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17ß-Estradiol Stimulates Resistin Gene Expression in 3T3-L1 Adipocytes via the Estrogen Receptor, Extracellularly Regulated Kinase, and CCAAT/Enhancer Binding Protein- Pathways

Department of Life Science, College of Science, National Central University, Chung-Li City, Taoyuan, Taiwan 32054

Address all correspondence and requests for reprints to: Dr. Yung-Hsi Kao, Department of Life Science, College of Science, National Central University, Chung-Li City, Taoyuan, Taiwan 32054. E-mail: ykao{at}cc.ncu.edu.tw.

Resistin is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. It can be regulated by sexual hormones, but the mechanism of estrogen’s actions is still not clear. Using 3T3-L1 adipocytes, we found that 17ß-estradiol (E₂) up-regulated resistin mRNA expression in a dose- and time-dependent manner. The concentration of E₂ that increased resistin mRNA levels by 100–250% was approximately 1 nM for a range of 1–24 h of treatment. Treatment with either actinomycin D or cycloheximide prevented E₂-stimulated resistin mRNA expression, suggesting that the effect of E₂ requires new mRNA and protein synthesis. Although E₂ was shown to increase activities of the estrogen receptor (ER) and MAPK kinase 1 and the association of nuclear ER and CCAAT/enhancer binding protein- with the resistin gene promoter, signaling was demonstrated to be blocked by pretreatment with either ICI182780 or PD98059. Neither SB203580 nor LY294002 changed the E₂-increased levels of resistin mRNA, but they respectively inhibited E₂-stimulated phosphorylation of p38 MAPK and Akt. These results imply the ER, ERK, and CCAAT/enhancer binding protein- are necessary for the E₂ stimulation of transcription from the resistin promoter. Moreover, PD98059, but not SB203580 or LY294002, antagonized E₂-increased resistin protein release. These data suggest that E₂ likely modifies the distribution of the resistin protein between the intracellular and extracellular compartments via an ERK-dependent pathway.

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