Abstract
Palm oil is enriched in vitamin E in the form of α-, γ-, and δ-tocotrienols. Dietary tocotrienol supplements have been shown to prevent atherosclerosis development in patients and preclinical animal models. However, the mechanistic basis for this health beneficial effect is not well established. Peroxisome proliferator-activated receptors α, γ, and δ (PPARα, PPARγ, and PPARδ) are ligand regulated transcription factors that play essential preventive roles in the development of atherosclerosis through regulating energy metabolism and inflammation. In this study, we presented data that the tocotrienol rich fraction (TRF) of palm oil activated PPARα, PPARγ, and PPARδ in reporter based assays. Importantly, TRF attenuated the development of atherosclerosis in ApoE−/− mice through inducing PPAR target gene liver X receptor alpha (LXRα) and its down-stream target genes apolipoproteins and cholesterol transporters, suggesting that modulating the activities of PPARs is a key aspect of the in vivo action of tocotrienols.
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