지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2009.9
- 수록면
- 179 - 185 (7page)
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초록· 키워드
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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.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Acknowledgements
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-510-018855943