본문 바로가기
  • 학술저널

표지

DBpia에서 서비스 중인 논문에 한하여 피인용 수가 반영됩니다. 내서재에 논문을 담은 이용자 수의 총합입니다.

초록·키워드 목차

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. #17β-estradiol #PPARγ #ER #Adipogenesis

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Acknowledgements
REFERENCES

DBpia에서 서비스 중인 논문에 한하여 피인용 수가 반영됩니다.
Insert title here
논문의 정보가 복사되었습니다.
붙여넣기 하세요.