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GLP-1-activated PKA inhibits voltage-gated potassium channels, prevents membrane repolarization, and prolongs VDC channel opening to promote Ca 2+ inward currents, contributing to GLP-1 stimulate insulin secretion, and the antagonistic effect of GLP-1R activation on Kv currents in βcells requires transactivation of epidermal growth factor receptors, accompanied by signal conduction of cAMP/PKA and phosphatidylinositol-3-kinase (PI3K)/PKCζ signaling (MacDonald et al., 2003)
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