Abstract Obesity is a global epidemic and is associated with a cluster of metabolic diseases that lead to premature mortality. Research in the past decade suggests that chronic, low-grade inflammation – a hallmark of obesity, is a major contributing factor for the pathophysiology of several cardiovascular and metabolic diseases, including atherosclerosis and type 2 diabetes. Evidence suggests that obesity leads to abnormal levels of adipokines, which is linked to insulin resistance and inflammation of the adipose tissue. Visfatin, an adipokine predominantly secreted by visceral adipose tissue and that circulates at increased levels in obesity has been associated with several inflammatory disorders and cancer. Whether visfatin functions as a pro-inflammatory or anti-inflammatory factor is still a subject of debate. We investigated the effect of visfatin on human endothelial cells at the level of gene expression, cytokine release, and interaction with leukocytes in vitro. We found that visfatin upregulates the gene expression of the cytokines – CCL2, IL6, GM-CSF, CXCL2, and CXCL8 (p<0.05) at the transcript level. Additionally, visfatin significantly upregulated the secretion of CXC-cytokines – CXCL2 and CXCL8, in a dose and time-sensitive manner. Finally, we explored if visfatin treatment has any effect on endothelial-leukocyte interaction; we found that visfatin-treated endothelial cells exhibited pronounced adhesion to monocytes (p<0.05). Visfatin also upregulated the expression of adhesion markers – ICAM1, VCAM1, and E-Selectin (p<0.05). Overall, these results consolidate the notion that extracellular visfatin is a marker for vascular and adipose inflammation and a potential target for therapeutic intervention.