Calcium affects insulin release and membrane potential in islet beta-cells.
Insulin release from perfused rat pancreas was compared with membrane potentials of single beta-cells from perifused mouse islets during glucose stimulation (11.1 mM) in the presence of varying Ca and Mg concentrations. Depolarization was associated with insulin release and hyperpolarization with its suppression, irrespective of Ca concentration. After sudden reduction of Ca and Mg (to 0.05 and 0.01 mM, respectively), glucose-stimulated insulin release was maintained while the cell membrane depolarized, leading to a reversed pattern of burst activity. Readdition of Ca and Mg caused suppression of insulin release that paralleled hyperpolarization of the cell membrane. This suppression was transient, lasting < 5 min, and was due mainly to readdition of Ca. Patterns of insulin release during reduction of Ca and Mg in the presence of valinomycin (1 microM), diphenylhydantoin (25 microgram/ml), and ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (0.037 and 1.0 mM) were also studied. In conclusion, the relative concentrations of Ca and Mg and the membrane potential per se are important in the release of insulin. Also, under certain experimental conditions, Ca can block glucose-stimulated insulin release, possibly by increasing K+ permeability.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002118:Calcium / Q000502:physiology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007473:Ion Channels / Q000502:physiology; D007515:Islets of Langerhans / Q000378:metabolism*; D008274:Magnesium / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D051381:Rats; D012636:Secretory Rate
D001786:Blood Glucose; D007328:Insulin; D007473:Ion Channels; D008274:Magnesium; D002118:Calcium