Thesis (M.A.) -- Boston University, 2013. / Increased free fatty acid (FFA) flux from adipocytes due to increased lipolysis, has a key contribution in the pathophysiology of metabolic disease. There is a lack of knowledge of the molecular components which determine the TG storing capacity and lipolysis in adipocytes. Studies from our lab and others have demonstrated the role of a lipid droplet associated protein, Fat Specific Protein 27 (FSP27, also called CIDEC), in regulating triglyceride accumulation and lipolysis in adipocytes, but its mechanism of action remains elusive. In the present study, we used cultured human primary adipocytes to define the role of FSP27 in regulating both basal and isoproterenol-stimulated lipolysis. Using a combination of RNAi and adenoviral mediated overexpression techniques, we have shown that FSP27 regulates ATGL-mediated lipolysis by down-regulating gene and protein expression of ATGL. Furthermore, our data shows that FSP27-mediated triglyceride accumulation is suppressed in the absence of ATGL. Our results support a model whereby FSP27 regulates ATGL-mediated lipolysis to accumulate triglycerides in human adipocytes