Abstract
the mechanism by which islet amyloid polypeptide (IAPP) inhibits insulin release is unclear. We hypothesized that reduced voltage-gated calcium channel activity and intracellular Ca(2+) concentration might contribute to IAPP-mediated inhibition of glucose-stimulated insulin release. rat islet beta cells were cultured and treated with various extracellular concentrations of IAPP, and insulin release was stimulated via addition of glucose. Activation voltage, high voltage-gated calcium channel currents, intracellular Ca(2+) concentration, and insulin secretion were detected by patch clamp electrophysiology, fluorescent digital imaging microscopy using calcium-sensitive fluorescent dye, and radioimmunoassay, respectively. high voltage-gated calcium channel currents, intracellular Ca(2+) concentration, and insulin secretion increased in a dose-dependent manner when rat beta cells were exposed to glucose. After short-term IAPP treatment (5 or 10 µM), these parameters decreased significantly in glucose-stimulated beta cells. However, no significant changes were observed with lower doses of IAPP. glucose-stimulated islet beta-cell high voltage-gated calcium channels were activated in conjunction with insulin secretion, while high extracellular concentrations of IAPP inhibited beta-cell high voltage-gated calcium channel activation and insulin secretion in a dose-dependent manner.
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