A Potential Role for GSK3βin Glucose-Driven Intrauterine Catch-Up Growth in Maternal Obesity

• DOI: 10.1210/en.2018-00899
• Publication Date: 2018-12-10T14:19:47Z
• Authors: Sarah Appel; Jon Grothe; Sarah Storck; Ruth Janoschek; Inga Bae-Gartz; Maria Wohlfarth; Marion Handwerk; Eva Hucklenbruch-...; Alexandra Gellhaus; Jörg Dötsch
• Keywords: Intrauterine growth restriction; Placental insufficiency

Obesity and unhealthy nutrition are increasing affect women of childbearing age 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 different intrauterine phases. Underlying molecular events remain elusive. Female mice were fed either a standard diet (SD) high-fat (HFD) after weaning until mating Pregnant euthanized at gestational day (G)15.5 G18.5, fetuses placentas removed for analysis. HFD displayed restriction (IUGR) G15.5, which disappeared indicating catch-up time period. Main placental findings indicate decreased canonical Wnt-GSK3β signaling lower proliferation rates goes along with smaller transfer zone. On other hand, glucose depots (glycogen cluster) in more strongly between G15.5 G18.5 compared SD mothers, transporter protein GLUT-1 was increased group. Maternal diet-induced obesity causes an IUGR phenotype beginning third week (G15.5) our mouse model. This reversed by end (G18.5) despite zone, probably based on GSK3β-mediated mobilization placenta supply to fetus.