Effect of dexamethasone on insulin binding, glucose transport, and glucose oxidation of isolated rat adipocytes

  • Olefsky J
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The authors have studied the in vitro effects of dexamethasone on isolated rat adipocytes at concentrations of dexamethasone therapeutically achieved in man. Glucose oxidation, glucose transport, and insulin binding were assessed. In dexamethasone treated cells, glucose oxidation was decreased by 30 to 40{%} both in the absence of insulin (basal state) and at low insulin levels (less than 25 $μ$U/ml). At maximally effective insulin levels (over 100 $μ$U/ml) no differences existed between control and treated cells. If glucose transport were the rate limiting step for glucose oxidation in the basal state and at low (submaximal) insulin levels, but not at maximally effective insulin concentrations, then these data could be explained by postulating that dexamethasone has a direct effect on glucose transport and does not affect intracellular oxidative pathways. The authors tested this hypothesis by directly assessing glucose transport in dexamethasone treated cells. Glucose transport was assessed by measuring the uptake of [14C]2 deoxy glucose. These studies demonstrated a 30 to 40{%} decrease in 2 deoxy glucose uptake by treated cells both in the basal state and at all insulin concentrations. Thus, a direct glucocorticoid effect on the glucose transport system seems to account for the decreased ability of dexamethasone treated cells to oxidize glucose. Since dexamethasone treatment leads to decreased insulin binding to adipocytes in vivo, they examined the possibility that the in vitro decreases in insulin mediated glucose transport could be due to decreased insulin receptors. Insulin binding to control and treated adipocytes was measured, and no differences were found. Therefore, in contrast to previously reported in vivo studies, adipocytes treated in vitro with dexamethasone retain a normal ability to bind insulin. Thus, these studies suggest that all of the in vitro effects of dexamethasone on glucose oxidation are due to direct inhibition of the glucose transport system.

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  • J. M. Olefsky

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