ACTH, lipotropin, and �-endorphin, which are all proteolytic products of pro-opiomelanocortin, are recovered from placental extracts (Genazzani, 1975; Odagiri, 1979). he physiological action of placental ACTH is unclear. As discussed, placental CRH stimulates synthesis and release of chorionic ACTH.
A human growth hormone variant (hGH-J that is not expressed in the pituitary is expressed in the placenta. The gene encoding hGH-V is located in the hGH-hPL gene cluster on chromosome 17. Sometimes referred to as placental growth hormone, hGH-V is a 191-amino-acid protein that difers in 15 amino acid positions from the sequence for hGH. Although hGH-V retains growth-promoting and antilipogenic functions similar to those of hGH, it has reduced diabetogenic and lactogenic functions relative to hGH (Vickers, 2009). Placental hGH-V presumably is synthesized in the syncytiotrophoblast. It is believed that hGH-V is present in maternal plasma by 21 to 26 weeks' gestation, rises in concentration until approximately 36 weeks, and remains relatively constant thereafter. There is a correlation between the levels of hGH-V in maternal plasma and those of insulin-like growth factor-I. lso, hGH-V secretion by trophoblast in vitro is inhibited by glucose in a dosedependent manner (Patel, 1995). Overexpression ofhGH-V in mice causes severe insulin resistance, making it a likely candidate to mediate insulin resistance of pregnancy (Liao, 2016).
Expression of relaxin has been demonstrated in human corpus luteum, decidua, and placenta (Bogic, 1995). This peptide is synthesized as a single, 105-amino-acid preprorelaxin molecule that is cleaved to A and B molecules. Relaxin is structurally similar to insulin and insulin-like growth factor. Two of the three relaxin genes-H2 and H3-are transcribed in the corpus luteum (Bathgate, 2002; Hudson, 1983, 1984). Decidua, placenta, and membranes express H 1 and H2 (Hansell, 1991).
The rise in maternal circulating relaxin levels seen in early pregnancy is attributed to corpus luteum secretion, and levels parallel those of hCG. Relaxin, along with rising progesterone levels, may act on myometrium to promote relaxation and the quiescence of early pregnancy (Chap. 21, p. 407). In addition, the production of relaxin and relaxin-like factors within the placenta and fetal membranes may play an autocrine-paracrine role in postpartum regulation of extracellular matrix remodeling (Qin, 1997a,b). One important relaxin function is enhancement of the glomerular iltration rate (Chap. 4, p. 66).
In pregnancy, circulating parathyroid hormone-related protein (PTH-rP) levels are significantly elevated within maternal but not fetal circulation (Bertelloni, 1994; Saxe, 1997). Many functions of this hormone have been proposed. PTH-rP synthesis is found in several normal adult tissues, especially in reproductive organs that include myometrium, endometrium, corpus luteum, and lactating mammary tissue. PTH-rP is not produced in the parathyroid glands of normal adults. Placentaderived PTH-rP may have an important function to regulate genes involved in transfer of calcium and other solutes. It also contributes to fetal mineral homeostasis in bone, amnionic luid, and the fetal circulation (Simmonds, 2010).