Effects of glucose on insulin release and 86Rb permeability in cultured neonatal and adult rat islets

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Abstract
Glucose‐induced insulin release and modifications in 86Rb outflow were studied in cultured neonatal and adult rat islets. The dose‐response curve for neonatal islets was steeper than for adult islets and the maximal response was clearly shifted towards lower glucose concentrations. In neonatal islets, glucose‐induced insulin release was inhibited by the Ca2+‐channel blocker, nifedipine. In the absence of glucose, the 86Rb outflow from neonatal islets was lower than from adult islets. Also, the glucose‐induced reduction in 86Rb outflow was less pronounced in neonatal islets. Altered K+ permeability in the B‐cell membrane could explain the change in glucose sensitivity of neonatal islets.