Abstract
Deep frying degrades the oil and generates harmful products. This study evaluated effects of reused palm oil (from frying pork or potato) on expression of cytochrome P450s (CYPs), the transporter (SLCO1B1), and lipid metabolism regulators; proliferator-activated receptors (PPAR) and sterol regulatory element binding protein (SREBP). Human hepatic carcinoma cell line (HepG2) cells were incubated with oleic acid (OA), new palm oil, or reused palm oils for 24hr. Fatty acid accumulation was examined by Nile red staining. Total RNA was extracted, followed by RT/qPCR of the target genes. Fatty acid accumulation was significantly different between the new and the reused oils. Expression of CYP1A2, CYP2C19, CYP2E1, CYP3A4, CYP4A11, and SLCO1B1 was induced by reused oils. Expression of PPAR-α was strongly increased in all treatments while SREBP-1a and SREBP-1c were suppressed. Modification of CYPs, PPAR-α, and SLCO1B1 by palm oil might increase the risk of fatty acid accumulation with associated oxidative stress. Therefore, consumption of palm oil or reused oil should be limited. PRACTICAL APPLICATIONS: Deep frying degrades the oil and generates harmful products. This study evaluated effects of reused palm oil (from frying pork or potato) on expression of cytochrome P450s (CYPs), the transporter (SLCO1B1), and lipid metabolism regulators; PPAR and SREBP in HepG2 cells. Both of the reused oils-induced profiles of all CYP and SLCO1B1, but the new oil upregulated CYP2E1, CYP3A4, and CYP4A11. PPAR-α was induced while SREBP-1a and SREBP-1c were suppressed by all treatments. Inductions of CYPs with suppression of SREBP-1a and SREBP-1c might contribute to an increased risk of fatty acid accumulation. These findings revealed the impacts of reused palm oil on metabolism via CYPs which related to oxidative stress for further study. Hence, consumption of palm oil or reused cooking oil should be of concern.
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