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A new experimental model of ATP-sensitive K+ channel-independent insulinotropic action of glucose: a permissive role of cAMP for triggering of insulin release from rat pancreatic beta-cells
http://hdl.handle.net/10091/17659
http://hdl.handle.net/10091/17659bb190326-8751-4b8f-92c6-15fe76ca3f9d
| 名前 / ファイル | ライセンス | アクション |
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H24Kou936_Takei.pdf (2.1 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2014-06-27 | |||||
| タイトル | ||||||
| タイトル | A new experimental model of ATP-sensitive K+ channel-independent insulinotropic action of glucose: a permissive role of cAMP for triggering of insulin release from rat pancreatic beta-cells | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| DOI | ||||||
| 関連識別子 | https://doi.org/10.1507/endocrj.EJ12-0388 | |||||
| 関連名称 | 10.1507/endocrj.EJ12-0388 | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Takei, Masahiro
× Takei, Masahiro× Dezaki, Katsuya× Ishii, Hiroaki× Nishio, Shin-ichi× Sato, Yoshihiko× Suzuki, Satoru× Yada, Toshihiko× Komatsu, Mitsuhisa |
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| 出版者 | ||||||
| 出版者 | JAPAN ENDOCRINE SOC | |||||
| 引用 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | ENDOCRINE JOURNAL. 60(5):599-607 (2013) | |||||
| 書誌情報 |
ENDOCRINE JOURNAL 巻 60, 号 5, p. 599-607, 発行日 2013-05 |
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| 内容記述 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 信州大学博士（医学）・学位論文・平成24年3月31日授与（甲第936号）・武井 真大 | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | In pancreatic beta-cells, glucose metabolism leads to closure of ATP sensitive K+ channels (K-ATP channel) and Ca2+ influx, which is regarded as a required step for triggering of insulin release. Here, we demonstrate that glucose triggers rapid insulin release independent from its action on K-ATP channels given the cellular cAMP is elevated. We measured insulin release from rat pancreatic islets by static and perifusion experiments. Changes in cytosolic free Ca2+ concentration ([Ca2+](i)) were monitored using fura-2 loaded rat pancreatic beta-cells. Glucose-induced insulin release was abolished when Ca2+ influx was inhibited by a combination of 250 mu M diazoxide, an opener of K-ATP channel, and 10 mu M nifedipine, a blocker of L-type voltage-dependent Ca2+ channels. However, with both nifedipine and diazoxide, glucose induced a 5-fold increase in insulin release in the presence of 10 mu M forskolin, an activator of adenylyl cyclase. In the presence of diazoxide, nifedipine, and forskolin, 22 mM glucose sharply increased the rate of insulin release within 2 min which peaked at 6 min: this was followed by a further gradual increase in insulin release. In contrast, it lowered [Ca2+](i) with a nadir at 2-3 min followed by a gradual increase in [Ca2+](i). The glucose effect was mimicked by 20 mM alpha-ketoisocaproic acid, a mitochondrial fuel, and it was nullified by 2 mM sodium azide, an inhibitor of mitochondrial electron transport. Cerulenin, an inhibitor of protein acylation, decreased the glucose effect. In conclusion, a rise in [Ca2+](i) through voltage-dependent Ca2+ channels is not mandatory for glucose-induced triggering of insulin release. | |||||
| 資源タイプ（コンテンツの種類） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Article | |||||
| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
