Jansen J B, Jebbink M C, Mulders H J, Lamers C B
Department of Gastroenterology and Hepatology, University Hospital, Leiden, The Netherlands.
Regul Pept. 1989 Jun-Jul;25(3):333-42. doi: 10.1016/0167-0115(89)90181-x.
To test the hypothesis, based on studies in healthy man and dog, that patients with impaired digestion due to severe pancreatic insufficiency have impaired postprandial cholecystokinin (CCK) secretion that can be improved by the addition of pancreatic enzymes, we have studied plasma CCK responses to a test meal with and without addition of pancreatic enzymes in 10 patients with pancreatic insufficiency and steatorrhea, in 8 patients with chronic pancreatitis without steatorrhea, and in 6 healthy subjects. The patients with steatorrhea had a significantly (P less than 0.001) lower integrated plasma CCK response to the meal (177 +/- 23 pM.150 min) than the healthy subjects (468 +/- 41 pM.150 min), while patients with chronic pancreatitis without steatorrhea had an intermediate integrated postprandial CCK secretion (327 +/- 101 pM.150 min). Addition of pancreatic enzymes to the meal significantly augmented the integrated CCK response in both the patients with steatorrhea to 483 +/- 72 pM.150 min (P less than 0.01) and in those without steatorrhea to 480 +/- 85 pM.150 min (P less than 0.05). These values were not significantly different from those in the healthy subjects (521 +/- 86 pM.150 min). Integrated CCK secretion in the three groups during bombesin infusion was similar (patients with steatorrhea 134 +/- 23 pM.20 min, patients without steatorrhea 131 +/- 33 pM.20 min, and healthy subjects 146 +/- 28 pM.20 min), indicating a normal capacity to secrete CCK in response to a humoral stimulus. These data are in agreement with the suggestions from previous studies that digestion of nutrients by pancreatic enzymes plays an important role in the regulation of plasma CCK secretion after feeding.
基于对健康人和狗的研究,我们提出一个假设:因严重胰腺功能不全导致消化功能受损的患者,其餐后胆囊收缩素(CCK)分泌受损,补充胰酶后可得到改善。为验证这一假设,我们对10例胰腺功能不全并伴有脂肪泻的患者、8例无脂肪泻的慢性胰腺炎患者以及6名健康受试者进行了研究,检测他们在进食试验餐时,添加和不添加胰酶情况下血浆CCK的反应。伴有脂肪泻的患者对该餐的血浆CCK综合反应(177±23 pM·150分钟)显著低于健康受试者(468±41 pM·150分钟)(P<0.001),而无脂肪泻的慢性胰腺炎患者餐后CCK综合分泌处于中间水平(327±101 pM·150分钟)。给餐中添加胰酶后,伴有脂肪泻的患者CCK综合反应显著增强至483±72 pM·150分钟(P<0.01),无脂肪泻的患者增强至480±85 pM·150分钟(P<0.05)。这些数值与健康受试者(521±86 pM·150分钟)相比无显著差异。在输注蛙皮素期间,三组的CCK综合分泌相似(伴有脂肪泻的患者为134±23 pM·20分钟,无脂肪泻的患者为131±33 pM·20分钟,健康受试者为146±28 pM·20分钟),表明对体液刺激分泌CCK的能力正常。这些数据与先前研究的观点一致,即胰酶对营养物质的消化在进食后血浆CCK分泌的调节中起重要作用。