Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes
Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes
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DOI：
10.1016/s0014-5793(01)03007-1
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发表时间：
2001-11-02
期刊：
影响因子：
3.5
通讯作者：
Chamberlain, LH
中科院分区：
文献类型：
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作者：
Chamberlain, LH
洛伐他汀处理引起3 T3-L1脂肪细胞中胰岛素响应性葡萄糖转运蛋白4（Glut 4）的下调和Glut 1的上调。这些蛋白质表达的变化与胰岛素刺激的葡萄糖转运的显著抑制有关。洛伐他汀对细胞胆固醇水平没有影响，但其作用被甲羟戊酸逆转，这表明抑制类异戊二烯生物合成会导致3 T3-L1脂肪细胞的胰岛素抵抗。这些发现支持了这样一种观点，即全身胰岛素抵抗可能是由于一般生化途径的扰动而引起的，而不是胰岛素信号传导的主要缺陷。(C)2001年由Elsevier Science B. V.代表欧洲生物化学学会联合会出版。
Lovastatin treatment caused down-regulation of the insulin-responsive glucose transporter 4 (Glut4) and up-regulation of Glut1 in 3T3-L1 adipocytes. These changes in protein expression were associated with a marked inhibition of insulin-stimulated glucose transport. Lovastatin had no effect on cell cholesterol levels, but its effects were reversed by mevalonate, demonstrating that inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes. These findings support the notion that whole body insulin resistance may arise as a result of perturbations in general biochemical pathways, rather than primary defects in insulin signalling. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.