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 μM did not. 3 At the stimulatory concentration of 10 mM glucose, all quinolones augmented insulin release in a dose-dependent manner. LFLX (100 μM) 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 μM) increased insulin release augmented by forskolin (5 μM) or 12-O-tetradecanoyl phorbol-13-acetate (100 nM) but not by raising the K+ concentration from 6 to 25 mM. 5 Verapamil (50 μM) or diazoxide (50 - 400 μM) 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.
|Number of pages||5|
|Journal||British Journal of Pharmacology|
|Publication status||Published - 1996|
- ATP-sensitive K channel
- Insulin release
- Quinolone antibiotics