DOI: 10.14457/tu.the.2015.649
title: The effect of rice bran oil in comparison to coconut oil on fat accumulation in 3T3-L1

description: Obesity has become a major health problem worldwide. It is associated with the development of type 2 diabetes, coronary heart disease, and hypertension. Rice bran oil (RO) and coconut oil (CO) have been shown to reduce blood cholesterol, lipid profiles and obesity in both human and animal studies. CO is the richest source of medium-chain fatty acids (MCFAs) comprising about 50% of lauric acid (LaA). RO contains mainly oleic acid (OA) and linoleic acid (LA). However, the direct effects of the coconut oil and RO on lipid accumulation and adipogenesis in vitro have not been previously investigated. Thus, the objectives of this study were to investigate the anti-obesity effects of RO and CO on lipid accumulation and adipogenesis in 3T3-L1 cells. The 3T3-L1 preadipocytes were induced to differentiate in the presence or absence of edible oils i.e. RO and CO, and fatty acids i.e. OA, LA, LaA, and PA. The cells were cultured in differentiated media with and without various concentrations of the treatments for 4 and 8 days. After incubation, the cells were measured cell viability by MTS assay, adipogenesis and lipid accumulation by Oil red O staining, and the expressions of PPARγ and C/EBPα mRNA by real time-PCR method. The results demonstrated that OA, LaA, RO and CO treatments at all concentrations did not significantly affect cell viability.  In contrast, the cells treated with PA (60 µg/mL) and LA (80, 100 µg/mL) for 8 days significantly reduced cell viability with more than 70% of surviving 3T3-L1 cells. However, PA (80, 100 µg/mL) and LaA (100 µg/mL) significantly reduced cell viability with less than 70% of surviving 3T3-L1 cells. The treatments of OA, LA, PA, LaA, RO, and CO inhibited adipogenesis and lipid accumulation in these cells as determined by decreased Oil red O staining. After 4 days of incubation, OA (20, 40, 60 µg/mL), LA (20, 40, 60 µg/mL), LaA (20 µg/mL), RO (100, 200, 300 µg/mL) significantly decreased lipid accumulation.  After 8 days of incubation, OA (20 µg/mL), LA (20, 40 µg/mL), LaA (20, 40 µg/mL), RO (100, 200 µg/mL), CO (100, 200, 300 µg/mL) significantly decreased lipid accumulation.  Moreover, the cells treated with LA (20, 40, 60 µg/mL), LaA (20, 40 µg/mL), CO (20, 40 µg/mL) for 8 days had significantly reduced adipocyte size. In gene expression, the treatments with LaA and CO for 4 and 8 days down-regulated PPARγ and C/EBPα while RO and LA treatments for 4 days suppressed only PPARγ. Moreover, OA (20, 40 µg/mL) for 8 days decreased the expression levels of PPARγ and C/EBPα, LA treatments (20, 40 µg/mL) for 4  days and (40 µg/mL) 8 days significantly decreased expression levels of PPARγ, and LA treatments (40 µg/mL) for 4 days and (20, 40 µg/mL) for 8 days significantly decreased expression levels of C/EBPα.  Therefore, LaA may be a bioactive compound in CO, as well as OA and LA may be bioactive compounds in RO for reducing adipogenesis and lipid accumulation. These properties of the fatty acids in CO and RO may be used to prevent obesity. However, further studies are required to explore more details of molecular mechanisms underlying the anti-obesity effects of CO, RO, and their bioactive compounds.