Transcriptomics of Beta3-adrenergic receptor in adipocyte catecholamine resistance. Mus musculus

To explore catecholamine resistance, mouse 3T3-L1adipocytes were exposed to inflammatory cytokine TNFalpha (heterologous desensitization), which similarly impaired stimulated lipolysis by beta-adrenergic agonists. Down-regulation of Adrb3 in response to both ligand exposure and inflammatory stimulation in vitro were triggered by induction of the pseudokinase TRIB1 downstream of the EPAC/RAP2A/PI-PLC pathway. TRIB1 in turn led to degradation of CEBPalpha, the primary transcriptional activator of Adrb3 expression.