Oral administration of fructose exacerbates liver fibrosis and hepatocarcinogenesis via increased intestinal permeability in a rat steatohepatitis model.

• 資料種別: 博士論文
• タイトル: Oral administration of fructose exacerbates liver fibrosis and hepatocarcinogenesis via increased intestinal permeability in a rat steatohepatitis model.
• 著者・編者: Seki, Kenichiro; Kitade, Mitsuteru; Nishimura, Norihisa; Kaji, Kosuke; Asada, Kiyoshi; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Takaya, Hiroaki; Sawada, Yasuhiko; Sato, Shinya; Nakanishi, Keisuke; Yoshiji, Hitoshi
• 著者標目: Seki, Kenichiro; Kitade, Mitsuteru; Nishimura, Norihisa; Kaji, Kosuke; Asada, Kiyoshi; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Takaya, Hiroaki; Sawada, Yasuhiko; Sato, Shinya; Nakanishi, Keisuke; Yoshiji, Hitoshi
• 出版事項: Impact Journals
• 出版年月日等: 2018-06-19
• 出版年（W3CDTF）: 2018-06-19
• 並列タイトル等: フルクトースの経口投与はラット脂肪性肝炎モデルにおいて腸管透過性亢進作用を介して肝線維化および肝発癌を悪化させる
• タイトル（掲載誌）: Oncotarget
• 巻号年月日等（掲載誌）: 9 47
• 掲載巻: 9
• 掲載号: 47
• 掲載ページ: 28638-28651
• ISSN（掲載誌）: ISSN : 1949-2553
• 授与機関名: 奈良県立医科大学
• 授与年月日: 2019-09-27
• 報告番号: 乙第1432号
• 学位: 博士（医学）
• 本文の言語コード: eng
• 件名標目: non-alcoholic steatohepatitis (NASH); fructose; hepatocarcinogenesis; intestinal permeability; endotoxin
• 対象利用者: 一般
• 一般注記: type:Thesis; Recent reports have revealed the impact of a western diet containing large amounts of fructose on the pathogenesis of non-alcoholic steatohepatitis (NASH). Fructose exacerbates hepatic inflammation in NASH by inducing increasing intestinal permeability. However, it is not clear whether fructose contributes to the progression of liver fibrosis and hepatocarcinogenesis in NASH. The aim of this study was to investigate the effect of fructose intake on NASH in a rat model. A choline-deficient/L-amino acid diet was fed to F344 rats to induce NASH. Fructose was administrated to one group in the drinking water. The development of liver fibrosis and hepatocarcinogenesis were evaluated histologically. Oral fructose administration exacerbated liver fibrosis and increased the number of preneoplastic lesions positive for glutathione S-transferase placental form. Fructose-treated rats had significantly higher expression of hepatic genes related to toll-like receptor-signaling, suggesting that fructose consumption increased signaling in this pathway, leading to the progression of NASH. We confirmed that intestinal permeability was significantly higher in fructose-treated rats, as evidenced by a loss of intestinal tight junction proteins. Fructose exacerbated both liver fibrosis and hepatocarcinogenesis by increasing intestinal permeability. This observation strongly supports the role of endotoxin in the progression of NASH.; 博士（医学）・乙第1432号・令和元年9月27日; Copyright © 2018 Impact Journals, LLC; Copyright © Seki et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0 https://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.; identifier:Oncotarget Vol.9 No.47 p.28638-28651 (2018 Jun); identifier:19492553; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3668; identifier:Oncotarget, 9(47): 28638-28651
• オンライン閲覧公開範囲: インターネット公開
• 関連情報（DOI）: 10.18632/oncotarget.25587
• 連携機関・データベース: 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• 提供元機関・データベース: 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

目次

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3668/1/011432.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3668/2/021432.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3668/3/031432.pdf fulltext