Gestational diabetes is an altered glucose metabolism state in pregnancy in previously healthy women. Children of mothers with gestational diabetes have an increased risk of obesity as adults. It is considered that this phenomenon is a product of fetal programming through epigenetic mechanisms like DNA methylation. Gene for serotonin transporter, transmembrane protein responsible for serotonin neurotransmitter cell intake has an important role in regulation of food intake, and weight control. It is included in etiopathogenesis of obesity. In this work, we had a hypothesis that DNA methylation of the gene for serotonin transporter could be involved in fetal programming of obesity in gestational diabetes. We investigated the possible relationship of gestational diabetes with the level of DNA methylation of the gene for serotonin transporter in the placental tissue of healthy newborns. For DNA methylation analysis we used bisulphite sequencing. The level of methylation of the gene for serotonin transporter was significantly lower in pregnancies complicated by gestational diabetes (N = 19) compared to pregnancies with no complications (N = 32), while polymorphism of the gene for serotonin transporter had no influence on methylation levels. Our results, for the first time, describe the methylation pattern of the promoter region of the gene for serotonin transporter in the human placenta, and present preliminary evidence for its possible role in developmental programming in gestational diabetes.