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LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance
http://hdl.handle.net/2297/37595
http://hdl.handle.net/2297/375952de38ee2-1028-4f07-b065-6d73c3756935
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-MISU-H-1649.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 | LECT2 functions as a hepatokine that links obesity to skeletal muscle 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 |
Lan, Fei
× Lan, Fei× Misu, Hirofumi× Chikamoto, Keita× Takayama, Hiroaki× Kikuchi, Akihiro× Mohri, Kensuke× Takata, Noboru× Hayashi, Hiroto× Matsuzawa-Nagata, Naoto× Takeshita, Yumie× Noda, Hiroyo× Matsumoto, Yukako× Ota, Tsuguhito× Nagano, Toru× Nakagen, Masatoshi× Miyamoto, Ken-ichi× Takatsuki, Kanako× Seo, Toru× Iwayama, Kaito× Tokuyama, Kunpei× Matsugo, Seiichi× Tang, Hong× Saito, Yoshiro× Yamagoe, Satoshi× Kaneko, Shuichi× Takamura, Toshinari |
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| 書誌情報 |
Diabetes 巻 63, 号 5, p. 1649-1664, 発行日 2014-05-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1939-327X | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA12037590 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.2337/db13-0728 | |||||
| 出版者 | ||||||
| 出版者 | American Diabetes Association | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance. © 2014 by the American Diabetes Association. | |||||
| 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 | |||||
