Differential chemoattractant response in adipocytes and macrophages to the action of acylation stimulating protein.

Abstract Obesity is characterized by chronic low-grade inflammation with increased adipose tissue pro-inflammatory cytokine production. Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2. Circulating ASP is increased in obesity, insulin resistance and metabolic syndrome. The present study examines the effects of normal (50 nM), high physiological (200 nM) and pathological (600 nM) levels of ASP on inflammatory changes in 3T3-L1 adipocytes and J774 macrophages and the underlying mechanisms involved. Treatment with ASP for 24 h increased monocyte chemoattractant protein-1 (MCP1, 800%, P 150%, P P P 468 and Ser 536 phosphorylation of p65 NFκB in a time- and concentration-dependent manner ( P 473 ( p  = 0.02). ASP and insulin stimulations of Ser 536 p65 NFκB phosphorylation were comparable (both p