title: Role of placental insufficiency and intrauterine growth restriction on the activation of fetal hepatic glucose production.
abstract: Glucose is the major fuel for fetal oxidative metabolism. A positive maternal-fetal glucose gradient drives glucose across the placenta and is sufficient to meet the demands of the fetus, eliminating the need for endogenous hepatic glucose production (HGP). However, fetuses with intrauterine growth restriction (IUGR) from pregnancies complicated by placental insufficiency have an early activation of HGP. Furthermore, this activated HGP is resistant to suppression by insulin. Here, we present the data demonstrating the activation of HGP in animal models, mostly fetal sheep, and human pregnancies with IUGR. We also discuss potential mechanisms and pathways that may produce and support HGP and hepatic insulin resistance in IUGR fetuses.
authors.affiliation: Perinatal Research Center, Department of Pediatrics, University of Colorado School of Medicine, Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: stephanie.wesolowski@ucdenver.edu.
authors.forename: Stephanie R
authors.initials: SR
authors.lastname: Wesolowski
authors.affiliation: Perinatal Research Center, Department of Pediatrics, University of Colorado School of Medicine, Colorado Anschutz Medical Campus, Aurora, CO, USA.
authors.forename: William W
authors.initials: WW
authors.lastname: Hay
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005333:Fetus / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism*; D010927:Placental Insufficiency / Q000503:physiopathology*; D011247:Pregnancy; D012756:Sheep
chemical_list: D005947:Glucose
keywords: Fetus; Glucose; IUGR; Insulin resistance; Liver