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Glucose-incretin interaction revisited
http://hdl.handle.net/10091/17576
http://hdl.handle.net/10091/17576d83316c0-ec6d-4fc2-bb08-14d9da3e4b6a
| 名前 / ファイル | ライセンス | アクション |
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Glucose-incretin_interaction_revisited.pdf (989.0 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2014-06-09 | |||||
| タイトル | ||||||
| タイトル | Glucose-incretin interaction revisited | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| DOI | ||||||
| 関連識別子 | https://doi.org/10.1507/endocrj.EJ11-0064 | |||||
| 関連名称 | 10.1507/endocrj.EJ11-0064 | |||||
| キーワード | ||||||
| 主題 | Glucose, Insulin secretion, ATP-sensitive K(+) channel, Incretin, cAMP | |||||
| 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 |
Ishii, Hiroaki
× Ishii, Hiroaki× Sato, Yoshihiko× Takei, Masahiro× Nishio, Shinichi× Komatsu, Mitsuhisa |
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| 信州大学研究者総覧へのリンク | ||||||
| 表示名 | Nishio, Shinichi | |||||
| URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.janagUkh.html | |||||
| 信州大学研究者総覧へのリンク | ||||||
| 表示名 | Komatsu, Mitsuhisa | |||||
| URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.HUnpHVkh.html | |||||
| 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. 58(7):519-525 (2011) | |||||
| 書誌情報 |
ENDOCRINE JOURNAL 巻 58, 号 7, p. 519-525, 発行日 2011-01-07 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Pancreatic beta cell dysfunction is pivotal to the development of diabetes, and restoration of insulin action is of primary importance. Here, we present a review of the mechanism of insulin secretion by pancreatic beta cells and discuss the mutual interaction of signaling pathways in stimulus-secretion coupling to better understand the scientific basis of pharmacological treatment for insulin secretion deficiency. Glucose stimulates insulin secretion via membrane depolarization by closure of ATP-sensitive K(+) channels (K(ATP) channels) and opening of L-type voltage-dependent Ca(2+) channels. The resultant elevation of cytosolic free Ca2+ triggers insulin exocytosis. This is termed the "K(ATP)-dependent pathway" and is shared by sulfonylurea, which closes K(ATP) channels. Glucose also stimulates insulin release independent of its action on K(ATP) channels. This is referred to as the "K(ATP)-independent pathway," the molecular basis of which remains elusive. In the pancreatic beta cell, incretin hormones increase cAMP level, which enhances glucose-stimulated insulin release by protein kinase A-dependent and -independent mechanisms. Importantly, cAMP does not directly augment Ca(2+)-stimulated insulin release per se. The stimulatory level of ambient glucose is an absolute requirement for incretin to enhance insulin release. Therefore, incretin/cAMP enhances K(ATP)-independent insulinotropic action of glucose. The robust glucose-lowering effect of DPP4 inhibitor add-on in diabetic patients with sulfonylurea secondary failure is intriguing. With the clinical availability of DPP4 inhibitor and GLP-1 mimetics, the importance of the interactions between cAMP signaling and K(ATP) channel-independent actions of glucose is reappraised. | |||||
| 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 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 0918-8959 | |||||
| 書誌レコードID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA10901436 | |||||
| PubMed | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | https://pubmed.ncbi.nlm.nih.gov/21701075 | |||||
| 関連名称 | 21701075 | |||||
| 権利 | ||||||
| 権利情報 | Copyright© The Japan Endocrine Society | |||||
| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| WoS | ||||||
| 表示名 | Web of Science | |||||
| URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000294533900001 | |||||
