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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/38940


    Title: Green tea (-)-epigallocatechin gallate inhibits insulin stimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor pathway
    Authors: Ku,HC;Chang,HH;Liu,HC;Hsiao,CH;Lee,MJ;Hu,YJ;Hung,PF;Liu,CW;Kao,YH
    Contributors: 物理研究所
    Keywords: ACTIVATED PROTEIN-KINASE;RESISTIN GENE-EXPRESSION;EPIGALLOCATECHIN GALLATE;MULTIFUNCTIONAL PROTEIN;CATECHIN-POLYPHENOLS;SIGNALING PATHWAY;CELLS;MECHANISMS;ADIPOCYTES;CANCER
    Date: 2009
    Issue Date: 2010-07-08 13:59:50 (UTC+8)
    Publisher: 中央大學
    Abstract: Ku HC, Chang HH, Liu HC, Hsiao CH, Lee MJ, Hu YJ, Hung PF, Liu CW, Kao YH. Green tea (-)-epigallocatechin gallate inhibits insulin stimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor pathway. Am J Physiol Cell Physiol 297: C121-C132, 2009. First published January 28, 2009; doi:10.1152/ajpcell.00272.2008.-Insulin and (-)-epigallocatechin gallate (EGCG) have been reported to regulate fat cell mitogenesis and adipogenesis, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated mitogenesis in 3T3-L1 preadipocytes. EGCG inhibited insulin stimulation of preadipocyte proliferation in a dose- and time-dependent manner. EGCG also suppressed insulin-stimulated phosphorylation of the insulin receptor-beta, insulin receptor (IR) substrates 1 and 2 (IRS1 and IRS2), and mitogen-activated protein kinase pathway proteins, RAF1, MEK1/2, and ERK1/2, but not JNK. Furthermore, EGCG inhibited the association of IR with the IRS1 and IRS2 proteins, but not with the IRS4 protein. These data suggest that EGCG selectively affects particular types of IRS and MAPK family members. Generally, EGCG was more effective than epicatechin, epicatechin gallate, and epigallocatechin in modulating insulin-stimulated mitogenic signaling. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and found that its expression was sensitive to growth phase, tissue type, and differentiation state. Pretreatment of preadipocytes with 67LR antiserum prevented the effects of EGCG on insulin-stimulated phosphorylation of IRS2, RAF1, and ERK1/2 and insulin-stimulated preadipocyte proliferation (cell number and bromodeoxyuridine incorporation). Moreover, EGCG tended to increase insulin-stimulated associations between the 67LR and IR, IRS1, IRS2, and IRS4 proteins. These data suggest that EGCG mediates anti-insulin signaling in preadipocyte mitogenesis via the 67LR pathway.
    Relation: AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
    Appears in Collections:[Graduate Institute of Physics] journal & Dissertation

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