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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/6379

    Title: 辛基苯酚對3T3-L1脂肪細胞中resistin的調節作用;Octylphenol regulation of resistin in 3T3-L1 adipocyte
    Authors: 吳敏華;Min-Hua Wu
    Contributors: 生命科學研究所
    Keywords: 辛基本酚;抗胰島素激素;脂肪細胞;Octylphenol;resistin;adipocyte
    Date: 2006-01-12
    Issue Date: 2009-09-22 10:18:31 (UTC+8)
    Publisher: 國立中央大學圖書館
    Abstract: 抗胰島素激素(resistin)是由脂肪細胞所分泌的荷爾蒙,其作用會降低了胰島素刺激脂肪細胞攝入葡萄糖的能力,而造成胰島素抗性,並且連結肥胖症和第二型糖尿病之間的關係。抗胰島素激素的表達量會受到許多荷爾蒙的調節,但整個調控機制仍然不清楚。然而環境荷爾蒙是由許多環境化合物所代謝產生,並且在累積中會影響到生物體內原本的生理活性,其中辛基苯酚(OP)結構和雌性素相似,並且會模仿雌性素的作用。故在本論文中,利用3T3-L1脂肪細胞做為研究細胞株,本研究發現OP會增加抗胰島素激素mRNA及蛋白質的產生,並且隨著OP的濃度及處理時間的不同而有程度上的差異。而在前處理轉錄抑制劑actinomycin D及轉譯抑制劑cycloheximide的情況下,OP刺激抗胰島素激素mRNA及蛋白質的表達量並不會受到改變,因此OP會增加抗胰島素激素mRNA及蛋白質的穩定性。實驗中也證實OP增加抗胰島素激素mRNA及蛋白質的表達會受到雌性素接受器抑制劑ICI182780及MEK1抑制劑U0126所抑制,顯示OP會經由ERα及MEK1訊息傳導途徑增加抗胰島素激素的產生,然而OP也會影響到ERα和抗胰島素激素負調節因子PPARγ之間的結合能力和PPARγ蛋白質表現,是否OP增加抗胰島素激素的產生之機制也與PPARγ的途徑有直接的關聯,將有待以釐清。 Resistin (Rstn) is an adipocyte-specific secretory hormone that can reduce the insulin-stimulated glucose uptake by adipocytes, resulting in insulin resistance, and link the obesity and type II diabetes. It can be regulated by many hormones, but the exact mechanisms of their action is still not clear. Environment hormones are derived from the metabolites of many environmental chemical compounds and have the biological activity in organisms. Octylphenol (OP) is one of environmental estrogens that has the structural similarity to estrogen and can mimic the action of estrogens. In this study using 3T3-L1 adipocytes as the research cell line, OP induced increases in Rstn mRNA and protein expression with significantly dose- and time-dependent differences was discovered. Also, pretreatment with either transcriptional inhibitor actinomycin D or translational inhibitor cycloheximide did not prevent the OP-stimulated Rstn mRNA and protein expression. This suggests that OP increases the stabilities of Rstn mRNA and protein. In addition, pretreatment with either estrogen receptor alpha (ER?) inhibitor ICI182780 or MEK1 inhibitor U0126 prevented the OP-induced increases in Rstn mRNA and protein expression, suggesting that the effect of OP requires the functional ER? and MEK1. Moreover, OP increased PPAR? (a negative regulator of Rstn) protein expression and the association of ER? with PPAR?. Further studies to demonstrating whether the effect of OP on Rstn gene expression is mediated directly via modulation of PPAR? is needed.
    Appears in Collections:[生命科學研究所 ] 博碩士論文

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