Foods rich in poly unsaturated fatty acids (PUFA) are vulnerable to oxidation. While it is well established that endogenously derived oxidized lipids are ligands of the transcription factor PPARγ, the binding ability of diet-derived oxidized lipids is unknown. Our two-fold objective was to determine the oxidized lipid content and PPARγ binding ability of commonly consumed foods. Extracted food lipids were assayed for the peroxide value, conjugated dienes, and aldehydes, and PPARγ binding was assessed by an in vitro PPARγ ligand screening assay. Oxidized lipids were present in all foods tested at the time of purchase, and oxidation did not increase during storage. The peroxide values for walnuts, sunflower seeds, and flax meal were significantly lower at the end of three months as compared to the day of purchase (peroxide value: 1.26 ± 0.13 vs. 2.32 ± 0.4; 1.65 ± 0.23 vs. 2.08 ± 0.09; 3.07 ± 0.22 vs. 9.94 ± 0.75 mEq/kg fat, p ≤ 0.05, respectively). Lipids extracted from French fries had the highest binding affinity (50.87 ± 11.76%) to PPARγ compared to other foods. Our work demonstrates that oxidized lipids are present in commonly consumed foods when purchased, and for the first time demonstrates that some contain ligands of PPARγ.

The objective of this study was to investigate if the level of oxidation of soybean oil determines the accumulation of lipids in 3T3‐L1 adipocytes.MethodsSoybean oil (SO) was unheated or heated for 3, 6 or 9 hours at 190°C to generate oils with increasing levels of oxidation as determined by the levels of conjugated dienes (CD) and conjugated trienes (CT). 3T3‐L1 cells were grown to confluence in 24 well plates and then exposed to DMEM supplemented with or without 0.1%, 0.01% and 0.001% of heated or unheated SO for 24 hrs either prior to or, after differentiation. After treatment, cells were stained with oil red O to determine the accumulation of lipids.ResultsProgressive heating of soybean oil created oils with increasing amounts of oxidized lipids (ratio of CD/CT was 1.92, 2.33, 3.1 and 3.56 for the unheated, 3hr, 6hr and 9hr heated oils, respectively). The intensity of oil red O staining was similar in 3T3‐L1 cells that were treated with vehicle or unheated oil for 24hr in undifferentiated cells but was lesser in the cells treated with 3hr heated SO. More interestingly, there was no oil red staining when cells were treated with the 6hr and 9hr heated oils, suggesting a loss of lipid accumulation. In experiments where SO was added to differentiated 3T3‐L1 cells for 24 hrs, there was no obvious effect of the oils on oil red O staining.ConclusionThese results demonstrate that exposure of pre‐adipocytes to oils with higher ratios of oxidized lipids inhibits the adipocyte lipid accumulation. Since this effect is not seen in cells that are differentiated, it suggests that heated oils could be suppressing regulators of adipocyte differentiation.Grant Funding Source : None