Adipokines, active substances secreted from adipocytes influence metabolic functions. Their levels have been shown to alter in pregnancy and it has been suggested that their dysregulation could be associated with complications of pregnancy, including gestational diabetes. Visfatin, is a novel adipokine (originally known as pre-B cell colony-enhancing factor) with multiple functions including insulin mimetic effects, and it has been found to have altered maternal plasma levels in obese women and during gestation. Leptin, one of the best characterised adipokines, has been reported to decrease contractility of the myometrium. We have therefore investigated the effect of visfatin on myometrial contractility and compared them to leptin. Myometrial strips from either term pregnant women having a caesarean section (with informed consent and ethical approval) or humanely killed rats were dissected, superfused with Krebs and the effects of visfatin or leptin at 1-100 nM studied. After establishment of regular contractions the adipokines were added for 20 minutes. In pregnant human myometrium, visfatin at 1nM had little effect on contractility but 10 nM produced a significant (paired T Test) decrease in the amplitude and integral of spontaneous contractions (47±18 % and 50±19 % respectively, mean + sem, control 100%; n= 4). Leptin at this concentration (10 nM) had only a small inhibitory effect (~ 5 – 10%) on contractions of rat or human myometrium. These data are the first to show that visfatin can inhibit myometrial contractility and that it may do so more potently than leptin. Increased output of adipokines associated with maternal adiposity, along with cholesterol, which we have previously demonstrated to inhibit contractility, may impair force production in uterine myocyte and contribute to uterine dystocia and the need for unplanned caesarean delivery in obese mothers.