title: Model for extrusion of insulin beta granules.
abstract: Considerable controversy surrounds the mechanisms of insulin secretion. This  hypothesis attempts to explain the events which may lead to insulin extrusion through the beta-cell membrane. The role of various effectors of insulin secretion on the activities of  membrane-bound enzymes is discussed. Glucose, without effect on these enzymes, did induce insulin secretion from insulin granules and plasma membranes in vitro. The model  proposes a mechanism whereby glucose may trigger first-phase insulin secretion; reinforcing mechanisms, such as raised levels of cyclic adenosine monophosphate, could augment subsequent secretion.
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism / Q000502:physiology; D005947:Glucose / Q000494:pharmacology; D005958:Glucosephosphates / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000166:cytology* / Q000378:metabolism; D008954:Models, Biological; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
chemical_list: D005958:Glucosephosphates; D007328:Insulin; D000255:Adenosine Triphosphate; D012964:Sodium; D000242:Cyclic AMP; D000251:Adenosine Triphosphatases; D005947:Glucose; D011188:Potassium