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Leptin activates ATP‐sensitive potassium channels in the rat insulin‐secreting cell line, CRI‐G1
Author(s) -
Harvey J.,
McKenna F.,
Herson P. S.,
Spanswick D.,
Ashford M. L. J.
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.527bd.x
Subject(s) - potassium channel , leptin , medicine , endocrinology , insulin , potassium , atp sensitive potassium channel , chemistry , microbiology and biotechnology , biology , obesity , diabetes mellitus , glibenclamide , organic chemistry
1 Whole‐cell current‐clamp recordings demonstrate that leptin (0.3–10 n m ) hyperpolarizes CRI‐G1 insulin‐secreting cells. This effect is slow on onset and is not reversed on washout of the leptin. 2 Voltage‐clamp recordings indicate that leptin activates a potassium conductance in the presence of intracellular ATP (5 mm), but has no effect in its absence. Following activation of ATP‐sensitive K + (K ATP ) current by diazoxide (0.2 m m ), addition of leptin did not alter cell membrane potential or potassium current further. 3 The leptin‐induced hyperpolarization and increased potassium conductance are completely inhibited by the application of the sulphonylureas tolbutamide (100 μ m ) and glibenclamide (0.5 μ m ). 4 Cell‐attached and inside‐out single‐channel recordings indicate that leptin activates tolbutamide‐sensitive K ATP channels in CRI‐G1 insulin‐secreting cells.