Dissociation by methylamine of insulin release from glucose-induced electrical activity in isolated mouse islets of Langerhans |
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Authors: | P. Lebrun I. Atwater L. M. Rosario A. Herchuelz W. J. Malaisse |
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Affiliation: | 1. Biophysics Department, School of Biological Sciences, University of East Anglia, Norwich, England;2. the Laboratory of Pharmacology, School of Medicine, Free University of Brussels, Brussels, Belgium;3. the Laboratory of Experimental Medicine, School of Medicine, Free University of Brussels, Brussels, Belgium;4. the Laboratory of Cell Biology and Genetics, NIADDK, National Institutes of Health, Bethesda, Md., USA |
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Abstract: | The effect of methylamine on electrical activity and simultaneously measured insulin release was investigated in single perifused islets of normal mice. Methylamine, (2 mmol/L or 6 mmol/L) failed to affect beta-cell input resistance and only caused a modest and transient inhibition of electrical activity of islets exposed to 11.1 mmol/L glucose. Methylamine (2 mmol/L) inhibited insulin release evoked by a five-minute rise in glucose concentration from 5.6 to 22.2 mmol/L, even when the glucose-induced electrical activity remained unaltered. Methylamine, at 2 or 5 mmol/L, partially inhibited insulin release but failed to affect the continuous electrical activity in islets exposed throughout to 22.2 mmol/L glucose. At 10 mmol/L, methylamine reduced both insulin release and electrical activity. These data reinforce the idea that the glucose-induced changes in beta-cell membrane potential represent an early event in the process of stimulus-secretion coupling and can be dissociated from the subsequent process of insulin release. |
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Keywords: | Address reprint requests to I. Atwater Laboratory of Cell Biology and Genetics National Institutes of Health Building 4 Room 312 Bethesda MD 20205. |
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