Molecular basis of cAMP signaling in pancreatic β cells

George G. Holz, Oleg G. Chepurny, Colin A. Leech, Woo Jin Song, Mehboob A. Hussain

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


Recent advances in conditional gene targeting and cyclic nucleotide research further our understanding of how the incretin hormone GLP-1 exerts a therapeutically important action to restore pancreatic insulin secretion in patients with type 2 diabetes mellitus (T2DM). These studies demonstrate that the pancreatic β-cell GLP-1 receptor has the capacity to signal through two distinct branches of the adenosine 3′,5′-cyclic monophosphate (cAMP) signal transduction network; one branch activates protein kinase A (PKA), and the second engages a cAMPregulated guanine nucleotide exchange factor designated as Epac2. Under normal dietary conditions, specific activation of the cAMP-PKA branch in mice dramatically augments glucose-stimulated insulin secretion (GSIS). However, under conditions of diet-induced insulin resistance, cAMP-Epac2 signaling in the control of GSIS becomes prominent. This chapter provides an update on GLP-1 receptor signaling in the islets of Langerhans, with special emphasis on key molecular events that confer “plasticity” in the β-cell cAMP signal transduction network. The reader is reminded that an excellent review of β-cell cAMP signaling can also be found in the prior first edition of this book.

Original languageEnglish (US)
Title of host publicationIslets of Langerhans, Second Edition
PublisherSpringer Netherlands
Number of pages39
ISBN (Electronic)9789400766860
ISBN (Print)9789400766853
StatePublished - Jan 1 2015


  • Cyclic amp
  • Diabetes
  • Epac2
  • Glp-1
  • Protein kinase a

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)


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