Increasing GLP-1–Induced β-Cell Proliferation by Silencing the Negative Regulators of Signaling cAMP Response Element Modulator-α and DUSP14

Abstract

Together, our data show that 1) the cAMP/protein kinase A/CREB and MAPK/ERK1/2 pathways can additively control beta-cell proliferation, 2) beta-cells have evolved several mechanisms limiting GLP-1-induced cellular proliferation, and 3) blocking these mechanisms increases the positive effect of GLP-1 on beta-cell mass.