Journal of Developmental Origins of Health and Disease

Review

Placental transport in response to altered maternal nutrition

F. Gacciolia1, S. Lagera1, T. L. Powella1 and T. Janssona1 c1

a1 Department of Obstetrics and Gynecology, Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, TX, USA

Abstract

The mechanisms linking maternal nutrition to fetal growth and programming of adult disease remain to be fully established. We review data on changes in placental transport in response to altered maternal nutrition, including compromized utero-placental blood flow. In human intrauterine growth restriction and in most animal models involving maternal undernutrition or restricted placental blood flow, the activity of placental transporters, in particular for amino acids, is decreased in late pregnancy. The effect of maternal overnutrition on placental transport remains largely unexplored. However, some, but not all, studies in women with diabetes giving birth to large babies indicate an upregulation of placental transporters for amino acids, glucose and fatty acids. These data support the concept that the placenta responds to maternal nutritional cues by altering placental function to match fetal growth to the ability of the maternal supply line to allocate resources to the fetus. On the other hand, some findings in humans and mice suggest that placental transporters are regulated in response to fetal demand signals. These observations are consistent with the idea that fetal signals regulate placental function to compensate for changes in nutrient availability. We propose that the placenta integrates maternal and fetal nutritional cues with information from intrinsic nutrient sensors. Together, these signals regulate placental growth and nutrient transport to balance fetal demand with the ability of the mother to support pregnancy. Thus, the placenta plays a critical role in modulating maternal–fetal resource allocation, thereby affecting fetal growth and the long-term health of the offspring.

(Received May 13 2012)

(Revised June 10 2012)

(Accepted July 05 2012)

(Online publication July 31 2012)

Key words

  • fetal programming;
  • maternal–fetal exchange;
  • obesity;
  • pregnancy;
  • trophoblast

Correspondence

c1 Address for correspondence: Dr T. Jansson, Department of Obstetrics and Gynecology, Center for Pregnancy and Newborn Research, University of Texas Health Science Center, Mail Code 7836, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. (Email jansson@uthscsa.edu)

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