2000年4月
The hepatic vagal reception of intraportal GLP-1 is via receptor different from the pancreatic GLP-1 receptor
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
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- 巻
- 80
- 号
- 1-2
- 開始ページ
- 14
- 終了ページ
- 21
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/S0165-1838(99)00086-7
- 出版者・発行元
- ELSEVIER SCIENCE BV
Glucagon-like peptide-1 (7-36)amide (tGLP-1), a representative humoral incretin, released into the portal circulation in response to a meal ingestion, exerts insulinotropic action through binding to the tGLP-1 receptor known to be a single molecular form thus far. We previously reported that the hepatic vagal nerve is receptive to intraportal tGLP-1, but not to non-insulinotropic full-length GLP-1-(1-37), through a mechanism mediated by specific receptor to the hormone. In the present study, we aimed to examine how modification of the receptor function alters this neural reception of tGLP-1, by using the specific agonist, exendin-4, and the specific antagonist, exendin (9-39)amide. of the receptor at doses known to exert their effects on the insulinotropic action of tGLP-1. Intraportal injection of 0.2 or 4.0 pmol tGLP-1, a periphysiological and pharmacological dose, respectively, facilitated significantly the afferent impulse discharge rate of the hepatic vagus in anesthetized rats, as reported previously. However, unexpectedly, intraportal injection of exendin-4 at a dose of 0.3 or 4.0 pmol, or of even 40.0 pmol, did not facilitate the efferents at all. Moreover, intraportal injection of exendin (9-39)amide at 100 times or more molar dose to that of tGLP-1, either 5 min before or 10 min after injection of 0.2 or 4.0 pmol tGLP-1, failed to modify the tGLP-1-induced facilitation of the afferents. The present results suggest that the neural reception of tGLP-1 involves a receptor mechanism distinct from that in the well-known humoral insulinotropic action. (C) 2000 Elsevier Science B.V. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/S0165-1838(99)00086-7
- ISSN : 0165-1838
- Web of Science ID : WOS:000086347400003