Transmembrane ion distribution and insulin secretion.
The sodium dependence of insulin release was studied with the in vitro perfused principal islet of channel catfish. When extracellular sodium was replaced with choline, glucose-induced insulin release and glucose enhancement of arginine-induced insulin release were selectively abolished. Lowering the extracellular pH from 7.6 to 7.1 had a similar selective effect on glucose-induced insulin release. It is suggested that the Na:H antiport is responsible for the sodium dependence of insulin release and that a lowered cytosolic pH preferentially inhibits the glucose sensing mechanism.
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D002397:Catfishes; D002462:Cell Membrane / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007515:Islets of Langerhans / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D017923:Sodium-Hydrogen Exchangers
D002352:Carrier Proteins; D007328:Insulin; D007473:Ion Channels; D017923:Sodium-Hydrogen Exchangers; D012964:Sodium; D005947:Glucose