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Somatostatin induces hyperpolarization in pancreatic islet α cells by activating a G protein‐gated K + channel
Author(s) -
Yoshimoto Yukiko,
Fukuyama Yuji,
Horio Yoshiyuki,
Inanobe Atsushi,
Gotoh Mitsukazu,
Kurachi Yoshihisa
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00076-9
Subject(s) - somatostatin , hyperpolarization (physics) , endocrinology , medicine , pertussis toxin , tolbutamide , g protein , chemistry , delta cell , potassium channel , secretion , glucagon , biology , signal transduction , biochemistry , insulin , organic chemistry , nuclear magnetic resonance spectroscopy
Somatostatin inhibits glucagon‐secretion from pancreatic α cells but its underlying mechanism is unknown. In mouse α cells, we found that somatostatin induced prominent hyperpolarization by activating a K + channel, which was unaffected by tolbutamide but prevented by pre‐treating the cells with pertussis toxin. The K + channel was activated by intracellular GTP (with somatostatin), GTPγS or Gβγ subunits. It was thus identified as a G protein‐gated K + (K G ) channel. RT‐PCR and immunohistochemical analyses suggested the K G channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin‐inhibition of glucagon‐secretion from pancreatic α cells.