Model for extrusion of insulin beta granules.
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.
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
D005958:Glucosephosphates; D007328:Insulin; D000255:Adenosine Triphosphate; D012964:Sodium; D000242:Cyclic AMP; D000251:Adenosine Triphosphatases; D005947:Glucose; D011188:Potassium