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 activates HOB1 motif within the A1 activation domain of c-JUN and promotes c-JUN’s binding to the AP-1 region (6). However, the regulation of CTRP3 under physiological conditions in vivo has not yet been established. Unlike most adipokines, circulating CTRP3 levels are increased with fasting (51), indicating that CTRP3 levels may be suppressed by either insulin or activated by glucagon signaling pathways. Further, CTRP3 levels are negatively associated with insulin and leptin levels in high fat fed mice (51). Taken together, these data show a potential reciprocal relationship between food intake and CTRP3. However, the clinical implications have yet to be explored, especially regarding the significance of the by-phasic regulation of CTRP3 and lipid metabolism.
