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Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3‐L1 adipocytes
Author(s) -
Chamberlain Luke H
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03007-1
Subject(s) - glut4 , insulin resistance , 3t3 l1 , lovastatin , glucose transporter , glut1 , insulin , medicine , glucose uptake , endocrinology , insulin receptor , chemistry , mevalonic acid , fgf21 , biology , biosynthesis , cholesterol , biochemistry , adipocyte , adipose tissue , gene , fibroblast growth factor , receptor
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.