The Stimulus-Secretion Coupling of Glucose-Induced Insulin Release. VII. A PROPOSED SITE OF ACTION FOR ADENOSINE-3′,5′-CYCLIC MONOPHOSPHATE
AUTOR(ES)
Brisson, Guy R.
RESUMO
Glucose-induced insulin release is thought to result from the following sequence of events in the beta cell: glucose metabolism leading to the production of a metabolic signal, net calcium uptake by the beta cell in response to the signal, and interaction between calcium and a microtubular-microfilamentous system, leading to emiocytosis of the secretory granules. Dibutyryl-cyclic AMP (db-cAMP) and theophylline are known to potentiate glucose-induced insulin release, their insulinotropic action being most marked at high glucose concentrations. Based on the above mentioned concepts, it was considered in the present experiments that the primary site of action of cAMP in the beta cell could correspond to either a facilitation of glucose metabolism, a modification of calcium distribution, or an interaction with the microtubular-microfilamentous system.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=302121Documentos Relacionados
- The stimulus-secretion coupling of glucose-induced insulin release. Metabolic and functional effects of NH4+ in rat islets.
- Bioregulation of lysosomal enzyme secretion from human neutrophils: roles of guanosine 3':5'-monophosphate and calcium in stimulus-secretion coupling.
- Amylin modulates beta-cell glucose sensing via effects on stimulus-secretion coupling.
- Partial pancreatectomy in the rat and subsequent defect in glucose-induced insulin release.
- Inhibitors of CDP-choline synthesis, action potential calcium channels, and stimulus-secretion coupling.