Inflammation is a key feature in adipose tissue, especially in association with obesity comorbidies. The novel adipokine acylation stimulating protein (ASP) is one factor implicated in the inflammatory response. The disruption of the alpha 7 nicotine acetylcholine receptor (alpha 7nAChR), an important component of the endogenous non-neural cholinergic defense system, may exacerbate sustained inflammatory phenotype. We examined cholinergic regulation of ASP-initiated inflammatory response in 3T3-L1 adipocytes. Our results show that preincubation of 3T3-L1 cells with alpha 7nAChR agonist GTS-21 significantly reduces ASP-mediated chemokine MCP-1 secretion, which is regulated though nuclear factor kappa B (NF kappa B) and signal transducer and activator of transcription 3 (STAT3). Treatment of 3T3-L1 cells with GTS-21 significantly reduced NF kappa B activation by DNA binding and STAT3 activation by disturbing post-translational modification.