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Year : 2020  |  Volume : 25  |  Issue : 1  |  Page : 105

The effect of trans-palmitoleic acid on cell viability and sirtuin 1 gene expression in hepatocytes and the activity of peroxisomeproliferator-activated receptor-alpha

1 Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
2 Department of Biochemistry, Faculty of Medicine; Finetech in Medicine Research Center, Iran University of Medical Sciences, Tehran, Iran
3 Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences; H. Aliasghar Children's Hospital, Iran University of Medical Sciences, Tehran, Iran
4 Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Iran University of Medical Sciences, Tehran, Iran

Correspondence Address:
Dr. Mitra Nourbakhsh
Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, 1449614535, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrms.JRMS_16_20

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Background: Accumulation of fatty acids in liver causes lipotoxicity which is followed by nonalcoholic fatty liver disease. The association between intakes of trans-fatty acids with metabolic diseases is still controversial. Accordingly, the objective of this study was to investigate the in vitro effects of trans-palmitoleic acid (tPA) and palmitic acid (PA) on lipid accumulation in hepatocytes, focusing on the gene expression of sirtuin 1 (SIRT1) as well as the transcriptional activity of peroxisome proliferator-activated receptor alpha (PPARα). Materials and Methods: In this experimental study, hepatocellular carcinoma (HepG2) cells were cultured and treated with various concentrations of tPA and PA (C16:0). The accumulation of triglyceride in the cells was measured by enzymatic method. Gene expression was evaluated by real-time polymerase chain reaction. The activity of PPARα was assessed by luciferase reporter assay after transfection of human embryonic kidney 293T cells by a vector containing the PPAR response element. Results: While concentration >1 mM for PA and cis-PA (cPA) reduced the viability of hepatocytes, tPA revealed an opposite effect and increased cell survival. Lipid accumulation in HepG2 cells after treatment with tPA was significantly lower than that in cells treated with PA. In addition, tPA at physiological concentration had no effect on the expression of SIRT1 while at high concentration significantly augmented its expression. There was a modest increase in PPARα activity at low concentration of tPA. Conclusion: tPA causes less lipid accumulation in hepatocytes with no detrimental effect on cell viability and might be beneficial for liver cells by the activation of SIRT1 and induction of PPARα activity.

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