Acylation Stimulating Protein (ASP, also known as C3a desArg) is one of activation fragments formed from the activation of complement cascade. ASP is produced through a process involving three proteins: C3, factor B and adipsin, which are secreted by adipocytes. Interactions of C3 with factor B and with adipsin result in production of C3a followed by desargination of the carboxyl terminus to generate ASP (C3a desArg). Human ASP contains 77 amino acids with 6 cysteins involved in disulfide bridges between residues 22–49, 23–56 and 36–57. ASP is a highly cationic molecule containing no carbohydrate. ASP has a primary role in regulation of lipid metabolism in adipocytes, where it stimulates glucose uptake, increase the activity of diacylglycerol acyltransferase, and inhibits hormone-sensitive lipase activity. In cellular studies, ASP increases fat storage through increased triglyceride synthesis and decreased intracellular lipolysis. In animal models, ASP deficient mice demonstrate reduced body weight, reduced leptin and reduced adipose tissue mass and ASP deficiency results in protection against development of obesity. In human, a number of studies have shown the relationship between ASP, obesity, diabetes and dyslipidemia. It was reported that concentration of circulating ASP is positively related to body adiposity and decreases after weight loss. Because ASP enhances triglyceride storage, whereas interfering with ASP production reduces body fat and protects against diet-induced obesity and insulin resistance, reducing the production of ASP and ASP receptor antagonists represents potential approaches for treating obesity and type 2 diabetes.