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Glucocorticoid-induced insulin resistance in vitro: evidence for both receptor and postreceptor defects.

Glucocorticoid excess in vivo has been shown to cause decreases in insulin sensitivity and insulin receptor binding in target tissues. It has not been previously possible to produce all of these changes in vitro because of limitations of the isolated rat adipocyte as an experimental model. We have studied the effects of glucocorticoid hormones on insulin binding and insulin action in differentiated mouse 3T3-L1 fatty fibroblasts, in an attempt to develop a complete in vitro model of the insulin resistance associated with glucocorticoid excess. Exposure of 3T3-L1 cells to dexamethasone, a synthetic glucocorticoid, resulted in decreased binding of insulin to its receptor and decreased insulin stimulation of 2-deoxyglucose uptake. Although some effect of dexamethasone on these parameters was observed after 24 h, more than 3 days were required for maximal inhibition of both binding and biological response. The magnitude of these changes was concentration dependent over a range of 0.1 –100 nM dexamethasone. Ex...