title: Maternal vitamin C deficiency during pregnancy results in transient fetal and placental growth retardation in guinea pigs.
abstract: OBJECTIVE
  Recently, we reported that preferential maternal-fetal vitamin C (vitC) transport across the placenta is likely to be impaired by prolonged maternal vitC deficiency. Maintenance of a basal maternal vitC supply at the expense of the fetus may impair fetal development; however, the knowledge of vitC's impact on intrauterine development is sparse. The aim of this study was to explore the effect of maternal vitC status on fetal and placental development in guinea pigs.
  
  
  METHODS
  Twenty pregnant Dunkin Hartley guinea pigs were randomized into four groups to receive diets either sufficient (918 mg/kg CTRL) or deficient (100 mg/kg DEF) in vitC. Cesarean sections at gestational day (GD) 45 or 56 allowed for fetal and placental measurements.
  
  
  RESULTS
  At GD45, body, brain and placental weights were significantly reduced in DEF pups compared with CTRL (p < 0.05, p < 0.001 and p < 0.05, respectively). DEF plasma vitC levels were ~6% of those of CTRL (p < 0.0001), and the fetal/maternal plasma vitC ratio was significantly reduced at GD56 in the DEF animals compared with controls (p = 0.035). Placental vitC levels were reduced in DEF animals (p < 0.0001) and the ascorbate oxidation ratio and glutathione elevated compared with controls (p < 0.0001).
  
  
  CONCLUSIONS
  Although no clinical differences between CTRL and DEF pups were observed at GD56, the present data suggest that vitC plays a role in early fetal development. Although no clinical differences between CTRL and DEF pups were observed at GD56, the present data suggest that vitC plays a role in early fetal development. Low maternal vitC intake during pregnancy may compromise maternal weight gain, placental function and intrauterine development.
authors.affiliation: Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, 9 Ridebanevej, 1870, Frederiksberg C, Denmark.
authors.forename: Janne Gram
authors.initials: JG
authors.lastname: Schjoldager
authors.forename: Maya Devi
authors.initials: MD
authors.lastname: Paidi
authors.forename: Maiken Marie
authors.initials: MM
authors.lastname: Lindblad
authors.forename: Malene Muusfeldt
authors.initials: MM
authors.lastname: Birck
authors.forename: Astrid Birch
authors.initials: AB
authors.lastname: Kjærgaard
authors.forename: Vibeke
authors.initials: V
authors.lastname: Dantzer
authors.forename: Jens
authors.initials: J
authors.lastname: Lykkesfeldt
authors.forename: Pernille
authors.initials: P
authors.lastname: Tveden-Nyborg
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000097:blood; D001206:Ascorbic Acid Deficiency / Q000097:blood*; D004032:Diet; D004195:Disease Models, Animal; D005065:Euthanasia; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005333:Fetus / Q000503:physiopathology*; D006168:Guinea Pigs; D016014:Linear Models; D039382:Maternal Nutritional Physiological Phenomena; D008431:Maternal-Fetal Exchange; D010920:Placenta / Q000503:physiopathology*; D011247:Pregnancy; D060347:Sodium-Coupled Vitamin C Transporters / Q000235:genetics / Q000378:metabolism
chemical_list: D060347:Sodium-Coupled Vitamin C Transporters; D001205:Ascorbic Acid