Although CTRP3, SP-1 and PPAR-gamma are induced during adipocyte differentiation, promoter activity assays demonstrate that PPAR-gamma, SP-1, and c-FOS are all negative regulators of CTRP3 expression (53, 56). Electrophoretic mobility shift assays confirmed that both SP-1 and PPAR-gamma (but not SRY, c-FOS, C/EBPβ, or PPAR-alpha) bind to the promoter region for CTRP3. To date only the transcription factor c-Jun has been shown to be an unequivocal positive regulator for CTRP3 transcription (28). The transcription factor c-Jun is one of three Jun family proteins which make up the activator protein-1 (AP-1) transcription factor group. Chromatin immunoprecipitation assay confirmed that c-Jun binds to the AP-1 region (-184/-177) of CTRP3 (28), whereas, other Jun and Fos members JunB, JunD, FosB, Fra-1, and Fra-2 were tested by a reporter gene assay and had no effect on CTRP3 promoter activity (28). Further, treatment of adipocytes, in vitro, or diet-induced obese rats, in vivo, with the glucagon-likepeptide-1 (GLP-1) receptor agonist, Exendin-4 (Ex-4), increased CTRP3 expression and circulating levels through activation of the Protein kinase A (PKA) pathway (37,40). Briefly, the activation ofGLP-1 receptor and PKA pathway
