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著者: Atsunori Saraya, Masaaki Yokokura, Tohru Gonoi, Susumu Seino
雑誌名: Eur J Pharmacol. 2004 Aug 16;497(1):111-7. doi: 10.1016/j.ejphar.2004.06.032.
Abstract/Text
Although fluoroquinolones are used widely in the treatment of various infectious diseases, some of the drugs are known to cause hypoglycemia as a side-effect. We have investigated the effects of three fluoroquinolone derivatives, levofloxacin, gatifloxacin, and temafloxacin, on insulin secretion and pancreatic beta-cell ATP-sensitive K(+) channel (K(ATP) channel) activity. While levofloxacin had only a small effect on insulin secretion and K(ATP) currents, gatifloxacin and temafloxacin stimulated insulin secretion and inhibited K(ATP) channel currents in a dose-dependent manner. We also determined the site of action of gatifloxacin and temafloxacin on the K(ATP) channel. In a reconstituted system, gatifloxacin and temafloxacin inhibited Kir6.2 Delta C26 channels, which function in the absence of the SUR subunit, indicating direct action of the drugs on the Kir6.2 subunits. These results suggest that stimulation of insulin secretion by inhibition of pancreatic beta-cell K(ATP) channels underlies the hypoglycemia caused by certain fluoroquinolones.
PMID 15321742 Eur J Pharmacol. 2004 Aug 16;497(1):111-7. doi: 10.1016/j.ejphar.2004.06.032.
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