肠道脂肪对进食刺激的胃酸分泌的抑制作用依赖于胆囊收缩素而非肽YY。
Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY.
作者信息
Zhao X T, Walsh J H, Wong H, Wang L, Lin H C
机构信息
Department of Medicine, Cedars-Sinai Burns and Allen Research Institute, Cedars-Sinai Medical Center, Los Angeles 90048, USA.
出版信息
Am J Physiol. 1999 Feb;276(2):G550-5. doi: 10.1152/ajpgi.1999.276.2.G550.
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 that 1) 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, and 3) 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.
小肠中的脂肪会减少进食刺激引起的胃酸分泌，并减缓胃排空。胆囊收缩素（CCK）是这种抑制作用的介质（一种肠抑胃素）。由于静脉注射的肽YY（PYY）会抑制胃酸分泌，脂肪释放的内源性PYY也可能是一种肠抑胃素。对四只狗进行了胃、十二指肠和中肠造瘘术。在肠道近端一半用60 mM油酸盐或缓冲液灌注前10分钟，单独或联合给予剂量为0.5 mg/kg的PYY抗体（抗PYY）或剂量为0.1 mg/kg的CCK-A受体拮抗剂（地伐西匹）。测量胃酸分泌和胃排空情况。我们发现：1）蛋白胨诱导的胃酸分泌受到肠道脂肪的抑制（P < 0.0001）；2）肠道脂肪对胃酸分泌的抑制作用可被CCK-A受体拮抗剂逆转（P < 0.0001），但不能被抗PYY逆转；3）脂肪引起的胃排空减慢可被CCK-A拮抗剂逆转（P < 0.05），但不能被抗PYY逆转。我们得出结论，肠道脂肪对蛋白胨餐诱导的胃酸分泌的抑制作用和胃排空的减慢取决于CCK，而不取决于循环中的PYY。
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