Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY.

Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY.
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肠脂肪诱导的对膳食刺激胃酸分泌的抑制取决于CCK,而不是肽YY。

DOI:
10.1152/ajpgi.1999.276.2.g550
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发表时间:
1999
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Lin,HC
Lin,HC
中科院分区:
--
文献类型:
--
作者:
Zhao,XT;Walsh,JH;Wong,H;Wang,L;Lin,HC

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小肠中的脂肪减少了膳食刺激的胃酸分泌,减缓了胃的排空。CCK是这种抑制作用(肠胃泌素)的中介物。由于静脉注射多肽YY(PYY)抑制酸的分泌,脂肪释放的内源性PYY也可能是一种肠胃泌素。四只狗被装备了胃瘘、十二指肠瘘和中肠瘘。PYY抗体(抗PYY)0.5 mg/kg或CCK-A受体拮抗剂DEVAZEPID(0.1 mg/kg)单独或联合应用10min,再用60 mM油酸或缓冲液灌胃。测定胃酸分泌和胃排空。我们发现:1)肠脂肪(P<0.0001)可抑制蛋白胨诱导的胃酸分泌;2)CCK-A受体拮抗剂(P<0.0001)可逆转肠脂肪对胃酸分泌的抑制,但抗PYY不能逆转其抑制作用;我们的结论是,抑制蛋白调餐诱导的胃酸分泌和肠道脂肪减慢胃排空依赖于CCK,而不是循环PYY。
Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that1) peptone-induced gastric acid secretion was inhibited by intestinal fat (P< 0.0001),2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist (P< 0.0001) but not by anti-PYY, and3) slowing of gastric emptying by fat was reversed by CCK-A antagonist (P< 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.
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