Data from: A potential role for GSK3beta in glucose-driven intrauterine catch-up growth in maternal obesity

Obesity and an unhealthy nutrition are on the rise and affect also women in childbearing age and hence, during pregnancy. Despite normal or even high birth weight the offspring suffers from long term metabolic risks. We hypothesized that fetal growth is disturbed during different intrauterine phases. Underlying molecular events remain elusive. Female mice were fed either a control diet (SD) or a high fat diet (HFD) after weaning until mating and during pregnancy. Pregnant mice were sacrificed at gestational time points G15.5 and G18.5 and fetuses and placentas were removed for analysis. HFD fetuses displayed intrauterine growth restriction (IUGR) at G15.5, which disappeared until G18.5, indicating an intrauterine catch-up growth during that time period. Main placental findings indicate decreased canonical Wnt-GSK3beta signaling and lower proliferation rates at G18.5 which goes along with a smaller placental transfer zone. On the other hand, glucose depots (glycogen cluster) in HFD placentas decreased stronger between G15.5 and G18.5 compared to placentas from SD mothers, and the glucose transporter protein GLUT-1 was increased at G18.5 in the HFD group. Maternal diet-induced obesity causes an IUGR phenotype at the beginning of the third week (G15.5) in our mouse model. This phenotype is reversed by the end of the third week (G18.5) despite of a smaller placental transfer zone, probably based on GSK3beta-mediated increased glucose mobilization in the placenta and hence an increased glucose supply to the fetus