Genistein enhances expression of genes involved in fatty acid catabolism through activation of PPARalpha.
Molecular and Cellular Endocrinology(2004)
Abstract
Although evidences are emerging that dietary isoflavones have beneficial effects in treatment of hyperlipidemia and cardiovascular diseases, the underlying molecular mechanism has not yet been extensively characterized. In this report, we showed that genistein, one of the major isoflavones, increased expression of genes involved in lipid catabolism such as carnitine palmitoyltransferase 1, liver form (CPT1L) in HepG2 cells, when assayed by real-time reverse-transcriptase polymerase chain reactions as well as Western blotting analysis. The increase in mRNA-level of CPT1L after genistein treatment was not changed in the presence of ICI182780, a potent inhibitor of estrogen receptor, suggesting that this effect of genistein was estrogen receptor-independent. Since these genes involved in fatty acid catabolism are considered putative downstream target genes of peroxisome proliferators-activated receptor α (PPARα), we examined whether expression of PPARα was modulated by genistein treatment. Interestingly, genistein induced expression of PPARα at both mRNA- and protein-level. Further, genistein activated transcriptional activity of PPARα, when determined by reporter gene analysis, suggesting genistein as a potential ligand for PPARα. Taken together, this study provides a picture of the regulatory action of genistein, as an activator of PPARα in fatty acid catabolism and potential use of genistein as lipid-lowering agent.
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Key words
Genistein,Carnitine palmitoyltransferase 1, liver form,Peroxisome proliferator-activated receptor,Fatty acid β-oxidation
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