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.