Increase in insulin release from rat pancreatic islets by quinolone antibiotics

N. Maeda, T. Tamagawa, I. Niki, H. Miura, K. Ozawa, G. Watanabe, K. Nonogaki, K. Uemura, A. Iguchi

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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.

Original languageEnglish
Pages (from-to)372-376
Number of pages5
JournalBritish Journal of Pharmacology
Issue number2
Publication statusPublished - 1996


  • ATP-sensitive K channel
  • Hypoglycaemia
  • Insulin release
  • Quinolone antibiotics


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