A cholecystokinin releasing peptide mediates feedback regulation of pancreatic secretion.
A cholecystokinin releasing peptide mediates feedback regulation of pancreatic secretion.
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胆囊收缩素释放肽介导胰腺分泌的反馈调节。
DOI：
10.1152/ajpgi.1989.256.2.g430
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Owyang,C
中科院分区：
文献类型：
--
作者：
Lu,L;Louie,D;Owyang,C
大鼠十二指肠胆胰液分流刺激胆囊收缩素（CCK）释放和胰酶分泌。十二指肠灌注胰蛋白酶抑制CCK释放和胰酶分泌。我们推测，胰液分流后胰腺酶分泌的增加是由小肠分泌的胰蛋白酶敏感肽介导的，该肽刺激CCK的释放。为了验证这一假设，通过手术准备大鼠胆胰套管和肠瘘。胆胰液的分流刺激淀粉酶的输出比基础水平高5倍，并使血浆CCK从基础水平0.5 +/- 0.05 pM增加到14 +/- 5 pM。用磷酸盐缓冲盐水快速灌注（3 ml/min）十二指肠可逆转淀粉酶输出的增加，并将血浆CCK降低至1.2 +/- 0.2。从供体大鼠收集的肠灌流液（3 ml/min）注入受体大鼠的十二指肠，转移胆胰液，使淀粉酶的输出增加到基础水平的三倍以上，并增加血浆CCK。肠灌流液的刺激活性被灭活处理胰蛋白酶，但不是由淀粉酶或脂肪酶。此外，煮沸并没有改变肠灌注液的刺激活性。用阿托品预处理的供体大鼠肠灌流液灌流不刺激受体大鼠淀粉酶分泌和CCK释放。通过使用分子膜排阻过滤器，保留了刺激活性（在1，000和5，000之间）。这些结果表明，反馈调节胰腺酶分泌介导的CCK释放肽的分泌从十二指肠胆碱能介导的。这种肽对胰蛋白酶敏感，分子量在1，000和5，000之间。
Diversion of bile pancreatic juice from the duodenum in rats stimulates cholecystokinin (CCK) release and pancreatic enzyme secretion. Intraduodenal perfusion of trypsin inhibits the release of CCK and pancreatic enzyme secretion. We hypothesized that the increased pancreatic enzyme secretion after pancreatic juice diversion is mediated by a trypsin-sensitive peptide secreted by the small intestine that stimulates release of CCK. To test this hypothesis, rats were surgically prepared with bile-pancreatic cannula and intestinal fistulas. Diversion of bile-pancreatic juice stimulated amylase output fivefold above basal and increased plasma CCK from a basal of 0.5 +/- 0.05 pM to 14 +/- 5 pM. Rapid perfusion (3 ml/min) of the duodenum with phosphate-buffered saline reversed the increase in amylase output and lowered the plasma CCK to 1.2 +/- 0.2. Administration of intestinal perfusate (3 ml/min) collected from a donor rat into the duodenum of a recipient rat with diversion of bile pancreatic juice increased amylase output threefold above basal and increased plasma CCK. The stimulatory activity of the intestinal perfusate was inactivated by treatment with trypsin but not by amylase or lipase. In addition, boiling did not alter the stimulatory activity of the intestinal perfusate. Perfusion of intestinal perfusate from donor rats pretreated with atropine did not stimulate amylase output and CCK release in recipient rats. By use of molecular membrane exclusion filters, stimulatory activity was retained (between 1,000 and 5,000). These results indicate that feedback regulation of pancreatic enzyme secretion is mediated by a CCK releasing peptide whose secretion from the duodenum is cholinergically mediated. This peptide is trypsin sensitive and has a molecular weight between 1,000 and 5,000.