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    請使用永久網址來引用或連結此文件: http://ir.meiho.edu.tw/ir/handle/987654321/3305


    題名: 探討穀維醇(-oryzanol)與預發芽糙米萃取物控制肝臟細胞糖代謝與脂肪細胞分化之功效
    作者: 沈國屏;郝繼隆
    關鍵詞: pre-germinated brown rice;insulin;TNF-;HepG2 cell
    日期: 2017-03-01
    上傳時間: 2017-03-06T06:12:02Z (UTC)
    摘要: This study is the first to examine the effects of pre-germinated brown rice (PGBR) extract in TNF- impaired insulin stimulated glucose uptake and insulin signaling. HepG2 cells were cultured in DMEM medium and added with 20M insulin or with 20M insulin and 30ng/ml TNF-. The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. However, TNF- inhibited glucose uptake into cells treated with insulin. Moreover, insulin increased the protein expressions of AMP-activated protein kinase (AMPK), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-3-kinase-(PI3K-), serine/threonine kinase PI3K-linked protein kinase B (Akt/PKB), glucose transporter-2 (GLUT-2), glucokinase (GCK), peroxisome proliferator activated receptor- (PPAR-) and PPAR-. TNF- activated MAPKs (p65, JNK1/2 and ERK1/2) which worsened the expressions of AMPK, IRS-1, PI3K-, Akt/PKB, GLUT-2, GCK, glucogen synthase kinase-3 (GSK-3), PPAR-and PPAR-. Once this relationship was established, we added PGBR extract (50, 100, 300 g/ml) to cell with 20M insulin and 30ng/ml TNF-. We found glucose levels of medium were lowered and that the protein expressions of AMPK, IRS-1, PI3K-, Akt/PKB, GLUT-2, GCK, GSK-3, PPAR-, PPAR- and p65, JNK1/2 were also improved. In conclusion, this study found that TNF- inhibited insulin stimulated glucose uptake and aggravated related proteins expressions, suggesting that it might cause insulin resistance. PGBR extract was found to improve this TNF-induced insulin resistance, suggesting that it might be used in the future to help control insulin resistance.
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