Potentiation of glucose uptake in 3T3-L1 adipocytes by PPARγ agonists is maintained in cells expressing a PPARγ dominant-negative mutant: Evidence for selectivity in the downstream responses to PPARγ activation

Abstract

Pharmacological agonists for the nuclear receptor PPARγ enhance glucose disposal in a variety of insulin-resistant states in humans and animals. The precise mechanisms whereby activation of PPARγ leads to increased glucose uptake in metabolically active cells remain to be determined. Notably, certain novel, synthetic PPARγ ligands appear to antagonize thiazolidinedione-induced adipogenesis yet stimulate cellular glucose uptake. We have explored the molecular mechanisms underlying the enhancement of glucose uptake produced by PPARγ agonists in 3T3-L1 adipocytes. Rosiglitazone treatment for 48 h significantly increased basal and insulin-stimulated glucose uptake and markedly increased the cell..