Effects of glucose on insulin release and 86Rb permeability in cultured neonatal and adult rat islets.
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.
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology*; D005985:Glyceraldehyde / Q000494:pharmacology; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012413:Rubidium; D012636:Secretory Rate / Q000187:drug effects; D013806:Theophylline / Q000494:pharmacology
D007328:Insulin; D005985:Glyceraldehyde; D013806:Theophylline; D009543:Nifedipine; D005947:Glucose; D012413:Rubidium; D011188:Potassium