Low birth weight is observed in rabbit offspring when maternal hypercholesterolemia is induced during gestation, but the related etiology is still unknown. Glucose is one of the most important substances during fetal development, and defect in glucose supply to fetus was related to pathophysiological mechanisms in intrauterine growth restriction. Thus, the aim of this work was to evaluate the impact of maternal hypercholesterolemia during rabbit gestation on the glucose metabolism and the routing of glucose transporters (SLC2 and SLC5 [previously known as GLUT and SGLT]) in placenta. In this study, maternal and offspring serum levels of glucose and insulin were evaluated for control and hypercholesterolemic groups, and the mRNA and protein expressions of placental SLCs were quantified by real-time RT-PCR and Western immunoblot, respectively. Our data demonstrate that maternal hypercholesterolemia during gestation: 1) induces offspring hypoglycemia; 2) does not modify the genetic and protein expressions of SLC2A1 and SLC2A4 (previously GLUT1 and GLUT4) in total placental extract; 3) downregulates the placental SLC5A1 (previously SGLT1) protein expression without affecting its mRNA levels; 4) impairs the translocation of SLC2A1 but not SLC2A4 from cytoplasmatic pool to the cell membrane surface. Then we assume that reduction of offspring birth weight in presence of maternal hypercholesterolemia may be related to the offspring's hypoglycemia and the reduction of the cell surface expression of placental SLC2A1.