空肠中一种葡萄糖依赖性机制可抑制胃酸分泌：这是一种通过肠高血糖素介导的反应吗？

A glucose-dependent mechanism in jejunum inhibits gastric acid secretion: a response mediated through enteroglucagon?

作者信息

Petersen B, Christiansen J, Holst J J

出版信息

Scand J Gastroenterol. 1985 Mar;20(2):193-7. doi: 10.3109/00365528509089656.

Abstract

In healthy subjects iso- and hyper-tonic glucose or saline was instilled intrajejunally and the effect on gastric acid secretion determined. Iso- and hyper-tonic glucose (100 ml; 300, 600, 900, 1200 mosm) reduced acid secretion dose-dependently (p less than 0.05), whereas iso- and hyper-tonic saline (100 ml; 300, 1000, 1500 mosm) was without influence. The enteroglucagon plasma levels increased during intrajejunal glucose but not during saline infusion. Gastrin and pancreatic glucagon levels were not affected. Hence, our results substantiate the concept of a non-osmosensitive, glucose-specific inhibitory mechanism of acid secretion located in the jejunum. Furthermore, enteroglucagon could be a possible humoral mediator of the inhibition.

摘要

在健康受试者中，将等渗和高渗葡萄糖或生理盐水经空肠内注入，并测定其对胃酸分泌的影响。等渗和高渗葡萄糖（100毫升；300、600、900、1200毫渗量）剂量依赖性地降低了胃酸分泌（p<0.05），而等渗和高渗生理盐水（100毫升；300、1000、1500毫渗量）则无影响。空肠内注入葡萄糖期间，肠高血糖素血浆水平升高，但注入生理盐水期间则未升高。胃泌素和胰高血糖素水平未受影响。因此，我们的结果证实了空肠中存在一种对酸分泌具有非渗透压敏感性、葡萄糖特异性抑制机制的概念。此外，肠高血糖素可能是这种抑制作用的一种潜在体液介质。