Bitter tastant quinine modulates glucagon-like peptide-1 exocytosis from clonal GLUTag enteroendocrine L cells via actin reorganization

Enteroendocrine L cells in the gastrointestinal tract secrete glucagon-like peptide-1 (GLP-1), which plays an important role in glucose homeostasis. Here we investigated the effect of bitter tastant quinine on GLP-1 secretion using clonal GLUTag mouse enteroendocrine L cells. We found that GLUTag ce...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2018-06, Vol.500 (3), p.723-730
Main Authors: Harada, Kazuki, Sakaguchi, Hidekazu, Sada, Shoko, Ishida, Rika, Hayasaka, Yuki, Tsuboi, Takashi
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Actin reorganization
Bitter taste receptors
ENDOPLASMIC RETICULUM
Enteroendocrine L cell
GASTROINTESTINAL TRACT
GLUCAGON
Glucagon-like peptide-1
GLUCOSE
Live-cell imaging
MESSENGER-RNA
MICE
QUININE
RECEPTORS
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Summary:Enteroendocrine L cells in the gastrointestinal tract secrete glucagon-like peptide-1 (GLP-1), which plays an important role in glucose homeostasis. Here we investigated the effect of bitter tastant quinine on GLP-1 secretion using clonal GLUTag mouse enteroendocrine L cells. We found that GLUTag cells expressed putative quinine receptors at mRNA levels. Although application of quinine resulted in an increase of intracellular Ca2+ levels, which was mediated by Ca2+ release from the endoplasmic reticulum and Ca2+ influx through voltage-sensitive Ca2+ channels, quinine had little effect on GLP-1 secretion. Total internal reflection fluorescence microscopy and immunocytochemistry revealed that GLP-1-containing vesicles remained unfused with the plasma membrane and facilitated actin polymerization beneath the plasma membrane after application of quinine, respectively. Interestingly, application of forskolin together with quinine induced GLP-1 exocytosis from the cells. These results suggest that quinine does not induce GLP-1 secretion because it facilitates Ca2+ increase and actin reorganization but not cAMP increase, and both Ca2+ and cAMP are essential for GLP-1 secretion. •Various bitter taste receptors were expressed in GLUTag cells.•Quinine increased the intracellular Ca2+ levels but did not promote GLP-1 secretion.•Quinine caused actin reorganization and suppressed exocytosis of GLP-1 vesicles.•Application of forskolin in quinine-treated GLUTag cells enhanced GLP-1 exocytosis.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.04.143