Insulinotropic action of glutamate is dependent on the inhibition of ATP-sensitive potassium channel activities in MIN 6 beta cells |
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Authors: | Katsuta Hidenori Ozawa Sachihiko Ninomiya Tomonori Shimoyama Tatsuhiro Ito Eisuke Tanaka Toshiaki Yamaguchi Shinya Katahira Hiroshi Nagamatsu Shinya Horie Minoru Ishida Hitoshi |
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Institution: | Third Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan. |
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Abstract: | To investigate the cellular mechanism of insulinotropic effect of glutamate in pancreatic beta cells, we utilized patch-clamp technique to monitor directly the activities of ATP-sensitive potassium channels (K(ATP) channels). Dimethylglutamate (5mM), a membrane-permeable analog of glutamate, augmented the insulin release induced by the stimulatory concentrations of glucose (p<0.05-0.01). In the cell-attached configurations, dimethylglutamate reversibly and significantly suppressed the K(ATP) channel activities (p<0.01). On the other hand, no significant effect was observed when glutamate itself was applied to the inside-out patches, whereas the prompt and reversible suppression was recorded in the case of ATP (p<0.01). These results indicate that the insulinotropic action of glutamate in beta cells could be derived from the inhibition of K(ATP) channel activities, probably due to generation of messengers via intracellular metabolism such as ATP. |
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Keywords: | Glutamate Insulin secretion Pancreatic β cells ATP-sensitive potassium channels (KATP channels) Patch-clamp technique |
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