The presence of hPL in the maternal circulation is much higher than in the fetal circulation, implying that these hormones may have a more significant role in the mother rather than the fetus. While hPL is not necessary for maintaining the pregnancy, both hPL and PRL serve as growth hormones for the fetus, stimulating the production of insulinlike growth factor (IGF)-I and IGF-II. Surprisingly, fetal growth hormone (GH) does not appear to regulate growth and does not affect birth weight. 

During the latter half of pregnancy when hPL levels are at their peak, the mother's energy metabolism undergoes a shift from an anabolic state to a catabolic state, also known as accelerated starvation. This shift leads to increased utilization of fat for energy while glucose usage decreases. Lipolysis, the breakdown of fats, is enhanced, and fatty acids become the primary source of energy. Insulin responsiveness in peripheral tissues decreases, resulting in increased pancreatic insulin secretion. Pregnancy also causes beta cell hyperplasia. Although this usually does not cause clinical issues, it can worsen pre-existing diabetes mellitus or lead to the development of diabetes for the first time during pregnancy. When diabetes resolves after delivery, it is referred to as gestational diabetes. Estrogens and progestins, which reduce insulin sensitivity, also contribute to the diabetogenic effects of pregnancy.

Human pregnancy lasts for an average of 40 weeks from the start of the last menstrual period, corresponding to an average fetal age of 38 weeks. Parturition, the process of childbirth, involves three stages: strong uterine contractions that push the fetus against the cervix and cause dilation and thinning of the cervix (lasting several hours), delivery of the fetus (less than 1 hour), and delivery of the placenta, accompanied by myometrial contractions to prevent bleeding (less than 10 minutes). The control mechanisms underlying parturition in humans are complex and not fully understood.

The placenta produces corticotropin-releasing hormone (CRH), which is identical to the CRH produced by the hypothalamus. CRH production by the placenta and levels of maternal serum CRH increase rapidly during late pregnancy and labor. The form of circulating CRH can either be free and bioactive or bound to a CRH-binding protein. Maternal levels of CRH-binding protein decrease significantly during late pregnancy and labor, leading to an increase in free CRH levels. Placental CRH also accumulates in the fetal circulation and stimulates fetal secretion of adrenocorticotropic hormone (ACTH). ACTH stimulates cortisol production in the fetal adrenal glands and estrogen production in the fetoplacental unit. While cortisol inhibits CRH production by the hypothalamus, it stimulates placental CRH production, creating a self-amplifying positive feedback loop. CRH itself promotes myometrial contractions by sensitizing the uterus to the effects of oxytocin and prostaglandins. Estrogens also directly and indirectly enhance myometrial contractility. This model suggests that the initiation of parturition is associated with cortisol-induced maturation of fetal systems, including the lungs and gastrointestinal tract.

The figure below provides an overview of energy utilization by the maternal and fetal compartments during pregnancy. It shows decreased maternal glucose usage, anti-insulin action of hPL produced by the placenta, and the utilization of amino acids and fatty acids for maternal energy production.

[Figure 44.36 - not included in paraphrase]
As with hCG, far less hPL is found in the fetal circulation than in the maternal circulation. This suggests that the hormones may play a more important role in the mother than in the fetus. hPL is not essential for the pregnancy.
Both hPL and PRL act as fetal growth hormones and stimulate production of the fetal growth-promoting hormones insulinlike growth factor (IGF)-I and IGF-II.
Ironically, fetal GH does not appear to regulate growth, and have normal birth weight.
Diabetogenicity of Pregnancy
Fig.
44.36 ). During the last half of pregnancy when hPL levels are highest, maternal energy metabolism shifts from an anabolic state in which nutrients are stored to a catabolic state sometimes described as accelerated starvation, in which maternal energy metabolism shifts toward fat utilization with sparing of glucose. As maternal use of glucose for energy decreases, lipolysis increases and fatty acids become major energy sources. Peripheral responsiveness to insulin decreases and pancreatic insulin secretion increases. Beta cell hyperplasia occurs in pregnancy. Although this does not usually lead to a clinical condition, pregnancy aggravates existing diabetes mellitus, and diabetes can develop for the first time in pregnancy. If the diabetes resolves spontaneously with delivery, the condition is referred to as gestational diabetes. Other hormones contributing to the diabetogenicity of pregnancy are estrogens and progestins, because both these hormones decrease insulin sensitivity.
Human pregnancy lasts an average of 40 weeks from the beginning of the last menstrual period (gestational age).
This corresponds to an average fetal age of 38 weeks. Par turition is the process whereby uterine contractions lead to childbirth. Labor consists of three stages: strong uterine contractions that force the fetus against the cervix, with dilation and thinning of the cervix (several hours); delivery of the fetus (<1 hour); and delivery of the placenta, along with contractions of the myometrium to halt bleeding (<10 minutes).
Control of parturition in humans is complex, and the exact mechanisms underlying its control are not well understood.
Placental CRH and the Fetal Adrenal Axis
The placenta produces corticotropin-releasing hormone (CRH), which is identical to the 41–amino acid peptide produced by the hypothalamus. Placental CRH production and maternal serum CRH levels increase rapidly during late pregnancy and labor. Moreover, circulating CRH is either in the form of free CRH, which is bioactive, or complexed to a CRH-binding protein. Maternal levels of CRH-binding protein plummet during late pregnancy and labor, so free CRH levels increase. Placental CRH also accumulates in the fetal circulation and stimulates fetal ACTH secretion. ACTH stimulates both fetal adrenal cortisol production and fetoplacental estrogen production. In contrast to the inhibitory effect of cortisol on hypothalamic CRH production, cortisol stimulates placental CRH production. This establishes a self-amplifying positive feedback. CRH itself promotes myometrial contractions by sensitizing the uterus to oxytocin and prostaglandins (see ). Estrogens also directly and indirectly stimulate myometrial contractility. Moreover, this model correlates the onset of parturition with cortisol-induced maturation of fetal systems, including the lungs and gastrointestinal tract.
824 SECTION8Berne & Levy Physiology •Fig. 44.36 Overviewofenergyusebythematernalandfetalcompartments.(ModifiedfromWhiteBA,PorterfieldSP.Endocrine Physiology. 4thed.Philadelphia:Mosby;2013.)Decreased maternal glucose use Antiinsulin action hPL Placenta Glucose Amino acids Fetus Lipolysis Proteolysis Amino acidsFatty acids for maternal use