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J. Biol. Chem., Vol. 269, Issue 4, 2516-2520, Jan, 1994
MA Turnbow, SR Keller, KM Rice and CW Garner
Insulin resistance resulting from prolonged exposure of intact animals or
cultured cells to glucocorticoids is often attributed to postreceptor
signaling defects. To better understand the specific effects of
glucocorticoids on insulin signaling, we have characterized the effect of
dexamethasone on the expression of an insulin signaling intermediate, the
insulin receptor substrate-1 (IRS-1) in 3T3-L1 adipocytes. Addition of
dexamethasone resulted in a 40-70% decline in steady-state IRS-1 protein
over 24-48 h of treatment. Dexamethasone did not significantly change the
degradation rate of IRS-1 protein but decreased the net rate of amino acid
incorporation into IRS-1 by 87%. Between 1 and 2.5 h of treatment with
dexamethasone, actinomycin D, or both drugs given simultaneously, the
concentration of IRS-1 mRNA declined with a half-life of 0.7-1.0 h.
However, after 4 h of dexamethasone treatment, IRS-1 mRNA concentrations
stabilized at approximately 35% of the control level. The
dexamethasone-induced decline in IRS-1 protein could be prevented by
simultaneous administration of the glucocorticoid antagonist mifepristone,
RU38486. These results suggest that in 3T3-L1 adipocytes the loss of IRS-1
protein after dexamethasone treatment can be accounted for chiefly by
inhibition of the synthesis of IRS-1 mRNA.
Dexamethasone down-regulation of insulin receptor substrate-1 in 3T3-L1 adipocytes
Department of Biochemistry and Molecular Biology, Texas Tech University Health Sciences Center, Lubbock 79430.
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