Placental efficiency and adaptation: endocrine regulation

Abstract

Size at birth is critical in determining life expectancy and is dependent primarily on the placental supply of nutrients. However, the fetus is not just a passive recipient of nutrients from the placenta. It exerts a significant acquisitive drive for nutrients, which acts through morphological and functional adaptations in the placenta, particularly when the genetically determined drive for fetal growth is compromised by adverse intrauterine conditions. These adaptations alter the efficiency with which the placenta supports fetal growth, which results in optimal growth for prevailing conditions in utero. This review examines placental efficiency as a means of altering fetal growth, the morphological and functional adaptations that influence placental efficiency and the endocrine regulation of these processes.

Figure 1. Unidirectional materno-fetal clearance of [¹⁴C]methylaminoisobutryic acid clearance across near term mouse placentas

Mean (±s.e.m.) unidirectional materno-fetal clearance of [¹⁴C]methylaminoisobutryic acid (MeAIB) clearance across near term mouse placentas with low (open columns) and high efficiencies (filled columns) induced by natural variations between the lightest and heaviest placentas within a litter (n= 11 litters) (A), undernutrition (UN, n= 10 litters) to 80% of ad libitum fed controls (n= 11 litters) (B) and feeding a high fat diet compared to controls (n= 5 litters per diet) (C). Data from Coan et al. 2008a; Jones et al. 2009 and P. M. Coan & A. L. Fowden unpublished observations.

Figure 2. Unidirectional materno-fetal transfer of [¹⁴C]methylaminoisobutryic acid across wild-type and null placentas

Mean (±s.e.m.) unidirectional materno-fetal transfer of [¹⁴C]methylaminoisobutryic acid (MeAIB) across wild-type (WT, open columns) and null placentas (filled columns) of 11β-HSD2^−/− (11β-hydroxysteroid dehydrogenase type 2)(A), Igf2P0^+/− (B), and Igf2^+/− mutant mice (C) at Day 15 or 16 and Day 18 or 19 of gestation calculated as counts transferred to the fetus per gram placenta in A and as clearance in B and C. Number of litters = 7–15 for each mutant at each gestational age. Data from Constancia et al. 2005, Sferruzzi-Perri et al. 2009 and Wyrwoll et al. 2009.

Figure 3. Schematic diagram of the regulation of placental phenotype by glucocorticoids and insulin like growth factors in relation to fetal growth and development

Circular profiles, circulating hormones; square profiles, regulated processes. Gene expression is shown in italics. IGF, insulin like growth factor; 11βHSD2, 11β-hydroxysteroid dehydrogenase type 2; mTOR, mammalian target of rapamycin.