High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte

doi:10.1002/jcp.26007

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Title:	High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte
Authors:	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
Contributors:	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
Keywords:	CD36 energy metabolism HDL GLUT4 obesity Palmitic acid
Date:	2017-11
Issue Date:	2018-11-30 15:53:06 (UTC+8)
Publisher:	Wiley
Abstract:	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.
Relation:	Journal of Cellular Physiology, v.232, n.11, pp.3020-3029
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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