here are ive genes in the growth hormone-placental lactogen gene cluster that are linked and located on chromosome 17. hPL is concentrated in syncytiotrophoblast, but similar to hCG, hPL is demonstrated in cytotrophoblasts before 6 weeks (Grumbach, 1964; Maruo, 1992). Within 5 to 10 days after conception, hPL is demonstrable in the placenta and can be detected in maternal serum as early as 3 weeks. Levels of mRNA for hPL in syncytiotrophoblast remain relatively con stant throughout pregnancy. his inding supports the idea that the hPL secretion rate is proportional to placental mass. Levels rise steadily until 34 to 36 weeks' gestation. The hPL produc tion rate near term-approximately 1 g/d-is by far the great est of aRY known hormone in humans. The hal-life of hPL in maternal plasma is between 10 and 30 minutes (Walker, 1991).
In late pregnancy, maternal serum concentrations reach levels of5 to 15 �g/mL (see Fig. 5-18).
Very little hPL is detected in fetal blood or in the urine of the mother or newborn. Amnionic fluid levels are somewhat lower than in maternal plasma. hPL is secreted primarily into the maternal circulation, with only very small amounts in cord blood. hus, its role in pregnancy is believed to be mediated through actions in maternal rather than in fetal tissues. None theless, interest continues for the possibility that hPL serves select functions in fetal growth.
cesses. First, hPL promotes maternal lipolysis with increased circulating free fatty acid levels. This provides an energy source for maternal metabolism and fetal nutrition. In vitro cytiotrophoblast (Coya, 2005). Prolonged maternal starvation in the irst half of pregnancy leads to higher hPL plasma con centrations.
Second, hPL may aid maternal adaptation to fetal energy requirements. For example, increased maternal insulin resistance ensures nutrient flow to the fetus. It also favors protein synthesis and provides a readily available amino acid source to the fetus. To counterbalance the greater insulin resistance and prevent maternal hyperglycemia, maternal insulin levels are increased. Both hPL and prolactin signal through the prolactin receptor to increase maternal beta cell proliferation to augment insulin secretion (Georgia, 2010). In animals, prolactin and hPL upregulate serotonin synthesis, which increases beta cell proliferation (Kim, 2010). Short-term changes in plasma glucose or insulin, however, have relatively little efect on plasma hPL levels. In vitro studies of syncytiotrophoblast suggest that hPL synthesis is stimulated by insulin and insulin-like growth factor-1 and inhibited by PGE2 and PGF2: (Bhaumick, 1987; Genbacev, 1977).
Last, hPL is a potent angiogenic hormone. It may serve an important function in fetal vasculature formation (Corbacho, 2002).
capacity to synthesize numer ous peptide hormones, including some that are analogous or related to hypothalamic and pituitary hormones. In contrast to their counterparts, some of these placental peptide/protein hormones are not subject to feedback inhibition.
he known hypothalamic-releasing or -inhibiting hormones include GnRH, CRH, thyrotropin-releasing hormone (TRH), growth hormone-releasing hormone, and somatostatin. For each, there is an analogous hormone produced in the human placenta (Petraglia, 1992; Siler-Khodr, 1988).