The Experts below are selected from a list of 7044 Experts worldwide ranked by ideXlab platform

George N Williams - One of the best experts on this subject based on the ideXlab platform.

Robert F Margolskee - One of the best experts on this subject based on the ideXlab platform.

  • loss of high frequency glucose induced ca2 oscillations in pancreatic islets correlates with impaired glucose tolerance in trpm5 mice
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Barbara Colsoul, Anica Schraenen, Katleen Lemaire, Roel Quintens, Leentje Van Lommel, Andrei Segal, Grzegorz Owsianik, Karel Talavera, Thomas Voets, Robert F Margolskee
    Abstract:

    Glucose homeostasis is critically dependent on insulin release from pancreatic β-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 Trpm5−/− cells. Ca2+-imaging and electrophysiological analysis show that glucose-induced oscillations of Vm 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.

  • loss of high frequency glucose induced ca2 oscillations in pancreatic islets correlates with impaired glucose tolerance in trpm5 mice
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Barbara Colsoul, Anica Schraenen, Katleen Lemaire, Roel Quintens, Andrei Segal, Grzegorz Owsianik, Karel Talavera, Thomas Voets, Leentje Van Lommel, Robert F Margolskee
    Abstract:

    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.

Katsuyuki Aoki - One of the best experts on this subject based on the ideXlab platform.

Adegboye O Adeyemo - One of the best experts on this subject based on the ideXlab platform.

Barbara Colsoul - One of the best experts on this subject based on the ideXlab platform.

  • loss of high frequency glucose induced ca2 oscillations in pancreatic islets correlates with impaired glucose tolerance in trpm5 mice
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Barbara Colsoul, Anica Schraenen, Katleen Lemaire, Roel Quintens, Leentje Van Lommel, Andrei Segal, Grzegorz Owsianik, Karel Talavera, Thomas Voets, Robert F Margolskee
    Abstract:

    Glucose homeostasis is critically dependent on insulin release from pancreatic β-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 Trpm5−/− cells. Ca2+-imaging and electrophysiological analysis show that glucose-induced oscillations of Vm 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.

  • loss of high frequency glucose induced ca2 oscillations in pancreatic islets correlates with impaired glucose tolerance in trpm5 mice
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Barbara Colsoul, Anica Schraenen, Katleen Lemaire, Roel Quintens, Andrei Segal, Grzegorz Owsianik, Karel Talavera, Thomas Voets, Leentje Van Lommel, Robert F Margolskee
    Abstract:

    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.