| 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 |
|
|
タイトル |
Myeloid Differentiation Factor 88 (MyD88)-Deficiency Increases Risk of Diabetes in Mice |
|
言語 |
en |
| 作成者 |
Hosoi, Toru
Yokoyama, Shota
Matsuo, Suguru
Akira, Shizuo
Ozawa, Koichiro
|
| 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 |
Copyright (c) 2010 Hosoi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| 主題 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| 内容記述 |
|
|
内容記述 |
Background: Multiple lines of evidence suggest innate immune response pathways to be involved in the development of obesity-associated diabetes although the molecular mechanism underling the disease is unknown. Recent observations suggest that saturated fatty acids can act as a ligand for toll-like receptor (TLR) 4, which is thought to mediate obesity-associated insulin resistance. Myeloid differentiation factor 88 (MyD88) is an adapter protein for TLR/IL-1 receptor signaling, which is involved in the activation of inflammatory pathways. To evaluate molecular mechanisms linking obesity-associated diabetes down-stream of TLR4, we investigated physiological role of MyD88 in high-fat diet (HFD)-induced obesity. Methodology/Principal Findings: In the present study, we found MyD88-deficient mice fed a HFD had increased circulating levels of insulin, leptin and cholesterol, as well as liver dysfunction (increased induction of ALT levels, increased activation of JNK and cleavage of PARP), which were linked to the onset of severe diabetes. On the other hand, TNF-α would not be involved in HFD-induced diabetes in MyD88-deficient mice, because TNF-α level was attenuated in MyD88-deficient mice fed with HFD. Conclusions/Significance: The present finding of an unexpected role for MyD88 in preventing diabetes may provide a potential novel target/strategy for treating metabolic syndrome. |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
Public Library Science |
| 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 |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.1371/journal.pone.0012537 |
| 関連情報 |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
http://dx.doi.org/10.1371/journal.pone.0012537 |
| 収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1932-6203 |
| 開始ページ |
|
|
開始ページ |
e12537-1 |
| 書誌情報 |
PLoS ONE
PLoS ONE
巻 5,
号 9,
p. e12537-1-e12537-7,
発行日 2010-09-02
|
| 旧ID |
30784 |
PLoS-One_5_e12537.pdf (524.4 KB)
