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

Kazuki Harada, Tetsuya Kitaguchi, Takashi Tsuboi

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2 Citations (Scopus)

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<sup>2+</sup> and cAMP concentration ([Ca<sup>2+</sup>]<inf>i</inf> and [cAMP]<inf>i</inf>, respectively), and GLP-1 exocytosis in GLUTag cells. Blockade of α1-AR inhibited adrenaline-induced [Ca<sup>2+</sup>]<inf>i</inf> increase and exocytosis but not [cAMP]<inf>i</inf> increase, while blockade of β1-AR inhibited adrenaline-induced [cAMP]<inf>i</inf> increase and exocytosis but not [Ca<sup>2+</sup>]<inf>i</inf> increase. Furthermore, overexpression of α2A-AR suppressed the adrenaline-induced [cAMP]<inf>i</inf> 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.

Original languageEnglish
Pages (from-to)1053-1058
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume460
Issue number4
DOIs
Publication statusPublished - 2015 May 12

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Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology
  • Medicine(all)

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