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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/61750


    Title: 綠茶表沒食子酸酯型唲茶素酸酯抑制第一型?皮素作用於脂肪細胞上攝入葡萄糖的訊息機制;Signaling mechanism of green tea (-)-epigallocatechin gallate inhibits the effects of endothelin-1 on 3T3-L1 adipocyte glucose uptake.
    Authors: 林庭瑄;Lin,Ting-Syuan
    Contributors: 生命科學系
    Keywords: 綠茶表沒食子酸酯型唲茶素酸酯;第一型?皮素;葡萄糖攝取;葡萄糖運送蛋白;訊息機制;EGCG;ET-1;glucose uptake;glucose transporter;signaling mechanism
    Date: 2013-10-29
    Issue Date: 2013-11-27 11:22:54 (UTC+8)
    Publisher: 國立中央大學
    Abstract: 本研究探討綠茶唲茶素中表沒食子酸酯型唲茶素酸酯(簡寫為EGCG)調控第一型內皮素(簡寫為ET-1 )在短時間(0.5小時)、中長時間(2小時)、長時間(6小時)刺激脂肪細胞攝入葡萄糖的訊息機制。利用3T3-L1脂肪細胞,實驗中發現,在ET-1處理0.5小時和2小時的環境下,預先處理PI3K的抑制劑LY294002及wortmannin時,EGCG無法抑制由ET-1所誘導的葡萄糖攝取作用,然而在前處理ERK/MAPK的抑制劑PD98059及U0126的組別中則無此效應,因此推測EGCG會使ET-1在短時間處理時所減弱葡萄糖攝取的作用與PI3K/AKT此訊息路徑相關。另一方面也發現,當脂肪細胞在已有JAK2的抑制劑AG490(50 ?M )的環境下,ET-1處理0.5小時、2小時的組別中會發現葡萄糖攝取有增加的趨勢,因此可推論EGCG的作用會與JAK2/STAT-3訊息相關。在脂肪細胞裡鑑定到一個EGCG接受子[已知為67-kDa laminin接受子 (67LR)]。在本研究中,預先處理67 LR 抗體時無論是在處理0.5、2、6小時ET-1的環境下,皆呈現EGCG無法抑制ET-1促進葡萄糖攝取的現象,因此推論EGCG會透過67LR來抑制由ET-1所誘導的葡萄糖攝取。另外本實驗中發現在ET-1處理0.5小時的環境下,預先處理抗氧化劑NAC時脂肪細胞本身及由ET-1所誘導的葡萄糖攝取的能力皆有增加的趨勢,因而推測NAC在短時間影響脂肪細胞本身及ET-1所促進的葡萄糖攝取作用與ROS的生成相關。而在預先處理AMPK抑制劑compound C的組別中,無論是在處理0.5、2、6小時ET-1的環境下,皆呈現EGCG無法抑制ET-1促進葡萄糖攝取的現象,因此推論EGCG會透過AMPK來抑制由ET-1所誘導的葡萄糖攝取現象。而當ET-1處理2小時和6小時,EGCG會藉由AMPK的路徑去減弱ET-1所促使的GLUT-1蛋白表現,進而減少葡萄糖攝取的作用。
    This study investigated the possible mechanism involved in EGCG modulation of ET-1-stimulated glucose uptake in 3T3-L1 adipocytes. We found that pretreatment with the PI3K inhibitors, such as LY294002 and wortmannin, inhibited EGCG-induced decreases on the acutely ET-1 stimulated glucose uptake in adipocytes. However, none of the ERK/MAPK inhibitors, such as PD98059 and U0126, significantly blocked the anti-ET-1 effects of EGCG on adipocyte glucose uptake. These data suggest that PI3K activation is necessary for the effects of EGCG on the acutely ET-1-stimulated glucose uptake in adipocytes. Interestingly, we observed that pretreatment with the JAK2/STAT3 inhibitors, such as AG490(50 ?M ), increased the basal glucose uptake and the ET-1-dependent glucose uptake, suggesting the JAK2/STAT3-dependent effect of EGCG. The EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] was identified in fat cells. Pretreatment of adipocytes with 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on ET-1-induced glucose uptake in adipocytes. These data suggest that EGCG exerts its anti-ET-1 actions on adipocyte glucose uptake via the 67LR. However, NAC(an antioxidant) acutely increased the basal glucose uptake and ET-1 stimulated glucose uptake, indicating that NAC possibly affected glucose uptake by suppressing not only the ET-1-dependent ROS production but also the ET-1-independent ROS production. Pretreatment with the AMPK inhibitor, such as compound C, blocked the anti-ET-1 effects of EGCG on adipocyte glucose uptake, and prevented the effects of EGCG on the chronically ET-1-stimulated GLUT-1 protein expression. This suggests that EGCG inhibits the chronically ET-1 action on adipocyte glucose uptake through the activation of AMPK pathway that results in alterations of GLUT-1 protein expression. Results of this study may help understand the mechanism of how green tea EGCG modulates hormone-mediated obesity.
    Appears in Collections:[生命科學研究所 ] 博碩士論文

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