Premium
Glucagon‐like peptide‐1 does not mediate amylase release from AR42J cells
Author(s) -
Zhou Jie,
MontroseRafizadeh Chahrzad,
Janczewski Andrzej M.,
Pineyro Marco A.,
Sollott Steven J.,
Wang Yihong,
Egan Josephine M.
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199912)181:3<470::aid-jcp11>3.0.co;2-p
Subject(s) - amylase , cholecystokinin , chemistry , phosphorylation , intracellular , glucagon , receptor , adenosine , tyrosine phosphorylation , endocrinology , medicine , secretion , calcium in biology , microbiology and biotechnology , biology , biochemistry , enzyme , hormone
In this study, AR42J pancreatic acinar cells were used to investigate if glucagon‐like peptide‐1 (GLP‐1) or glucagon might influence amylase release and acinar cell function. We first confirmed the presence of GLP‐1 receptors on AR42J cells by reverse trasncriptase‐polymerase chain reaction (RT‐PCR), Western blotting, and partial sequencing analysis. While cholecystokinin (CCK) increased amylase release from AR42J cells, GLP‐1, alone or in the presence of CCK, had no effect on amylase release but both CCK and GLP‐1 increased intracellular calcium. Similar to GLP‐1, glucagon increased both cyclic adenosine monophosphate (cAMP) and intracellular calcium in AR42J cells but it actually decreased CCK‐mediated amylase release (n = 20, P < 0.01). CCK stimulation resulted in an increase in tyrosine phosphorylation of several cellular proteins, unlike GLP‐1 treatment, where no such increased phosphorylation was seen. Instead, GLP‐1 decreased such protein phosphorylations. Genestein blocked CCK‐induced phosphorylation events and amylase secretion while vanadate increased amylase secretion. These results provide evidence that tyrosine phosphorylation is necessary for amylase release and that signaling through GLP‐1 receptors does not mediate amylase release in AR42J cells. J. Cell. Physiol. 181:470–478, 1999. Published 1999 Wiley‐Liss, Inc.