Cardiovascular disease, including ischemic heart disease, is the major cause of morbidity and mortality in developed countries.1 Obese states are closely linked to the development of metabolic dysfunction and cardiovascular disorders.2,3 It is well established that adipose tissue secretes various hormonal factors, also known as adipokines, and affects nearby or remote organs in a paracrine, and endocrine manner.3–5 Increasing evidence indicates that dysregulated adipokine production caused by excess fat accumulation contributes to obesity-associated complications.4 Most adipokines are upregulated in obese states and usually act as proinflammatory mediators that promote the disease process.4 Conversely, a few adipokines are downregulated by obesity, and these factors typically exert beneficial actions on obesity-linked disorders. Article see p 3159 Adiponectin is a widely-studied antiinflammatory adipokine. Its concentration in the bloodstream is reduced in obese subjects. Experimental studies have shown that adiponectin protects against the development of various obesity-inducible metabolic and cardiovascular disorders.3,4,6 In the past few years, it has become appreciated that adiponectin is a member of the large C1q/tumor necrosis factor–related protein (CTRP) family. These family members contain a conserved collagen tail domain and a globular C1q-like domain at the C terminus.7,8 Recent studies show that, like adiponectin, some CTRPs function as adipokines that display diverse biological activities in the context of …