Abstract
Extracellular regulated kinases (ERKs) mediate the inhibitory effect of tumor necrosis factor α (TNF-α) on uncoupling protein-1 (UCP-1), but not on lipid accumulation. TNF-α-induced ERK-dependent peroxisome proliferator activator receptor γ (PPARγ) phosphorylation could be responsible for UCP-1 downregulation. Thus, the negative effect of TNF-α on UCP-1 mRNA expression at 4–5 h, under basal conditions or in cells treated with the PPARγ agonist, rosiglitazone, was reversed by the MEK1 inhibitor PD98059. In contrast, fatty acid synthase and malic enzyme mRNA downregulation was not prevented. Moreover, rosiglitazone has no positive effect on adipogenic gene expression or lipid accumulation. Therefore, there is a differential regulation of thermogenic and adipogenic differentiation by PPARγ, which might account for the differences in the TNF-α regulation through ERKs.
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