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Glucocorticoids impair KATP-independent signals to reduce ionic fluxes in glucose-stimulated β-cells. This is further exacerbated by HSD11B1, which increases availability of more active glucocorticoid (11-DHC/cortisone→corticosterone/cortisol) in a paracrine manner. However, insulin secretion is preserved because glucocorticoids reprogram the β-cell signaling cassette toward a cAMP phenotype most likely through upregulation of specific Adcy isoforms.
