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  1. 050 医学部, 大学院医学系研究科
  2. 0507 学位論文
  3. 博士(医学)

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
bb190326-8751-4b8f-92c6-15fe76ca3f9d
名前 / ファイル ライセンス アクション
H24Kou936_Takei.pdf H24Kou936_Takei.pdf (2.1 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2014-06-27
タイトル
言語 en
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
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ journal article
著者 Takei, Masahiro

× Takei, Masahiro

WEKO 17409

Takei, Masahiro

Search repository
Dezaki, Katsuya

× Dezaki, Katsuya

WEKO 17410

Dezaki, Katsuya

Search repository
Ishii, Hiroaki

× Ishii, Hiroaki

WEKO 17411

Ishii, Hiroaki

Search repository
Nishio, Shin-ichi

× Nishio, Shin-ichi

WEKO 17412

Nishio, Shin-ichi

Search repository
Sato, Yoshihiko

× Sato, Yoshihiko

WEKO 17413

Sato, Yoshihiko

Search repository
Suzuki, Satoru

× Suzuki, Satoru

WEKO 17414

Suzuki, Satoru

Search repository
Yada, Toshihiko

× Yada, Toshihiko

WEKO 17415

Yada, Toshihiko

Search repository
Komatsu, Mitsuhisa

× Komatsu, Mitsuhisa

WEKO 17416

Komatsu, Mitsuhisa

Search repository
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
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
DOI
関連識別子
識別子タイプ DOI
関連識別子 https://doi.org/10.1507/endocrj.EJ12-0388
関連名称
関連名称 10.1507/endocrj.EJ12-0388
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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