Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 220, Issue 1-2, Pages 51-58Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2004.03.011
Keywords
genistein; carnitine palmitoyltransferase 1, liver form; peroxisome proliferator-activated receptor; fatty acid beta-oxidation
Categories
Ask authors/readers for more resources
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 genistem, 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 genistem 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 alpha (PPARalpha), we examined whether expression of PPARalpha was modulated by genistein treatment. Interestingly, genistein induced expression of PPARalpha at both mRNA- and protein-level. Further, genistein activated transcriptional activity of PPARalpha, when determined by reporter gene analysis, suggesting genistein as a potential ligand for PPARalpha. Taken together, this study provides a picture of the regulatory action of genistein, as an activator of PPARalpha in fatty acid catabolism and potential use of genistein as lipid-lowering agent. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available