Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes

被引：126

作者：

Chamberlain, LH ^{[1
]}

机构：

[1] Univ Glasgow, Inst Biomed & Life Sci, Div Biochem & Mol Biol, Glasgow G12 8QQ, Lanark, Scotland

来源：

FEBS LETTERS | 2001年 / 507卷 / 03期

关键词：

Glut4; Glut1; lovastatin; cholesterol; isoprenoid; adipocyte;

D O I：

10.1016/S0014-5793(01)03007-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：357 / 361

页数：5

共 21 条

[1] Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver [J].