In pig production, the selection of hyperprolific animals has lead to an increased rate of intrauterine growth-retarded piglets in litters. Intrauterine growth retardation (IUGR) is an important economic issue inducing a higher mortality rate, a lower growth capacity, a higher muscular lipid content in carcasses and less tender meat. The maternal and fetal environments interact through the placenta to maintain nutrient supply of the fetus. The aim of this work was to explore placental adaptive mechanisms throughout pregnancy in IUGR piglets. Possible changes in placental morphometry and gene expression of the IUGR piglet were prospected, using a natural IUGR pig model. Placental samples from 18 pairs of control (normal birth weight) and IUGR fetuses at gestation days (gd) 45, 71 and 112 were analyzed by stereology. The expression of 10 candidate genes potentially associated with placental development and IUGR was examined by RT-qPCR. The DNA methylation of the insulin-like growth factor 2 (IGF2) imprinting gene was evaluated by pyrosequencing. Glycemia and fructosemia were measured in IUGR and control fetuses at gd 71 and 112. No morphometric abnormality was found in the IUGR placenta. An increased expression of the IGF2 gene, however, was observed in the IUGR chorionic tissue at gd 71 (31.48, P , 0.05). No difference was shown, however, in the DNA methylation levels of the IGF2 gene. Fructosemia was significantly reduced in IUGR fetuses at gd 71, but not at gd 112, whereas glycemia remained normal at both stages. IGF2 affects the placental growth and the placental permeability by modulating the nutrient transport levels. This increase could be a compensatory mechanism from the placenta to meet the fetal nutrient demand and maintain fetal growth at mid-gestation. Indeed, there was a tendency for the expression of glucose transporter GLUT3 to be reduced at gd 71.