LPS is a well-established endotoxin used as a model of systemic immune response, in vivo. In cell culture models LPS inhibits adipose tissue differentiation, induces insulin resistance, and prevents the expression of CTRP3 (59). Whereas, CTRP3 has been shown to specifically block the binding of LPS to its receptor TLR4 (13,30) and inhibit the inflammatory response (30). Further, in animalmodels intraperitoneal injection (IP) injection of CTRP3 (0.4ug/g body weight) significantly reduced the LPS-induced (IP) inflammatory response (65). Although intravenous administration of CTRP3 was unable to prevent LPS-induced inflammation, this is thought to be a dose related limitation and future studies are ongoing to determine the clinically relevant levels of CTRP3 administration needed to inhibit a systematic immune response. Further, CTRP3 potently inhibited LPS-induced IL-6 in monocytes isolated from healthy subjects but not in monocytes derived from subject with T2D (31, 70). Similarly, the anti-inflammatory effects of CTRP3 have also been observed in isolated primary human colonic fibroblasts (21). Combined, these data show promise for the use of CTRP3 and CTRP3-mediated pathways as a potential anti-inflammatory mediator. However, neither chronic CTRP3
