British Journal of Nutrition

Full Papers

Metabolism and Metabolic Studies

Prolonged maternal vitamin C deficiency overrides preferential fetal ascorbate transport but does not influence perinatal survival in guinea pigs

Janne G. Schjoldagera1, Pernille Tveden-Nyborga1 and Jens Lykkesfeldta1 c1

a1 Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, 9 Ridebanevej, DK-1870 Frederiksberg C, Denmark

Abstract

Human and guinea pig fetuses are completely dependent on an adequate maternal vitamin C (vitC) intake. Shortage of micronutrients can have negative implications for fetal health and pregnancy outcome; however, knowledge of maternal vitC deficiency's impact on fetal development is sparse and reports of pregnancy outcome have been divergent. The present study investigated whether maternal vitC deficiency affects pregnancy outcome and plasma vitC distribution between the mother and the offspring in a guinea pig model. A total of eighty pregnant Dunkin Hartley guinea pigs were randomised into two weight-stratified groups receiving either a deficient (100 mg/kg DEF) or a control (923 mg/kg CTRL) diet. VitC levels were measured in plasma during pregnancy and postpartum, and in the plasma and brain of newborns. Pregnancy outcome was recorded with respect to birth weight and perinatal survival and were similar between groups. Plasma vitC in dams declined throughout gestation in both groups (P< 0·01). Compared with maternal plasma vitC, plasma vitC of newborn pups was found to be significantly lower in the DEF group (P< 0·001) and higher in the CTRL group (P< 0·001), respectively. Brain vitC levels were significantly reduced in DEF newborn pups (P< 0·001). The present results indicate that preferential transport of vitC from the mother to the fetus is overridden during sustained maternal vitC deficiency, maintaining maternal vitC concentration at the expense of the offspring. This contradicts the notion that a fetus is protected from vitC deficiency by the placental Na-dependent vitC co-transporter, SVCT2, thus fetal development may be susceptible to the negative effects of maternal vitC deficiency.

(Received October 04 2012)

(Revised January 24 2013)

(Accepted January 24 2013)

(Online publication April 16 2013)

Key Words:

  • Vitamin C;
  • Deficiency;
  • Fetuses;
  • Pregnancy outcomes

Footnotes

  Abbreviations: CTRL, control group; DEF, deficient group; SVCT2, sodium-dependent vitamin C co-transporter 2; vitC, vitamin C

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