Loss of high-frequency glucose-induced Ca2+ oscillations in pancreatic islets correlates with impaired glucose tolerance in Trpm5-/- mice

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  • Barbara Colsoul
  • Anica Schraenen
  • Katleen Lemaire
  • Roel Quintens
  • Leentje Van Lommel
  • Andrei Segal
  • Grzegorz Owsianik
  • Karel Talavera
  • Thomas Voets
  • Robert F. Margolskee
  • Zaza Kokrashvili
  • Patrick Gilon
  • Bernd Nilius
  • Frans C. Schuit
  • Rudi Vennekens

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Glucose homeostasis is critically dependent on insulin release from pancreatic beta-cells, which is strictly regulated by glucose-induced oscillations in membrane potential (V(m)) and the cytosolic calcium level ([Ca(2+)](cyt)). We propose that TRPM5, a Ca(2+)-activated monovalent cation channel, is a positive regulator of glucose-induced insulin release. Immunofluorescence revealed expression of TRPM5 in pancreatic islets. A Ca(2+)-activated nonselective cation current with TRPM5-like properties is significantly reduced in Trpm5(-/-) cells. Ca(2+)-imaging and electrophysiological analysis show that glucose-induced oscillations of V(m) and [Ca(2+)](cyt) have on average a reduced frequency in Trpm5(-/-) islets, specifically due to a lack of fast oscillations. As a consequence, glucose-induced insulin release from Trpm5(-/-) pancreatic islets is significantly reduced, resulting in an impaired glucose tolerance in Trpm5(-/-) mice.


Original languageEnglish
Pages (from-to)5208-5213
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number11
Publication statusPublished - Mar 2010


  • Ca2+ signaling, insulin release, pancreatic beta cells, transient receptor potential ion channels, glucose sensing

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