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  1. 30 大学院医学系研究科・医学部
  2. 30D 学位論文
  3. 博士論文 本文
  4. 2015年度

Substitution in Amino Acid 70 of Hepatitis C Virus Core Protein Changes the Adipokine Profile via Toll-Like Receptor 2/4 Signaling

http://hdl.handle.net/10076/00016979
http://hdl.handle.net/10076/00016979
9836d562-e07b-44cd-94d7-b767c2f06d35
名前 / ファイル ライセンス アクション
2015DM037.pdf 2015DM037 (1.3 MB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2017-07-04
タイトル
タイトル Substitution in Amino Acid 70 of Hepatitis C Virus Core Protein Changes the Adipokine Profile via Toll-Like Receptor 2/4 Signaling
言語 en
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_db06
資源タイプ doctoral thesis
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
著者 浦城, 聡子

× 浦城, 聡子

en Uraki, Satoko

ja-Kana ウラキ, サトコ

ja 浦城, 聡子

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抄録
内容記述タイプ Abstract
内容記述 Background & Aims It has been suggested that amino acid (aa) substitution at position 70 from arginine (70R) to glutamine (70Q) in the genotype 1b hepatitis C virus (HCV) core protein is associated with insulin resistance and worse prognosis. However, the precise mechanism is still unclear. The aim of this study was to investigate the impact of the substitution at position 70 in HCV core protein on adipokine production by murine and human adipocytes. Methods The influence of treatment with HCV core protein (70R or 70Q) on adipokine production by both 3T3-L1 and human adipocytes were examined with real-time PCR and enzyme-linked immunosorbent assay (ELISA), and triglyceride content was also analyzed. The effects of toll-like receptor (TLR)2/4 inhibition on IL-6 production by 3T3-L1 induced by HCV core protein were examined. Results IL-6 production was significantly increased and adiponectin production was reduced without a change in triglyceride content by treatment with 70Q compared to 70R core protein in both murine and human adipocytes. IL-6 induction of 3T3-L1 cells treated by 70Q HCV core protein was significantly inhibited with anti-TLR2 antibody by 42%, and by TLR4 inhibitor by 40%. Conclusions Our study suggests that extracellular HCV core protein with substitution at position 70 enhanced IL-6 production and reduced adiponectin production from visceral adipose tissue, which can cause insulin resistance, hepatic steatosis, and ultimately development of HCC.
内容記述
内容記述タイプ Other
内容記述 本文 / Department of Internal Medicine, Mie University School of Medicine
内容記述
内容記述タイプ Other
内容記述 14p
書誌情報
発行日 2016-03-25
DOI
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0131346
権利
権利情報 (C) 2015 Uraki 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
フォーマット
内容記述タイプ Other
内容記述 application/pdf
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
出版者
出版者 三重大学
出版者(ヨミ)
値 ミエダイガク
関係URI
関連名称 https://doi.org/10.1371/journal.pone.0131346
学位名
学位名 博士(医学)
学位授与機関
学位授与機関識別子Scheme kakenhi
学位授与機関識別子 14101
学位授与機関名 三重大学
学位授与年月日
学位授与年月日 2016-03-25
学位授与番号
学位授与番号 甲医学第1774号
ノート
資源タイプ(三重大)
値 Doctoral Dissertation / 博士論文
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