English  |  正體中文  |  简体中文  |  Items with full text/Total items : 17433/19733 (88%)
Visitors : 6263019      Online Users : 815
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31692


    標題: High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte
    作者: Wen, Su-Ying
    Velmurugan, Bharath Kumar
    Day, Cecilia Hsuan
    Shen, Chia-Yao
    Chun, Li-Chin
    Tsai, Yi-Chieh
    Lin, Yueh-Min
    Chen, Ray-Jade
    Kuo, Chia-Hua
    Huang, Chih-Yang
    貢獻者: Taipei City Hosp, Renai Branch, Dept Dermatol
    Mackay Jr Coll Med Nursing & Management, Ctr Gen Educ
    Ton Duc Thang Univ, Fac Appl Sci, Ho Chi Minh City, Vietnam
    MeiHo Univ, Dept Nursing
    Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm
    China Med Univ, Grad Inst Basic Med Sci
    Changhua Christian Hosp, Dept Pathol
    Jen Teh Jr Coll Med Nursing & Management, Dept Med Technol
    Taipei Med Univ, Sch Med, Dept Surg
    Univ Taipei, Dept Sports Sci
    China Med Univ, Grad Inst Chinese Med Sci
    Asia Univ, Dept Biol Sci & Technol
    關鍵字: CD36
    energy metabolism
    HDL
    GLUT4
    obesity
    Palmitic acid
    日期: 2017-11
    上傳時間: 2018-11-30 15:53:06 (UTC+8)
    出版者: Wiley
    摘要: In our previous study palmitic acid (PA) induced lipotoxicity and switches energy metabolism from CD36 to GLUT4 in H9c2 cells. Low level of high density lipoprotein (HDL) is an independent risk factor for cardiac hypertrophy. Therefore, we in the present study investigated whether HDL can reverse PA induced lipotoxicity in H9c2 cardiomyoblast cells. In this study, we treated H9c2 cells with PA to create a hyperlipidemia model in vitro and analyzed for CD36 and GLUT4 metabolic pathway proteins. CD36 metabolic pathway proteins (phospho-AMPK, SIRT1, PGC1 alpha, PPAR alpha, CPT1 beta, and CD36) were decreased by high PA (150 and 200 mu g/mu l) concentration. Interestingly, expression of GLUT4 metabolic pathway proteins (p-PI3K and pAKT) were increased at low concentration (50 mu g/mu l) and decreased at high PA concentration. Whereas, phospho-PKC., GLUT4 and PDH proteins expression was increased in a dose dependent manner. PA treated H9c2 cells were treated with HDL and analyzed for cell viability. Results showed that HDL treatment induced cell proliferation efficiency in PA treated cells. In addition, HDL reversed the metabolic effects of PA: CD36translocation was increased and reduced GLUT4 translocation, but HDL treatment significantly increased CD36 metabolic pathway proteins and reduced GLUT4 pathway proteins. Rat neonatal cardiomyocytes showed similar results. In conclusion, HDL reversed palmatic acid-induced lipotoxicity and energy metabolism imbalance in H9c2 cardiomyoblast cells and in neonatal rat cardiomyocyte cells.
    關聯: Journal of Cellular Physiology, v.232, n.11, pp.3020-3029
    Appears in Collections:[醫務管理系(所)] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML120View/Open
    jcp.26007.pdf1792KbAdobe PDF0View/Open


    All items in CNU IR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback