Glucagon-like peptide-1 activation of TCF7L2-dependent Wnt signaling enhances pancreatic beta cell proliferation

J Biol Chem. 2008 Mar 28;283(13):8723-35. doi: 10.1074/jbc.M706105200. Epub 2008 Jan 23.

Abstract

The insulinotropic hormone GLP-1 (glucagon-like peptide-1) is a new therapeutic agent that preserves or restores pancreatic beta cell mass. We report that GLP-1 and its agonist, exendin-4 (Exd4), induce Wnt signaling in pancreatic beta cells, both isolated islets, and in INS-1 cells. Basal and GLP-1 agonist-induced proliferation of beta cells requires active Wnt signaling. Cyclin D1 and c-Myc, determinants of cell proliferation, are up-regulated by Exd4. Basal endogenous Wnt signaling activity depends on Wnt frizzled receptors and the protein kinases Akt and GSK3beta but not cAMP-dependent protein kinase. In contrast, GLP-1 agonists enhance Wnt signaling via GLP-1 receptor-mediated activation of Akt and beta cell independent of GSK3beta. Inhibition of Wnt signaling by small interfering RNAs to beta-catenin or a dominant-negative TCF7L2 decreases both basal and Exd4-induced beta cell proliferation. Wnt signaling appears to mediate GLP-1-induced beta cell proliferation raising possibilities for novel treatments of diabetes.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Line
  • Cell Proliferation / drug effects
  • Cell Separation
  • Cyclic AMP / metabolism
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cyclin D1 / genetics
  • Enzyme Activation
  • Exenatide
  • Frizzled Receptors / metabolism
  • Glucagon-Like Peptide 1 / pharmacology*
  • Glycogen Synthase Kinase 3 / metabolism
  • Humans
  • Insulin / pharmacology
  • Insulin-Secreting Cells / cytology*
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / metabolism*
  • Ligands
  • Mice
  • Peptides / pharmacology
  • Rats
  • Receptors, Glucagon / metabolism
  • Signal Transduction / drug effects*
  • TCF Transcription Factors / genetics
  • TCF Transcription Factors / metabolism*
  • Transcription Factor 7-Like 2 Protein
  • Venoms / pharmacology
  • Wnt Proteins / metabolism*
  • beta Catenin / metabolism

Substances

  • Cyclic AMP Response Element-Binding Protein
  • Frizzled Receptors
  • Insulin
  • Ligands
  • Peptides
  • Receptors, Glucagon
  • TCF Transcription Factors
  • TCF7L2 protein, human
  • Tcf7l2 protein, mouse
  • Transcription Factor 7-Like 2 Protein
  • Venoms
  • Wnt Proteins
  • beta Catenin
  • Cyclin D1
  • Glucagon-Like Peptide 1
  • Exenatide
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases
  • Glycogen Synthase Kinase 3