The stimulus-secretion coupling of glucose-induced insulin release. XLVII. The possible role of calmodulin
Abstract
Pancreatic islets contain calmodulin. This protein activates adenylate cyclase in a subcellular fraction of rat islets in a calcium-dependent fashion. The Km for calmodulin was close to 0.1 microM, well below the concentration of endogenous calmodulin. Trifluoperazine and the trifluoromethylphenothiazine derivative of domperidone inhibited glucose-stimulated insulin release without affecting glucose oxidation by the islets. When insulin release was inhibited by 30% or more, this inhibition coincided with a reduction in the 45Ca net uptake by the islets. Both drugs suppressed the increment in adenylate cyclase activity evoked by calmodulin in a particulate fraction derived from the islets. However, the drugs also decreased basal and NaF-stimulated adenylate cyclase activities. Within limits, these data are compatible with the participation of endogenous calmodulin in the normal process of insulin release.
Citations
Role of calmodulin in thyroid hormone stimulation in vitro of human erythrocyte Ca2+-ATPase activity
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