| Item type |
デフォルトアイテムタイプ_（フル）(1) |
| 公開日 |
2023-03-18 |
| タイトル |
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|
タイトル |
Obesity-induced endoplasmic reticulum stress causes chronic inflammation in adipose tissue |
|
言語 |
en |
| 作成者 |
Kawasaki, Noritaka
Asada, Rie
Saito, Atsushi
Kanemoto, Soshi
Imaizumi, Kazunori
|
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 権利情報 |
|
|
権利情報 |
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareALike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/ |
| 内容記述 |
|
|
内容記述 |
Adipose tissue plays a central role in maintaining metabolic homeostasis under normal conditions. Metabolic diseases such as obesity and type 2 diabetes are often accompanied by chronic inflammation and adipose tissue dysfunction. In this study, we observed that endoplasmic reticulum (ER) stress and the inflammatory response occurred in adipose tissue of mice fed a high-fat diet for a period of 16 weeks. After 16 weeks of feeding, ER stress markers increased and chronic inflammation occurred in adipose tissue. We found that ER stress is induced by free fatty acid (FFA)-mediated reactive oxygen species (ROS) generation and up-regulated gene expression of inflammatory cytokines in 3T3-L1 adipocytes. Oral administration to obese mice of chemical chaperons, which alleviate ER stress, improved chronic inflammation in adipose tissue, followed by the suppression of increased body weight and improved insulin signaling. These results indicate that ER stress plays important pathophysiological roles in obesity-induced adipose tissue dysfunction. |
|
言語 |
en |
| 内容記述 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
This work was partly supported by grants from the Japan Society for the Promotion of Science KAKENHI (#22020030, #22800049), Sumitomo Foundation, Mochida Memorial Foundation for Medical and Pharmaceutical Research, Astellas Foundation for Research on Metabolic Disorders, Takeda Science Foundation, The Pharmacological Research Foundation Tokyo, Daiichi-Sankyo Foundation of Life Science, and The Naito Foundation. |
| 出版者 |
|
|
出版者 |
Nature Research |
| 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 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 関連情報 |
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.1038/srep00799 |
| 関連情報 |
|
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|
識別子タイプ |
PMID |
|
|
関連識別子 |
23150771 |
| 関連情報 |
|
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1038/srep00799 |
| 収録物識別子 |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
2045-2322 |
| 開始ページ |
|
|
開始ページ |
799 |
| 書誌情報 |
Scientific Reports
Scientific Reports
巻 2,
p. 799,
発行日 2012-11-12
|
| 旧ID |
48728 |
SciRep_2_799.pdf (1.1 MB)
