Glucagon-like peptide-1 inhibits gastric emptying via vagal afferent-mediated central mechanisms
Glucagon-like peptide-1 inhibits gastric emptying via vagal afferent-mediated central mechanisms
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DOI：
10.1152/ajpgi.1997.273.4.g920
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发表时间：
1997-10-01
影响因子：
4.5
通讯作者：
Ulusoy, NB
中科院分区：
文献类型：
--
作者：
Imeryuz, N;Yegen, BC;Ulusoy, NB
外源性施用胰高血糖素样肽-1-(7-36)酰胺(GLP-1)（一种促胰岛素激素）可抑制人体胃排空和胃酸分泌。 GLP-1 作为胃功能调节剂的作用尚不清楚。在胃瘘大鼠中，迷走神经传入神经支配和外周给予 GLP-1 受体拮抗剂 exendin-(9-39) 酰胺可增强葡萄糖餐的排空，而脑室内 exendin 则无效。外周和中枢施用GLP-1可减弱盐水排空率，并且通过相应途径用毒蜥外泌肽预处理可逆转GLP-1的抑制作用。迷走神经传入去神经消除了 GLP-1 对胃排空的中枢和外周作用。外周胆碱能或肾上腺素能阻断均未改变脑池内注射 GLP-1 导致甲基纤维素膳食排空的延迟。脑池内给予 GLP-1 可抑制清醒幽门结扎大鼠的胃酸分泌，而全身 GLP-1 则无效。这些结果支持GLP-1受体参与胃功能的中枢和外周调节的观点。此外，迷走神经传入神经介导 GLP-1 对胃运动功能的抑制作用。 GLP-1可能是一种候选脑肠肽，可作为胃功能的生理调节剂。
Exogenous administration of glucagon-like peptide-1-(7-36) amide (GLP-1), an insulinotropic hormone, inhibits gastric emptying and acid secretion in humans. The role of GLP-1 as a regulator of gastric function is elusive. In gastric fistula rats, vagal afferent denervation and peripheral administration of the GLP-1 receptor antagonist exendin-(9-39) amide enhanced emptying of a glucose meal, whereas intracerebroventricular exendin was ineffective. The rate of saline emptying was attenuated by peripheral as well as by central administration of GLP-1, and pretreatment with exendin by the respective routes reversed the inhibition by GLP-1. Vagal afferent denervation abolished the central and peripheral action of GLP-1 on gastric emptying. Neither peripheral cholinergic nor adrenergic blockade altered the delay of methyl cellulose meal emptying by intracisternal GLP-1 injection. Acid secretion in conscious pylorus-ligated rats was inhibited by intracisternal GLP-1 administration, whereas systemic GLP-1 was ineffective. These results support the notion that GLP-1 receptors participate in the central and peripheral regulation of gastric function. Furthermore, vagal afferent nerves mediate the inhibitory action of GLP-1 on gastric motor function. GLP-1 may be a candidate brain-gut peptide that acts as a physiological modulator of gastric function.