Visfatin is a novel-secreted 52kDa adipokine that appears to mimic the action of insulin, inducing glucose transport into mammalian cells. We examined visfatin expression in a cohort of pregnant women to determine if pregnancy influenced visfatin gene expression, circulating levels of visfatin, or local concentrations of visfatin in either omental fat or placenta. Samples of female omental fat, blood and placenta were collected over a 2-year period and frozen at -80 degrees C until they were employed in a series of various assays. Samples were collected during delivery in pregnant women, at hysterectomy in lean women and at bariatric surgery in obese and obese diabetic women. Visfatin expression and concentrations were measured in four cohorts of women: lean controls, pregnant women at term, obese (BMI>40) and obese diabetic women (BMI>40). Visfatin expression was seven times higher in omental fat of pregnant women than in lean women. Immunohistochemistry (IHC) demonstrated that the visfatin gene transcript was translated to protein. An immunoblot confirmed that visfatin protein was much higher in pregnant women than in obese women. Serum visfatin was 20.8ng/ml (n=7) in lean women as compared to 40.3ng/ml in pregnant women (n=4); thus the increased visfatin mRNA levels in omental fat were not reflected in increased serum visfatin. We measured visfatin mRNA content of human placenta and found that placenta expresses substantial amounts of visfatin. GAP-DH, a housekeeping gene that is highly expressed in most human cells had a threshold value (Ct) of 20.9 versus a Ct of 22.4 for visfatin. Again, IHC confirmed that placental visfatin mRNA was translated into visfatin protein. [(3)H] 2-deoxyglucose transport was measured in partially differentiated 3T3-L1 preadipocytes. At a concentration of 2nM, visfatin and insulin produced nearly identical increases in glucose transport. Taken together, these data suggest there is a selective increase in visfatin gene expression in pregnant women at term. Since visfatin also potently and efficaciously induced glucose transport in a cell culture model, any hypothetical role for visfatin in pregnancy should include the possibility that it may function in regulation of maternal/fetal glucose metabolism or distribution.