In our previous report, we showed that $PPAR{gamma}$ does not influence adipogenesis in females with functioning ovaries, indicating that $PPAR{gamma}$ 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 $17{eta}$-estradiol (E) inhibits 3T3-L1 cell adipogenesis by preventing $PPAR{gamma}$ activity. E decreased triglyceirde accumulation in differentiated 3T3-L1 cells compared with control group. E also decreased the expression of $PPAR{gamma}$ mRNA as well as $PPAR{gamma}$ dependent adipocyte-specific genes, such as adipocyte fatty acid binding protein and tumor necrosis factor $alpha$. In addition, E not only decreased luciferase reporter activity by $PPAR{gamma}$, but also transfection of estrogen receptor $alpha$ ($ER{alpha}$) or $ER{eta}$ led to decreases in $PPAR{gamma}$ reporter gene activation. Moreover, E-activated ERs significantly decreased the luciferase reporter gene activation induced by $PPAR{gamma}$ transfection, suggesting that estrogen-activated ERs inhibit $PPAR{gamma}$-dependent transactivation. Accordingly, our results demonstrate that E inhibits the action of $PPAR{gamma}$ on adipogenesis through E activated ER, providing evidence that lack of estrogen may potentiate $PPAR{gamma}$ action on adipogenesis.