Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 119, Issue 4, Pages 3363-3372Publisher
WILEY
DOI: 10.1002/jcb.26501
Keywords
fatty acid metabolism; glucose metabolism; hypoxia; insulin signaling pathway; ischemia; palmitic acid
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Funding
- China Medical University
- Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence [DMR-104-007, MOHW106-TDU-B-212-113004]
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Metabolic syndrome is a risk factor for the development of cardiovascular diseases. Myocardial cell damage leads to an imbalance of energy metabolism, and many studies have indicated that short-term hypoxia during myocardial cell injury has a protective effect. In our previous animal studies, we found that short-term hypoxia in the heart has a protective effect, but long-term hypoxia increases myocardial cell injury. Palmitic acid (PA)-treated H9c2 cardiomyoblasts and neonatal rat ventricle cardiomyocytes were used to simulate hyperlipidemia model, which suppress cluster of differentiation 36 (CD36) and activate glucose transporter type 4 (GLUT4). We exposed the cells to short- and long-term hypoxia and investigated the protective effects of hypoxic preconditioning on PA-induced lipotoxicity in H9c2 cardiomyoblasts and neonatal rat cardiomyocytes. Preconditioning with short-term hypoxia enhanced both CD36 and GLUT4 metabolism pathway protein levels. Expression levels of phospho-PI3K, phospho-Akt, phospho-AMPK, SIRT1, PGC1, PPAR, CD36, and CPT1 induced by PA was reversed by short-term hypoxia in a time-dependent manner. PA-induced increased GLUT4 membrane protein level was reduced in the cells exposed to short-term hypoxia and si-PKC. Short-term hypoxia, resveratrol and si-PKC rescue H9c2 cells from apoptosis induced by PA and switch the metabolic pathway from GLUT4 dependent to CD36 dependent. We demonstrate short-term hypoxic preconditioning as a more efficient way as resveratrol in maintaining the energy metabolism of hearts during hyperlipidemia and can be used as a therapeutic strategy.
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