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KMID : 0603820090150030179
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Journal of Experimental & Biomedical Science
2009 Volume.15 No. 3 p.179 ~ p.185
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Repression of PPARγ Activity on Adipogenesis by 17β-estradiol in Differentiated 3T3-L1 Cell
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Yoon Mi-Chung
Jeong Sun-Hyo
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Abstract
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In our previous report, we showed that PPARγ does not influence adipogenesis in females with functioning ovaries, indicating that PPARγ activity on adipogenesis is associated with sex-related factors. Among the sex-related factors, estrogen has been recognized as a major factor in inhibiting adiposgenesis in females. Thus, we hypothensized that 17β-estradiol (E) inhibits 3T3-L1 cell adipogenesis by preventing PPARγ activity. E decreased triglyceirde accumulation in differentiated 3T3-L1 cells compared with control group. E also decreased the expression of PPARγ mRNA as well as PPARγ dependent adipocyte-specific genes, such as adipocyte fatty acid binding protein and tumor necrosis factor α. In addition, E not only decreased luciferase reporter activity by PPARγ, but also transfection of estrogen receptor α (ERα) or ERβ led to decreases in PPARγ reporter gene activation. Moreover, E-activated ERs significantly decreased the luciferase reporter gene activation induced by PPARγ transfection, suggesting that estrogen-activated ERs inhibit PPARγ-dependent transactivation. Accordingly, our results demonstrate that E inhibits the action of PPARγ on adipogenesis through E activated ER, providing evidence that lack of estrogen may potentiate PPARγ action on adipogenesis.
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KEYWORD
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17β-estradiol, PPARγ, ER, Adipogenesis
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