We have demonstrated previously that treatment of 3T3-L1 adipocytes with tumour necrosis factor-α (TNF) results in a rapid (4 h) and significant (75–80%) reduction in the rate of transcription of the GLUT4 gene. Control of GLUT4 gene transcription has been suggested at least in part to reside with the CCAAT-enhancer-binding protein (C/EBP) family (α, β and δ isoforms) of transcription factors. Using electrophoretic mobility shift assays, we have examined the ability of TNF to alter the occupation of the C/EBP site in the GLUT4 promoter. The data suggest that in fully differentiated adipocytes the C/EBP site is a ligand for predominantly α/α homodimers; however, after exposure to TNF, a shift in occupancy of the site occurs and the ligands become α/β heterodimers and β/β homodimers. Partner selection in dimer formation appears to be controlled by selective translocation of the β-isoform from the cytosol to the nucleus after exposure of the cells to TNF.

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