Wisén O, Rössner S, Johansson C
Department of Medicine, Karolinska Hospital, Stockholm, Sweden.
Metabolism. 1988 May;37(5):436-41. doi: 10.1016/0026-0495(88)90043-1.
We previously found that massively obese patients respond with less gastric acid secretion in response to vagal stimulation. This is compatible with the described association between experimental obesity and altered vagal function in the rat. To confirm this observation, the pancreatic and biliary responses to vagal stimulation were examined in nine nondiabetic obese patients against a background secretin infusion of 15 CU x h-1, and monitored after a subsequent injection of 75 IDU of cholecystokinin. Two separate marker perfusion systems were used in the stomach and duodenum, respectively, and blood samples were drawn for hormone analyses. In contrast to controls having normal body weight, the obese patients failed to respond with increments of pancreatic enzyme secretion and duodenal bile acids after stimulation with modified sham feeding. Cholecystokinin stimulated the pancreatic secretion of trypsin, amylase, and lipase, the emptying of bile acids, and the release of gastrin, but the patients' responses were only half that of the controls. In the resting state the obese had higher outputs of bile and pancreatic enzymes and higher plasma levels of pancreatic polypeptide compared with controls, but the pancreatic bicarbonate secretion rate was not different. The almost complete suppression of the basal gastric acid secretion by a low dose of intravenous (IV) secretin in controls did not occur in the obese. We conclude that massive obesity is associated with a reduced pancreatic and biliary response to vagal stimulation. Compared with controls, the digestive functions of the obese patients seem to be less sensitive to stimulation by exogenous cholecystokinin.(ABSTRACT TRUNCATED AT 250 WORDS)
我们之前发现,极度肥胖患者对迷走神经刺激的胃酸分泌反应较弱。这与大鼠实验性肥胖和迷走神经功能改变之间所描述的关联相符。为证实这一观察结果,在9名非糖尿病肥胖患者中,于持续输注15 CU x h-1促胰液素的背景下,检测其对迷走神经刺激的胰腺和胆汁反应,并在随后注射75 IDU胆囊收缩素后进行监测。分别在胃和十二指肠使用两个独立的标记物灌注系统,并采集血样进行激素分析。与体重正常的对照组相比,肥胖患者在模拟假饲刺激后,胰腺酶分泌和十二指肠胆汁酸未出现增加反应。胆囊收缩素刺激了胰蛋白酶、淀粉酶和脂肪酶的胰腺分泌、胆汁酸排空以及胃泌素释放,但患者的反应仅为对照组的一半。在静息状态下,与对照组相比,肥胖患者胆汁和胰腺酶的分泌量更高,血浆胰多肽水平也更高,但胰腺碳酸氢盐分泌率并无差异。对照组中低剂量静脉注射促胰液素几乎完全抑制基础胃酸分泌的情况在肥胖患者中未出现。我们得出结论,极度肥胖与胰腺和胆汁对迷走神经刺激的反应减弱有关。与对照组相比,肥胖患者的消化功能对外源性胆囊收缩素的刺激似乎不太敏感。(摘要截选至250词)