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Increase in insulin release from rat pancreatic islets by quinolone antibiotics
Author(s) -
Maeda N.,
Tamagawa T.,
Niki I.,
Miura H.,
Ozawa K.,
Watanabe G.,
ogaki K.,
Uemura K.,
Iguchi A.
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15201.x
Subject(s) - insulin , tolbutamide , diazoxide , medicine , endocrinology , chemistry , drug interaction , pharmacology , quinolone , forskolin , pancreatic islets , lomefloxacin , antibiotics , islet , biology , stimulation , norfloxacin , biochemistry , ciprofloxacin , pharmacokinetics
1 The present study was undertaken to elucidate the mechanism(s) of hypoglycaemia caused by quinolone antibiotics. We investigated the effects of various quinolone antibiotics on insulin release in rat pancreatic islets. 2 At a non‐stimulatory concentration of 3 mM glucose, lomefloxacin (LFLX) or sparfloxacin at 1 mM and pipemidic acid (0.1‐1 mM) induced slight insulin release but tosufloxacin or enoxacin up to 100 μ m did not. 3 At the stimulatory concentration of 10 mM glucose, all quinolones augmented insulin release in a dose‐dependent manner. LFLX (100 μ m ) shifted the dose‐response curve of glucose‐induced insulin release to the left without altering the maximal response. 4 At 10 mM glucose, LFLX (100 μ m ) increased insulin release augmented by forskolin (5 μ m ) or 12‐0‐tetradecanoyl phorbol‐13‐acetate (100 nM) but not by raising the K + concentration from 6 to 25 mM. 5 Verapamil (50 μ m ) or diazoxide (50–400 μ m ) antagonized the insulinotropic effect of LFLX. 6 These data suggest that quinolone antibiotics may cause hypoglycaemia by increasing insulin release via blockade of ATP‐sensitive K + channels.