Extracellular bicarbonate ions and insulin secretion.
The role of bicarbonate ions in insulin release was studied with incubated and perifused isolated rat islets of Langerhans. In the absence of NaHC03, the early phase of glucose-induced secretion was completely abolished and the second phase inhibited by approximately 65%. The insulinotropic effect of the sugar was totally restored after reintroduction of the ion in the medium. The monophasic secretory after reintroduction of the ion in the medium. The monophasic secretory response to tolbutamide was also markedly diminished by omission of NaHC03, WHereas the release evoked by a high concentration of K+ was very little affected. CO2 wwas unable to substitute for HC03minus, but small concentrations of the anion (3to 5mM) WEre sufficient to ensure a normal response to glucose.
D000818:Animals; D000941:Antigens; D001639:Bicarbonates / Q000494:pharmacology*; D002245:Carbon Dioxide; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D014044:Tolbutamide / Q000494:pharmacology
D000941:Antigens; D001639:Bicarbonates; D007328:Insulin; D002245:Carbon Dioxide; D014044:Tolbutamide; D005947:Glucose; D011188:Potassium