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Biochem Biophys Res Commun. 2015 May 15;460(4):1053-8. doi: 10.1016/j.bbrc.2015.03.151. Epub 2015 Apr 3.

Integrative function of adrenaline receptors for glucagon-like peptide-1 exocytosis in enteroendocrine L cell line GLUTag.

Author information

1
Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan.
2
Cell Signaling Group, Waseda Bioscience Research Institute in Singapore (WABIOS), 11 Biopolis Way #05-02 Helios, Singapore 138667, Singapore; Organization for University Research Initiatives, Waseda University, #304, Block 120-4, 513 Wasedatsurumaki-cho, Shinjuku-ku, Tokyo 162-0041, Japan.
3
Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan. Electronic address: takatsuboi@bio.c.u-tokyo.ac.jp.

Abstract

Adrenaline reacts with three types of adrenergic receptors, α1, α2 and β-adrenergic receptors (ARs), inducing many physiological events including exocytosis. Although adrenaline has been shown to induce glucagon-like peptide-1 (GLP-1) secretion from intestinal L cells, the precise molecular mechanism by which adrenaline regulates GLP-1 secretion remains unknown. Here we show by live cell imaging that all types of adrenergic receptors are stimulated by adrenaline in enteroendocrine L cell line GLUTag cells and are involved in GLP-1 exocytosis. We performed RT-PCR analysis and found that α1B-, α2A-, α2B-, and β1-ARs were expressed in GLUTag cells. Application of adrenaline induced a significant increase of intracellular Ca(2+) and cAMP concentration ([Ca(2+)]i and [cAMP]i, respectively), and GLP-1 exocytosis in GLUTag cells. Blockade of α1-AR inhibited adrenaline-induced [Ca(2+)]i increase and exocytosis but not [cAMP]i increase, while blockade of β1-AR inhibited adrenaline-induced [cAMP]i increase and exocytosis but not [Ca(2+)]i increase. Furthermore, overexpression of α2A-AR suppressed the adrenaline-induced [cAMP]i increase and exocytosis. These results suggest that the fine-turning of GLP-1 secretion from enteroendocrine L cells is established by the balance between α1-, α2-, and β-ARs activation.

KEYWORDS:

Adrenaline; Adrenergic receptors; Enteroendocrine L cell; Exocytosis; Glucagon-like peptide-1

PMID:
25843795
DOI:
10.1016/j.bbrc.2015.03.151
[Indexed for MEDLINE]

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