The size and composition of a baby at birth is largely dependent on the net flux of solute and water across the placenta over the length of that pregnancy. We have tested the hypothesis that the rate of transfer across the placenta can be adapted in relation to the demands of fetal growth and metabolism, and that such adaptation is modified dependent on maternal nutritional status.

Initial evidence to support the concept of adaptation in our laboratory came from work where we investigated the activity of the System A amino acid transporter in microvillous membrane vesicles isolated from the syncytiotrophoblast of placentas from babies with a range of normal birthweights. We found that the activity of the transporter (per mg membrane protein) was inversely related to the size and weight of the baby at birth. This was consistent with epidemiology data from others suggesting that placental efficiency (g fetus produced per g placental weight at birth) is greater in small for gestational age than in appropriate for gestational age babies. Subsequent work on both wild type and genetically modified mice has now provided experimental evidence for adaptation of a range of determinants of placental exchange capacity, at different times in gestation.

In recent studies on the effects of maternal obesity on placental function a high BMI was found to be associated with altered myometrial and fetoplacental vascular contractility and on placental transporter activity, in the absence of any significant effect on fetal growth. These could be adaptations in placental function, in the face of altered maternal nutrition, maintaining normal fetal growth.

Therefore, our data, and those of others, suggest that placental function is adapted in relation to the demands of fetal growth and metabolism. Adaptations in specific transfer mechanisms, perhaps at different times in gestation, will have effects on final body composition of the baby; we postulate that these will alter homeostatic set points with life long consequences.