Background and Objective: Metabolic syndromes may be induced or exacerbated by environmental exposure to industrial pollutants that act as endocrine disruptors, such as the widely used chemical surfactant Nonylphenol (NP). We previously examined the effects of NP on fat metabolism in mice and found that developmental exposure led to increased weight gain and adipogenesis of adult males. We further observed that NP could induce adipogenesis for human preadipocyte cells. However, the effects of NP on adipogenesis for human preadipocyte cells are not clear enough. This study examined the mechanisms of NP on lipogenesis upon human preadipocytes. Materials and Methods: Human preadipocytes were incubated with NP plus the cAMP-dependent Protein Kinase A (PKA) inhibitor H89 or the Extracellular Signal-regulated Kinase (ERK) inhibitor U0126 under differentiation-inducing conditions. The cells after incubation were harvested for western blotting and real-time PCR measurements of lipogenic markers. Results: With human preadipocytes, NP stimulated lipogenesis by increasing c/EBPα mRNA expression and both proliferator-activated receptor-γ (PPARγ mRNA and protein expression and reducing PPARα protein expression. The cells incubation with U0126 for the first day inhibited NP-induced upregulation of c/EBPα mRNA, PPARγ mRNA and PPARγ protein expressions. H89 did not affect NP-stimulated expression of FASN and PPARγ mRNA but decreased NP-induced PPARα protein expression. Conclusion: This study demonstrated that NP-stimulated lipogenesis by increasing c/EBPα mRNA expression and both PPARγ mRNA and protein expression and reducing PPARα protein expression. The action mechanism of NP looks mediates through PKA and ERK cascades.