Giving combined medium-chain fatty acids and glucose protects against cancer-associated skeletal muscle atrophy. 10

• Material Type: 博士論文
• ISSN: 1347-9032
• Title: Giving combined medium-chain fatty acids and glucose protects against cancer-associated skeletal muscle atrophy.
• Volume: 110 10
• Author/Editor: Mori, Takuya; Ohmori, Hitoshi; Luo, Yi; Mori, Shiori; Miyagawa, Yoshihiro; Nukaga, Shota; Goto, Kei; Fujiwara-Tani, Rina; Kishi, Shingo; Sasaki, Takamitsu; Fujii, Kiyomu; Kawahara, Isao; Kuniyasu, Hiroki
• Author Heading: Mori, Takuya; Ohmori, Hitoshi; Luo, Yi; Mori, Shiori; Miyagawa, Yoshihiro; Nukaga, Shota; Goto, Kei; Fujiwara-Tani, Rina; Kishi, Shingo; Sasaki, Takamitsu; Fujii, Kiyomu; Kawahara, Isao; Kuniyasu, Hiroki
• Publication, Distribution, etc.: Wiley / Japanese Cancer Association
• Publication Date: 2019-10; 110 10
• Publication Date (W3CDTF): 2019-10
• Alternative Title: 中鎖脂肪酸と糖質の併用摂取は癌関連骨格筋萎縮から保護する
• Periodical title: Cancer science
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2020-03-16
• Date Granted (W3CDTF): 2020-03-16
• Dissertation Number: 甲第733号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第733号
• Text Language Code: eng
• Subject Heading: cachexia; glucose; medium-chain fatty acid; sarcopenia; Warburg effect
• Target Audience: 一般
• Note (General): type:Thesis; Skeletal muscle volume is associated with prognosis of cancer patients. Maintenance of skeletal muscle is an essential concern in cancer treatment. In nutritional intervention, it is important to focus on differences in metabolism between tumor and skeletal muscle. We examined the influence of oral intake of glucose (0%, 10%, 50%) and 2% medium-chain fatty acid (lauric acid, LAA, C12:0) on tumor growth and skeletal muscle atrophy in mouse peritoneal metastasis models using CT26 mouse colon cancer cells and HT29 human colon cancer cells. After 2 weeks of experimental breeding, skeletal muscle and tumor were removed and analyzed. Glucose intake contributed to prevention of skeletal muscle atrophy in a sugar concentration-dependent way and also promoted tumor growth. LAA ingestion elevated the level of skeletal muscle protein and suppressed tumor growth by inducing tumor-selective oxidative stress production. When a combination of glucose and LAA was ingested, skeletal muscle mass increased and tumor growth was suppressed. Our results confirmed that although glucose is an important nutrient for the prevention of skeletal muscle atrophy, it may also foster tumor growth. However, the ingestion of LAA inhibited tumor growth, and its combination with glucose promoted skeletal muscle integrity and function, without stimulating tumor growth. These findings suggest novel strategies for the prevention of skeletal muscle atrophy.; 博士（医学）・甲第733号・令和2年3月16日; © 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License(https://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.; identifier:Cancer science Vol.110 No.10 p.3391-3399 (2019 Oct); identifier:13479032; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3724; identifier:Cancer science, 110(10): 3391-3399
• DOI: info:doi/10.1111/cas.14170; https://doi.org/info:doi/10.1111/cas.14170
• Persistent ID (NDL): info:ndljp/pid/11551885; https://dl.ndl.go.jp/pid/11551885
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2020-10-06T21:18:06+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10564/3724
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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