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Pioglitazone and other antidiabetic thiazolidinediones appear to overcome insulin resistance by affecting an unidentified early event in insulin action. Because attempts to determine changes in insulin receptors in tissues from thiazolidinedione‐treated diabetic animals are complicated by drug‐induced reduction of hyperinsulinemia and consequent receptor up‐regulation, 3T3‐L1 cells were utilized here as an in vitro model system. After the excess insulin required for optimal differentiation of 3T3‐L1 adipocytes was removed from the culture medium, there was an increase in specific binding of insulin to the cell surface that was further augmented 25 and 47% in cells treated with pioglitazone for 12 and 24 h, respectively (EC50 about 0.6 μM, maximal at 5–25 μM). Pioglitazone increased the number of insulin receptors without changing binding affinity. Specific IGF‐I binding was not affected by pioglitazone in the 3T3‐L1 cells. Glycerol 3‐phosphate dehydrogenase activity, a marker of adipocyte differentiation, was also increased in a dose‐dependent manner by pioglitazone (maximal at 10–25 μM). Tunicamycin, which inhibits the N‐linked glycosylation of newly synthesized insulin receptors that is required for their translocation to the cell surface, decreased specific insulin binding by about 50% after 24 h, and this decrease remained unchanged when pioglitazone was simultaneously present. Pioglitazone increased not only cell surface insulin receptors, but also total cellular insulin receptors (quantitated either by specific insulin binding or by immunoblotting) and insulin receptors mRNA. In addition, among several structurally related thiazolidinediones there was a positive correlation between in vivo antihyperglycemic activity and their ability to increase insulin binding in vitro, suggesting a possible common molecular mechanism for these actions. © 1995 Wiley‐Liss, Inc.
Drug Development Research – Wiley
Published: Jun 1, 1995
Keywords: cultured cells; insulin; insulin‐like growth factor I; insulin resistance
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