Metabolic syndrome is defined as a cluster of risk factors which directly increase the risk of CVD, T2D, and allcause mortality (4, 26). One of the major defining risk factors for metabolic syndrome is a chronic state of low-grade inflammation marked by elevated circulating proinflammatory cytokines (TNF, IL-6, and C-reactive protein). The adipose tissue immune response plays amajor role in the development of the chronic proinflammatory state (22, 26). Whereas, CTRP3 is a potential anti-inflammatory mediator, and is negatively associated with the proinflammatory cytokines TNF, IL-6, and C-reactive protein (5, 11, 12, 14, 48, 50, 52, 65, 83). In animal models, diet-induced obesity results in decreased CTRP3 levels concurrent with an elevation in TNF and IL-6 (50). Similarly, diet-induced obese Ctrp3-knockout mice have an enhanced elevation of IL-6 and TNF levels (71). Further, transgenic overexpression of CTRP3 attenuates the high-fat diet induced rise in cytokine levels and more than doubles circulating soluble gp130 (sgp130) levels (50). Circulating sgp130 is a potent inhibitor of inflammatory cytokines such as IL-6 (24).On another note, although essential for regulating platelet aggregation, excessive levels of
