The Role of Placental Hormones in Mediating Maternal Adaptations to Support Pregnancy and Lactation

Abstract

During pregnancy, the mother must adapt her body systems to support nutrient and oxygen supply for growth of the baby in utero and during the subsequent lactation. These include changes in the cardiovascular, pulmonary, immune and metabolic systems of the mother. Failure to appropriately adjust maternal physiology to the pregnant state may result in pregnancy complications, including gestational diabetes and abnormal birth weight, which can further lead to a range of medically significant complications for the mother and baby. The placenta, which forms the functional interface separating the maternal and fetal circulations, is important for mediating adaptations in maternal physiology. It secretes a plethora of hormones into the maternal circulation which modulate her physiology and transfers the oxygen and nutrients available to the fetus for growth. Among these placental hormones, the prolactin-growth hormone family, steroids and neuropeptides play critical roles in driving maternal physiological adaptations during pregnancy. This review examines the changes that occur in maternal physiology in response to pregnancy and the significance of placental hormone production in mediating such changes.

Keywords: cardiovascular; endocrine; fetal growth; hormones; maternal adaptations; metabolism; placenta; pregnancy.

Figure 1

Schematic diagram highlighting the main physiological modifications in the maternal physiology in response to pregnancy. Many of the changes described in the figure for women during pregnancy also occur in other species, including mice. Respiratory system (Macrae and Palavradji, ; Weinberger et al., ; Contreras et al., ; Hegewald and Crapo, ; Frise et al., ; Lomauro and Aliverti, ; Soma-Pillay et al., 2016); cardiovascular system (Adamova et al., ; Li et al., ; Pieper, ; Soma-Pillay et al., 2016); hematological system (Shakhmatova et al., ; Chang and Streitman, ; Rodger et al., ; Soma-Pillay et al., 2016); spleen (Maroni and De Sousa, ; Sasaki et al., ; Norton et al., 2009); renal system (Davison and Dunlop, ; Atherton et al., ; Krutzén et al., ; Elsheikh et al., ; Cheung and Lafayette, ; Lumbers and Pringle, ; Pieper, ; Soma-Pillay et al., 2016); pancreas (Ziegler et al., ; Ernst et al., ; Ohara-Imaizumi et al., ; Baeyens et al., 2016); adipose tissue (Catalano et al., ; Hauguel-De Mouzon et al., ; Lain and Catalano, ; Nien et al., ; Hadden and Mclaughlin, ; Valsamakis et al., ; Musial et al., 2016); skeletal muscle (Alperin et al., , ; Musial et al., 2016); bone (Shahtaheri et al., ; Ulrich et al., ; Hellmeyer et al., ; Salles, 2016); digestive tract (Everson, ; Fudge and Kovacs, ; Pieper, 2015); liver (Munnell and Taylor, ; Van Bodegraven et al., ; Lain and Catalano, ; Bacq, 2013); mammary tissue (Elling and Powell, ; Neville et al., ; Sternlicht, ; Pang and Hartmann, 2007); immune system (Clarke and Kendall, ; Kendall and Clarke, ; Veenstra Van Nieuwenhoven et al., ; Norton et al., ; Mor and Cardenas, ; Saito et al., ; Racicot et al., ; Groen et al., ; Zöllner et al., ; Edey et al., 2018); nervous system (Shingo et al., ; Gregg, ; Roos et al., ; Hoekzema et al., 2017).

Figure 2

Summary of expression profiles, interactions and maternal physiological effects of placental-derived hormones. PRL, prolactin; PL, placental lactogen; PLF, proliferins; PRP, proliferin-related proteins; GH, growth hormone; GHRH, growth hormone releasing hormone; IGF1/2, insulin-like growth factor-1/2; E2, estrogen; P4, progesterone; MEL, melatonin; SER, serotonin; KISS, kisspeptin; OXY, Oxytocin; TRH, thyrotropin-releasing hormone; RELAX, relaxin; ACTIV, activin; CG, chorionic gonadotropin; LEP, leptin; PTHrP, parathyroid hormone-related protein.