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胰高血糖素样肽-1延缓大鼠胃排空和小肠转运:通过中枢或肠神经系统机制介导的作用。

Glucagon-like peptide-1 retards gastric emptying and small bowel transit in the rat: effect mediated through central or enteric nervous mechanisms.

作者信息

Tolessa T, Gutniak M, Holst J J, Efendic S, Hellström P M

机构信息

Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.

出版信息

Dig Dis Sci. 1998 Oct;43(10):2284-90. doi: 10.1023/a:1026678925120.

Abstract

This study investigated effects of glucagon-like peptide-1(7-36)amide (GLP-1) on gastric emptying, small intestinal transit, and contractility of smooth muscle strips in rats. GLP-1 at doses of 10 and 20 pmol/kg/min administered intravenously dose-dependently retarded transit of the small intestine (P < 0.001), while only the higher dose of 20 pmol/kg/min retarded gastric emptying (P < 0.01). GLP-1 at concentrations up to 10(-4) M did not affect the basal tone or contractility of the gastrointestinal muscle strips that were stimulated with electric field stimulation or acetylcholine. Our results demonstrate that small intestinal transit seems more sensitive than gastric emptying to inhibition by GLP-1 at physiologic levels in plasma. Furthermore, this inhibition appears to be mediated through central mechanisms rather than through peripheral actions. Thus, GLP-1 is suggested to inhibit gastric emptying and small intestinal transit through an indirect effect via central or enteric nervous mechanisms.

摘要

本研究调查了胰高血糖素样肽-1(7-36)酰胺(GLP-1)对大鼠胃排空、小肠转运及平滑肌条收缩性的影响。静脉注射剂量为10和20 pmol/kg/min的GLP-1可剂量依赖性地延缓小肠转运(P < 0.001),而仅较高剂量20 pmol/kg/min可延缓胃排空(P < 0.01)。浓度高达10(-4) M的GLP-1不影响经电场刺激或乙酰胆碱刺激的胃肠肌条的基础张力或收缩性。我们的结果表明,在生理水平的血浆中,小肠转运对GLP-1抑制的敏感性似乎高于胃排空。此外,这种抑制似乎是通过中枢机制而非外周作用介导的。因此,提示GLP-1通过中枢或肠神经系统机制的间接作用抑制胃排空和小肠转运。

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