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下丘脑室旁核内注射食欲素和葡萄糖对清醒大鼠胃酸分泌的影响。

Effects of orexin and glucose microinjected into the hypothalamic paraventricular nucleus on gastric acid secretion in conscious rats.

机构信息

Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Neurogastroenterol Motil. 2012 Feb;24(2):e94-102. doi: 10.1111/j.1365-2982.2011.01789.x. Epub 2011 Oct 17.

DOI:10.1111/j.1365-2982.2011.01789.x
PMID:22004243
Abstract

BACKGROUND

Orexin-A is a novel peptide that appears to play a role in regulation of gastric acid secretion. However, little is known about sites of its action. In addition, evidences suggest that some of orexin-A neurons respond to glucose. In this study, we address the hypothesis which demonstrates that orexin-A and glucose act in the hypothalamic paraventricular nucleus (PVN) to increase gastric acid secretion and juice volume in pyloric-ligated conscious rats.

METHODS

Male Wistar rats were implanted with guide canula directed to the PVN. Orexin-A (3-10 μg), glucose (350-750 ng) SB334867 (6-20 μg) were microinjected. The effect of pretreatment with an orexin-1 receptor antagonist, SB334867, on orexin-A and D-glucose induced acid secretion was assessed. Gastric acid secretion was measured using the pylorus-ligation method, and the amount of gastric acid was determined by titration with 0.01 N NaOH to a pH of 7.0.

KEY RESULTS

Intraparaventricular injection of orexin-A or D-glucose stimulated gastric acid secretion in a dose-dependent manner. The PVN injections of orexin-A receptor antagonist, SB334867, were associated with gastric acid secretion decrease and inhibited effects of PVN-injected orexin-A. Orexin-stimulated gastric acid secretion was decreased (~40%) after PVN lesions. Glucose-stimulated gastric acid secretion was also suppressed by intraperitoneal (IP) injection of SB334867. In addition, it was observed that co-injection of orexin-A and glucose at ineffective doses increased gastric secretion significantly.

CONCLUSIONS & INFERENCES: We suggest that orexin-A and glucose effects on the PVN stimulate gastric acid secretion. This stimulatory effect is probably mediated by orexin-1 receptors.

摘要

背景

食欲素-A 是一种新型肽,似乎在调节胃酸分泌中发挥作用。然而,人们对其作用部位知之甚少。此外,有证据表明,一些食欲素-A 神经元对葡萄糖有反应。在这项研究中,我们提出了一个假设,即食欲素-A 和葡萄糖在下丘脑室旁核(PVN)中起作用,以增加幽门结扎清醒大鼠的胃酸分泌和胃液量。

方法

雄性 Wistar 大鼠被植入导向 PVN 的引导套管。微注射食欲素-A(3-10μg)、葡萄糖(350-750ng)、SB334867(6-20μg)。评估了食欲素-1 受体拮抗剂 SB334867 预处理对食欲素-A 和 D-葡萄糖诱导的胃酸分泌的影响。采用幽门结扎法测量胃酸分泌量,用 0.01NNaOH 滴定至 pH7.0 确定胃酸量。

主要结果

脑室旁注射食欲素-A 或 D-葡萄糖可刺激胃酸分泌,呈剂量依赖性。PVN 注射食欲素-A 受体拮抗剂 SB334867 与胃酸分泌减少有关,并抑制 PVN 注射食欲素-A 的作用。PVN 损伤后食欲素刺激的胃酸分泌减少(~40%)。葡萄糖刺激的胃酸分泌也被腹腔内(IP)注射 SB334867 抑制。此外,观察到在无效剂量下共注射食欲素-A 和葡萄糖可显著增加胃液分泌。

结论和推论

我们认为食欲素-A 和葡萄糖对 PVN 的作用刺激胃酸分泌。这种刺激作用可能是通过食欲素-1 受体介导的。

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