Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 11, Pages 5208-5213Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0913107107
Keywords
Ca2+ signaling; insulin release; pancreatic beta-cells; transient receptor potential ion channels; glucose sensing
Categories
Funding
- FWO Vlaanderen
- European Union [FP6-518153]
- Belgian Ministry for Science Policy [P6/40, P6/28]
- Excellentiefinanciering [EF/95/010]
- Research Foundation-Flanders [G.0172.03, 1.5.206.09, G. 0565.07]
- Katholieke Universiteit Leuven [2004/07, 2004/11, 2008/16]
- National Institutes of Health [DC03055]
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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 (Vm) and the cytosolic calcium level ([Ca2+](cyt)). We propose that TRPM5, a Ca2+-activated monovalent cation channel, is a positive regulator of glucose-induced insulin release. Immunofluorescence revealed expression of TRPM5 in pancreatic islets. A Ca2+-activated nonselective cation current with TRPM5-like properties is significantly reduced in Trpm(5-/-) cells. Ca2+-imaging and electrophysiological analysis show that glucose- induced oscillations of V-m and [Ca2+](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.
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