Hidalgo L, Clavé P, Estorch M, Rodríguez-Espinosa J, Rovati L, Greeley G H, Capellà G, Lluís F
Department of Surgery, Hospital de Mataró, Mataró, Spain.
Neurogastroenterol Motil. 2002 Oct;14(5):519-25. doi: 10.1046/j.1365-2982.2002.00355.x.
Our aim was determine the relationship between cholecystokinin (CCK)-A receptor blockade, glucose levels, insulin secretion and gastric emptying in humans, and to assess the effect of CCK-A blockade on pancreatic polypeptide secretion. After a 12-h fast, six healthy volunteers were given [99mTc]iminodiacetic acid monosodium salt (IDA) intravenously (5 mCi). One hour later they were offered a 577 kcal liquid meal containing [99mTc]diethylenetriaminepentaacetic acid (DTPA) (2 mCi) and glucose (105 g). Scintigraphic gastric and gallbladder activity, and plasma glucose, insulin and pancreatic polypeptide responses were monitored. In a second experiment, a continuous intravenous infusion of loxiglumide (7.5 mg kg h(-1)) was started 60 min before and continued until 120 min after test meal ingestion to block the CCK-A receptors. Gallbladder emptying was blocked by loxiglumide. Loxiglumide accelerated gastric emptying, increased insulin secretion without alteration of glucose profiles, and abolished all phases of the postprandial pancreatic polypeptide response. Blockade of peripheral CCK-A receptors accelerates gastric emptying of liquids with an increase in postprandial insulin levels. The lack of changes in glycaemia suggests that alternative homeostatic mechanisms also control postprandial glucose levels. Inhibition of pancreatic polypeptide release may reflect an independent effect of loxiglumide on vagal control involved in pancreatic polypeptide release.
我们的目的是确定人类体内胆囊收缩素（CCK）-A受体阻断、血糖水平、胰岛素分泌和胃排空之间的关系，并评估CCK-A受体阻断对胰多肽分泌的影响。在禁食12小时后，给6名健康志愿者静脉注射[99mTc]亚氨基二乙酸单钠盐（IDA）（5毫居里）。1小时后，给他们提供一份含有[99mTc]二乙三胺五乙酸（DTPA）（2毫居里）和葡萄糖（105克）的577千卡流食。监测闪烁扫描的胃和胆囊活性以及血浆葡萄糖、胰岛素和胰多肽反应。在第二个实验中，在摄入测试餐之前60分钟开始持续静脉输注洛西格列胺（7.5毫克·千克·小时-1），并持续至摄入测试餐之后120分钟，以阻断CCK-A受体。洛西格列胺可阻断胆囊排空。洛西格列胺加速胃排空，增加胰岛素分泌而不改变血糖水平，并消除餐后胰多肽反应的所有阶段。外周CCK-A受体的阻断加速了液体的胃排空，同时餐后胰岛素水平升高。血糖水平没有变化表明，其他稳态机制也控制餐后血糖水平。胰多肽释放的抑制可能反映了洛西格列胺对参与胰多肽释放的迷走神经控制的独立作用。
