The Programming Power of the Placenta

Abstract

Size at birth is a critical determinant of life expectancy, and is dependent primarily on the placental supply of nutrients. However, the placenta is not just a passive organ for the materno-fetal transfer of nutrients and oxygen. Studies show that the placenta can adapt morphologically and functionally to optimize substrate supply, and thus fetal growth, under adverse intrauterine conditions. These adaptations help meet the fetal drive for growth, and their effectiveness will determine the amount and relative proportions of specific metabolic substrates supplied to the fetus at different stages of development. This flow of nutrients will ultimately program physiological systems at the gene, cell, tissue, organ, and system levels, and inadequacies can cause permanent structural and functional changes that lead to overt disease, particularly with increasing age. This review examines the environmental regulation of the placental phenotype with particular emphasis on the impact of maternal nutritional challenges and oxygen scarcity in mice, rats and guinea pigs. It also focuses on the effects of such conditions on fetal growth and the developmental programming of disease postnatally. A challenge for future research is to link placental structure and function with clinical phenotypes in the offspring.

Maternal and fetal genomes interplay through phosphoinositol 3-kinase(PI3K)-p110α signaling to modify placental resource allocation

“…This occurred despite reduced placental expression of the amino acid transporter gene Slc38a1 in litters of α/+ dams (also at D19 along with decreased Slc38a2). Similar disparity between Slc38a gene expression and transport of MeAIB in vivo has been observed in placentas in which growth regulatory genes (15) or the maternal environment have been affected in rodents (3)(4)(5)(6)(7). These findings suggest that there are temporal differences between the expression, translation, and membrane trafficking of amino acid transporters in the placenta and that measuring placental expression of Slc38a genes provides little information with respect to actual transport function in vivo.…”

“…As the interface between the mother and fetus, the placenta is central to this tug-of-war over nutrient allocation. Genetic and dietary manipulations during pregnancy as well as reciprocal crosses between breeds of different sizes indicate that the placenta can adapt dynamically to both fetal signals of nutrient demand and maternal signals of nutrient availability to ensure appropriate allocation of available resources (3)(4)(5)(6)(7)(8)(9). The fetus and mother, therefore, have to cooperate to optimize both offspring and maternal fitness, but to date, little is known about the relative importance of fetal versus maternal genomes in balancing resource allocation at the placental level.…”

Competition for Materno-Fetal Resource Partitioning in a Rabbit Model of Undernourished Pregnancy

“…Despite these inconveniences, MFR protocols applied in specific periods of the pregnancy, such as the preimplantation period, in which the embryo’s requirements are low and the mother presents an anabolic status, could reduce productive costs and be an alternative strategy in farms [9, 10]. However, the advantages and disadvantages of such managements need to be further investigated, since inadequate nutrition from early gestation can influence placentation processes (specifically the allocation of trophectoderm and inner cell mass within the blastocyst [11]), which may impair placental development and function [12], compromising pregnancy outputs. In fact, experimental studies suggest that impaired placental structure or function ( e .…”

Vitamin D deficiency and impaired placental function: potential regulation by glucocorticoids?

“…In addition to facilitating the direct exchange of oxygen and nutrients between mother and fetus, the placenta functions in a specialized endocrine capacity to produce hormones essential for maternal physiological adaptations to pregnancy (Evain-Brion & Malassine 2003). As such, a healthy placenta is vital for normal fetal growth and development, whereas impaired placental function disrupts fetal growth outcomes and may also result in long-term health complications in offspring via developmental programming mechanisms (Burton et al 2016, Sferruzzi-Perri & Camm 2016.…”