ROLE OF CCK IN THE CONTROL OF GASTRIC-EMPTYING AND GASTRIC SECRETORY RESPONSE TO FATTY MEAL IN HUMANS

Exogenous CCK is known to affect gastric motility and secretion but its physiological role in the control of gastric functions is unknown. In this study involving 10 young healthy subjects, 500 ml of standard meal without or with addition of 15 % soybean oil was given and the gastric emptying rate and the pH profile and plasma levels of gastrin, CCK and somatostatin were determined in separate tests with placebo or with antagonism of type A CCK-receptors (loxiglumide, 1200 mg p.o.). The emptying half-time was 44 and the addition of oil prolonged the emptying by about 50 %. Pretreatment with loxiglumide, significantly accelerated fat-induced retardation of gastric emptying. Standard meal resulted in an immediate rise in median gastric pH to about 6.0 and this was followed by gradual decline within about 3h to pre-meal values of about 2.0. After the meal, plasma gastrin rose by 57 %, CCK by 177 % and somatostatin by 39 %. Addition of fat significantly prolonged the pK decline after meal while reducing the increment in plasma gastrin and enhancing plasma CCK levels. Loxiglumide significantly reduced the median postprandial pH (from control 4.8 to 2.5) and reversed the changes in the pH profile caused by the addition of fat, The increments in plasma gastrin and CCK were markedly augmented, while those of somatostatin were significantly attenuated. These results indicate that endogenous CCK released by fatty meal delays gastric emptying and inhibits gastric acid and plasma gastrin responses in humans and this is mediated, at least in part, by somatostatin.