『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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登録内容 (EID=148371)

EID=148371EID:148371, Map:0, LastModified:2018年5月23日(水) 17:08:26, Operator:[[ADMIN]], Avail:TRUE, Censor:0, Owner:[馬渡 一諭], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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審査 (推奨):
カテゴリ (推奨):
共著種別 (推奨):
学究種別 (推奨):
組織 (推奨):
著者 (必須): 1. (英) Nazari Hossein (日) (読)
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2.髙橋 章 ([徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.予防環境栄養学])
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3.原田 永勝
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4.馬渡 一諭
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5. (英) Nakano Masayuki (日) (読)
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6.岸 和弘
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7.蛯名 洋介
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8.中屋 豊
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題名 (必須): (英) Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2.  (日)    [継承]
副題 (任意):
要約 (任意): (英) There is crosstalk in intracellular signaling between Angiotensin II (Ang II) and insulin. We hypothesized that the underlying mechanism might be related to changes in cytoskeleton. In the presence of 100 nM of Ang II, insulin-induced glucose uptake was decreased and insulin-induced actin filament organization was inhibited. PKC inhibitors, including GF109203x and p38MAPK inhibitor (SB203580) neither improved insulin-induced actin reorganization nor glucose uptake. In contrast, the Ang II-induced inhibition of glucose uptake and actin filament disorganization was reversed by 10 micromol ERK 1/2 MAPK inhibitor (PD98059). Pretreatment of Ang II increased ERK1/2 phosphorylation and inhibited insulin-induced Akt phosphorylation. The effect of Ang II on ERK1/2 phosphorylation was blocked by Ang II type 1 receptor antagonists, RNH6270 and PD98059 but not by SB203580 or Guanosine-5'-O-(2-ThioDiphosphate), a G-protein inhibitor. We next tested the effect of broad-spectrum matrix metalloproteinase (MMP) inhibitor (GM6001) on Ang II-inhibition of insulin signaling pathway. GM6001 did not improve Ang II-induced actin filament disorganization and did not inhibit ERK1/2 phosphorylation. From these data in L6 myotube, we conclude that Ang II negatively regulates the insulin signal not through MMP signaling pathway but specifically through MMP-independent ERK1/2 activation pathway, providing an alternative molecular mechanism for angiotensin-induced insulin resistance.  (日)    [継承]
キーワード (推奨): 1. (英) Angiotensin II (日) (読) [継承]
2. (英) Cell Line (日) (読) [継承]
3.グルコース (glucose) [継承]
4. (英) Humans (日) (読) [継承]
5.インスリン (insulin) [継承]
6. (英) MAP Kinase Signaling System (日) (読) [継承]
7. (英) Mitogen-Activated Protein Kinase 1 (日) (読) [継承]
8. (英) Mitogen-Activated Protein Kinase 3 (日) (読) [継承]
9.リン酸化 (phosphorylation) [継承]
10. (英) Proto-Oncogene Proteins c-akt (日) (読) [継承]
11. (英) Receptor, Angiotensin, Type 1 (日) (読) [継承]
12. (英) Stress Fibers (日) (読) [継承]
発行所 (推奨):
誌名 (必須): The Journal of Medical Investigation : JMI ([徳島大学.医学部])
(pISSN: 1343-1420, eISSN: 1349-6867)

ISSN (任意): 1343-1420
ISSN: 1343-1420 (pISSN: 1343-1420, eISSN: 1349-6867)
Title: The journal of medical investigation : JMI
Title(ISO): J Med Invest
Supplier: 徳島大学
Publisher: Tokushima Daigaku Igakubu
 (NLM Catalog  (Webcat Plus  (医中誌Web  (J-STAGE  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 54 [継承]
(必須): 1,2 [継承]
(必須): 19 27 [継承]
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年月日 (必須): 西暦 2007年 2月 初日 (平成 19年 2月 初日) [継承]
URL (任意):
DOI (任意): 10.2152/jmi.54.19    (→Scopusで検索) [継承]
PMID (任意): 17380010    (→Scopusで検索) [継承]
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機関リポジトリ : 111490 [継承]
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備考 (任意): 1.(英) Article.Affiliation: Department of Nutrition and Metabolism, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Hossein Nazari, Akira Takahashi, Nagakatsu Harada, Kazuaki Mawatari, Masayuki Nakano, Kazuhiro Kishi, Yousuke Ebina and Yutaka Nakaya : Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2., The Journal of Medical Investigation : JMI, Vol.54, No.1,2, 19-27, 2007.
欧文冊子 ● Hossein Nazari, Akira Takahashi, Nagakatsu Harada, Kazuaki Mawatari, Masayuki Nakano, Kazuhiro Kishi, Yousuke Ebina and Yutaka Nakaya : Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2., The Journal of Medical Investigation : JMI, Vol.54, No.1,2, 19-27, 2007.

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