par Best, Leonard;Lebrun, Philippe 
;Saceda, Miguel
Référence Biochemical pharmacology, 33, 13, page (2033-2039)
Publication Publié, 1984
;Saceda, MiguelRéférence Biochemical pharmacology, 33, 13, page (2033-2039)
Publication Publié, 1984
Article révisé par les pairs
| Résumé : | The possible participation of enzymatic methylation reactions in the process of insulin release was investigated in rat pancreatic islets. The combination of 3-deazaadenosine and DL-homocystein impaired the incorporation of 3H-methyl from L-[methyl-3H]methionine into endogenous islet proteins and phospholipids, but failed to affect turnover in the phosphatidylinositol cycle. The inhibitors of methylation decreased insulin release evoked by D-glucose or the combinations of D-glucose and gliclazide, L-leucine and L-glutamine, or Ba2+ and theophylline. The inhibitors of methylation did not impair either the oxidation of D-glucose or affect its capacity to decrease K+ conductance, stimulate Ca2+ inflow and provoke 45Ca accumulation in pancreatic islets. It is proposed that, in the process of insulin secretion, a methyl acceptor protein and/or phospholipid play(s) a limited modulatory role in the coupling of cytosolic Ca2+ accumulation to exocytosis. |
