et al 1994). One histochemical study was able to detect the expression of CCK1 receptors in some D cells of the human stomach (Schmitz et al 2001) whereas another immunostaining reported that most of the gastric D cells in the dog and guinea pig were immunoreactive for the CCK2 receptor (Helander et al 1997).…”

“…Besides the direct stimulation by CCK, indirect pathways via the vagal nerve have been proposed for the regulation of the pancreas and gallbladder (Mawe 1991;Owyang and Logsdon 2004;Singer and Niebergall-Roth 2009). CCK also plays a role in the intestinal phase in the control of gastric functions that negatively regulate meal-stimulated gastric acid secretion and gastrin release (Lloyd et al 1992a, b), possibly via somatostatin release (Schmidt et al 1994). The hindbrain is a direct or indirect target of peripherally released CCK which is related to the regulation of feeding behavior and satiety.…”