Konturek J W, Thor P, Maczka M, Stoll R, Domschke W, Konturek S J
Dept. of Medicine, University of Münster, Germany.
Scand J Gastroenterol. 1994 Jul;29(7):583-90. doi: 10.3109/00365529409092476.
Exogenous cholecystokinin (CCK) is known to affect gastric motor and secretory activities, but its physiologic role in the control of gastric functions is unknown.
In this study involving 10 young healthy subjects and 10 duodenal ulcer (DU) patients, 500 ml of a 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, pancreatic polypeptide (PP), and somatostatin were determined in separate tests with placebo or with antagonism of type-A CCK receptors (loxiglumide, 1200 mg orally).
In healthy controls and DU patients the emptying half-time was 44 and 34 min, respectively, and the addition of oil prolonged the emptying by about 50%. Pretreatment with loxiglumide significantly reduced fat-induced retardation of gastric emptying in both healthy controls and DU patients. A standard meal in healthy subjects resulted in an immediate rise in median gastric pH to about 6.0, and this was followed by gradual decrease within about 3 h to premeal values of about 2.0. After the meal, plasma gastrin rose by 57%, CCK by 177%, PP by 100%, and somatostatin by 39%. Addition of fat significantly attenuated and prolonged the pH decrease after the meal while reducing the increment in plasma gastrin and enhancing plasma CCK and PP 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, whereas those of somatostatin and PP were significantly attenuated. DU patients showed lower postprandial pH (3.0) in tests with or without fat and higher increments in plasma gastrin. CCK antagonism failed to affect significantly the pH profile or the increments in plasma gastrin in DU patients.
These results indicate that endogenous CCK released by a fatty meal delays gastric emptying and inhibits gastric acid and plasma gastrin responses in healthy subjects, but in DU patients the inhibitory effect of CCK is less pronounced, suggesting a defect in the action of this hormone on gastrin release and gastric acid secretion.
已知外源性胆囊收缩素（CCK）会影响胃的运动和分泌活动，但其在胃功能控制中的生理作用尚不清楚。
在这项涉及10名年轻健康受试者和10名十二指肠溃疡（DU）患者的研究中，给予500毫升不含或添加15%大豆油的标准餐，并在分别使用安慰剂或拮抗A型CCK受体（洛谷酰胺，口服1200毫克）的试验中测定胃排空率、pH值变化曲线以及胃泌素、CCK、胰多肽（PP）和生长抑素的血浆水平。
在健康对照组和DU患者中，排空半衰期分别为44分钟和34分钟，添加油后使排空时间延长约50%。洛谷酰胺预处理显著降低了健康对照组和DU患者中脂肪诱导的胃排空延迟。健康受试者进食标准餐后，胃中位pH值立即升至约6.0，随后在约3小时内逐渐降至餐前约2.0的水平。进食后，血浆胃泌素升高57%，CCK升高177%，PP升高100%，生长抑素升高39%。添加脂肪显著减弱并延长了餐后pH值的下降，同时降低了血浆胃泌素的升高幅度，并提高了血浆CCK和PP水平。洛谷酰胺显著降低了餐后中位pH值（从对照组的4.8降至2.5），并逆转了添加脂肪引起的pH值变化曲线。血浆胃泌素和CCK的升高明显增强，而生长抑素和PP的升高则显著减弱。在有或无脂肪的试验中，DU患者餐后pH值较低（3.0），血浆胃泌素升高幅度较高。CCK拮抗作用未能显著影响DU患者的pH值变化曲线或血浆胃泌素的升高。
这些结果表明，脂肪餐释放的内源性CCK可延迟健康受试者的胃排空，并抑制胃酸和血浆胃泌素反应，但在DU患者中，CCK的抑制作用不太明显，提示该激素在胃泌素释放和胃酸分泌作用方面存在缺陷。
