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A liver-derived secretory protein, selenoprotein P, causes insulin resistance
http://hdl.handle.net/2297/25782
http://hdl.handle.net/2297/257828f5a8213-a35a-40a1-8bbb-9e5419203578
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-MISU-H-483.pdf (1.8 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | A liver-derived secretory protein, selenoprotein P, causes insulin resistance | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 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 |
Misu, Hirofumi
× Misu, Hirofumi× Takamura, Toshinari× Takayama, Hiroaki× Hayashi, Hiroto× Matsuzawa-Nagata, Naoto× Kurita, Seiichiro× Ishikura, Kazuhide× Ando, Hitoshi× Takeshita, Yumie× Ota, Tsuguhito× Sakurai, Masaru× Yamashita, Tatsuya× Mizukoshi, Eishiro× Yamashita, Taro× Honda, Masao× Miyamoto, Kenichi× Kubota, Tetsuya× Kubota, Naoto× Kadowaki, Takashi× Kim, Han-Jong× Lee, In-kyu× Minokoshi, Yasuhiko× Saito, Yoshiro× Takahashi, Kazuhiko× Yamada, Yoshihiro× Takakura, Nobuyuki× Kaneko, Shuichi |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学医薬保健研究域医学系 | |||||
| 書誌情報 |
Cell Metabolism 巻 12, 号 5, p. 483-495, 発行日 2010-11-03 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1550-4131 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11978571 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.cmet.2010.09.015 | |||||
| 出版者 | ||||||
| 出版者 | Elsevier | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secretory proteins, termed hepatokines. Here, we demonstrate that selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance. Using serial analysis of gene expression (SAGE) and DNA chip methods, we found that hepatic SeP mRNA levels correlated with insulin resistance in humans. Administration of purified SeP impaired insulin signaling and dysregulated glucose metabolism in both hepatocytes and myocytes. Conversely, both genetic deletion and RNA interference-mediated knockdown of SeP improved systemic insulin sensitivity and glucose tolerance in mice. The metabolic actions of SeP were mediated, at least partly, by inactivation of adenosine monophosphate-activated protein kinase (AMPK). In summary, these results demonstrate a role of SeP in the regulation of glucose metabolism and insulin sensitivity and suggest that SeP may be a therapeutic target for type 2 diabetes. © 2010 Elsevier Inc. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.elsevier.com/locate/issn/15504131 | |||||
