Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed to analyze the impact of maternal and fetal common LEP variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24-28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12 LEP variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal LEP polymorphisms may affect maternal glucose metabolism in pregnancy.