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The Incretins and β-Cell Health: Contrasting Glucose-Dependent Insulinotropic Polypeptide and Glucagon-Like Peptide-1 as a Path to Understand Islet Function in Diabetes Lene Jessen, David D'Alessio Gastroenterology Volume 137, Issue 6, Pages (December 2009) DOI: /j.gastro Copyright © 2009 AGA Institute Terms and Conditions
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Figure 1 Incretin actions on β-cells and plausible sites of differential effects. Although there is considerable overlap between pathways, GLP-1r activation may up-regulate IRS-2 expression through transactivation of the EGF receptor, resulting in more potent cytoprotective actions on β-cells. Other mechanisms could also mediate the differential effects of the incretins on β-cell functions. Akt/PKB, Akt-protein kinase B; cAMP, cyclic adenosine monophosphate; CREB, cAMP response element-binding protein; EGF, epidermal growth factor; Epac, guanine nucleotide exchange factor; ER, endoplasmic reticulum; Foxo1, forkhead box O1; IRS-2, insulin receptor substrate-2; MAPK, mitogen-activated protein kinase; NFAT, nuclear factor of activated T cells; NF-κB, nuclear factor-κ B; PDX-1, pancreas duodenum homeobox 1; PI-3K, phosphatidylinositol 3-kinase; PKA, protein kinase A; PKC, protein kinase C; VDCC, voltage-dependent calcium channels. Gastroenterology , DOI: ( /j.gastro ) Copyright © 2009 AGA Institute Terms and Conditions
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