Gap junctions and B-cell function.
The development of gap junctions between pancreatic B-cells was quantitatively assessed in freeze-fracture replicas of isolated rat islets under various conditions of insulin secretion. Stimulation of insulin secretion by glucose in vitro and by glibenclamide in vivo raised the number of gap junctions between B-cells; glibenclamide alone caused an increase in the size of individual gap junctions. In addition, gap junctions of control and stimulated B-cells showed a packing of particles different from that observed under experimental conditions causing functional uncoupling. The results suggest that gap junctions (and probably coupling) are involved in the secretory activity of B-cells.
D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D002462:Cell Membrane / Q000502:physiology; D004140:Dinitrophenols / Q000494:pharmacology; D005614:Freeze Fracturing; D005947:Glucose / Q000502:physiology; D005905:Glyburide / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007365:Intercellular Junctions / Q000502:physiology*; D007515:Islets of Langerhans / Q000502:physiology*; D008854:Microscopy, Electron; D051381:Rats
D004140:Dinitrophenols; D007328:Insulin; D002245:Carbon Dioxide; D005947:Glucose; D005905:Glyburide