Maternal obesity is a risk factor for many complications during pregnancy that often include impaired placental function. The most common obesity-related complication is intrauterine growth restriction (IUGR), a growth disorder occurring in adverse conditions during pregnancy. Fetal growth and development require balanced function of various placental proteins, such as growth factors and proteins involved in serotonin signaling and cellular metabolism. Previous studies have shown that changes in the expression of the aforementioned proteins in the placenta are associated with IUGR and maternal obesity. Therefore, their expression in the placenta could be disrupted due to maternal obesity, which could potentially lead to the occurrence of IUGR. In addition to the placenta, the expression of these proteins could also be altered in fetal tissues (brain and liver). This will be investigated by measuring the expression levels of selected proteins in the placenta and fetal brain and liver of a mouse model of maternal diet-induced obesity, characterized by offspring IUGR. In the same model, changes in tissue structure will be investigated and potentially impaired cellular pathways in the placenta will be examined. Knowledge about the potentially related roles of serotonin balance and placental cellular metabolism as mediators and modulators of the effect of maternal obesity on offspring health may contribute to a better understanding of the mechanisms underlying fetal growth disorders.