Insulin resistance(IR) is a hallmark of pregnancy. Because increased visceral fat(VF) is associated with IR in non-pregnant states, we reasoned that fat accretion might be important in the development of IR during pregnancy. To determine if VF depots increase in pregnancy and if VF contributes to IR, we studied three groups of 6-month old female SD rats, 1)Non-pregnant sham-operated(Non-Preg, n=6), 2)Pregnant sham-operated(Preg, n=6), and 3)Pregnant rats in which VF was surgically removed one month prior to mating(PVF-, n=6). VF doubled by Day 19 of pregnancy(Non-Preg 5.1±0.3g, Preg 10.0±1.0, p<0.01) and PVF- has similar amounts of VF compared to Non-Preg (PVF- 4.6±0.8g). Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp in late gestation in chronically catheterized rats. The glucose infusion rate (GIR) was highest in the Non-Preg (19.4±2.0mg/kg/min), lowest in Preg (11.1 ±1.4mg/kg/min) and intermediate in PVF- (14.7±0.6mg/kg/min; p<0.001 between all groups). During the clamp, Non-Preg had greater hepatic insulin sensitivity than Preg (hepatic glucose production (HGP) Non-Preg 4.5±1.3, Preg 9.3±0.5mg/kg/min, p<0.001). With decreased VF, hepatic insulin sensitivity was similar to non-pregnant levels in PVF-(HGP 4.9±0.8mg/kg/min). Both pregnant groups had lower peripheral glucose uptake compared to Non-Preg. In parallel with hepatic insulin sensitivity, hepatic triglyceride (TG) content was increased in pregnancy (Non-Preg 1.9±0.4 vs. Preg 3.2±0.3mg/g) and decreased with removal of VF (PVF- 1.3±0.4mg/g, p<0.05). Accretion of visceral fat is an important component to the development of hepatic IR in pregnancy and accumulation of hepatic triglycerides is a mechanism by which visceral fat may modulate insulin action in pregnancy.