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At least 19 recordsLinked to original sources
PubMed2000

Hormonal placental function tests for fetal assessment in high risk pregnancies.

BACKGROUND: Biochemical tests of fetal well-being such as placental hormone levels have not always shown direct benefits for mothers and babies. OBJECTIVES: The objective of this review was to assess the effects of measuring placental hormone levels during high risk pregnancies. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group trials register and MEDLINE. We also contacted study authors. SELECTION CRITERIA: Adequately controlled trials comparing availability with no availability of hormone placental tests in high risk pregnancy. DATA COLLECTION AND ANALYSIS: Trial quality was assessed and data were extracted by two reviewers and this was checked by a colleague. Study authors were contacted for additional information. MAIN RESULTS: Two trials involving 3355 women were included. Methodological quality of the trials was acceptable, but results for only 230 out of 2733 women (abnormal hormone levels) were available from one trial. One trial compared oestriol levels reported promptly with levels measured but not reported. The overall perinatal mortality rate was 30.5 per 1000 live births weighing 500 grams or more. No beneficial effects of oestriol measurement on fetal outcome could be identified (odds ratio of perinatal death 0.87, 95% confidence interval 0.35 to 2.18). For abnormal test results only, the reported oestriol group showed a statistically non-significant trend to less perinatal mortality (odds ratio 0.48, 95% confidence interval 0.15 to 1.60). The other trial compared human placental lactogen measurements reported promptly with measurements not reported until after pregnancy. For abnormal test results, the reported group showed significantly less perinatal mortality with four (3.4%) deaths compared to 17 (15%) in the control group (odds ratio 0.25, 95% confidence interval 0.10 to 0.61). Data from normal test results was not available for this trial. REVIEWER'S CONCLUSIONS: The measurement of human placental lactogen levels may be of some value in high risk pregnancies, but there is not enough evidence to evaluate the use of hormone placental tests generally.

Female↗
PubMed1989

Effects of human growth hormone upon term placental hormone secretion in vitro.

The role of human growth hormone (hGH) on placental hormone secretion at term was investigated in two in vitro models: placental explants and cultured trophoblastic cells. Physiological concentrations of hGH caused a significant dose-dependent increase in placental lactogen and progesterone secretion. In the explant model it stimulated estradiol secretion. In order to determine whether this stimulatory effect on estradiol is exerted via aromatase, an isolated cell culture was utilized where androstenedione was supplied as substrate. In this model, hGH exerted a mild inhibitory effect. In conclusion, hGH at levels present in the fetal circulation exerts a significant stimulatory effect upon placental function as reflected by both peptide and steroid hormone production and secretion. The effect of estradiol secretion is the end result of an inhibitory effect on androgen aromatization and a stimulatory effect on earlier steps.

Androstenediols↗
PubMed1999

Altered arterial concentrations of placental hormones during maximal placental growth in a model of placental insufficiency.

Pregnant ewes were exposed chronically to thermoneutral (TN; 20+/-2 degrees C, 30% relative humidity; n=8) or hyperthermic (HT; 40+/-2 degrees C 12 h/day, 35+/-2 degrees C 12 h/day, 30% relative humidity, n=6) environments between days 37 and 93 of pregnancy. Ewes were killed following 56 days of exposure to either environment (days in treatment (dit)), corresponding to 93+/-1 day post coitus (dpc). Maternal core body temperatures (CBT) in HT ewes were significantly elevated above the TN ewes (HT; 39.86+/-0.1 degrees C vs TN; 39.20+/-0.1 degrees C; P<0.001). Both groups of animals displayed circadian CBT, though HT ewes had elevated amplitudes (HT; 0.181+/-0.002 degrees C vs TN; 0.091+/-0.002 degrees C; P<0.001) and increased phase shift constants (HT; 2100 h vs TN; 1800 h; P<0.001). Ewes exposed to chronic heat stress had significantly reduced progesterone and ovine placental lactogen (oPL) concentrations from 72 and 62 dpc respectively (P<0.05), corresponding to approximately 30 dit. However, when compared with the TN ewes, HT cotyledonary tissue oPL mRNA and protein concentrations were not significantly different (P>0.1). Prolactin concentrations rose immediately upon entry into the HT environment, reaching concentrations approximately four times that of TN ewes, a level maintained throughout the study (HT; 216.31+/-32.82 vs TN; 54. 40+/-10.0; P<0.0001). Despite similar feed intakes and euglycemia in both groups of ewes, HT fetal body weights were significantly reduced when compared with TN fetuses (HT; 514.6+/-48.7 vs TN; 703. 4+/-44.8; P<0.05), while placental weights (HT; 363.6+/-63.3 vs TN; 571.2+/-95.9) were not significantly affected by 56 days of heat exposure. Furthermore, the relationship between body weight and fetal length, the ponderal index, was significantly reduced in HT fetuses (HT; 3.01+/-0.13 vs TN; 3.57+/-0.18; P<0.05). HT fetal liver weights were also significantly reduced (HT; 27.31+/-4.73 vs TN; 45.16+/-6.16; P<0.05) and as a result, the brain/liver weight ratio was increased. This study demonstrates that chronic heat exposure lowers circulating placental hormone concentrations. The observation that PL mRNA and protein contents are similar across the two treatments, suggests that reduced hormone concentrations are the result of impaired trophoblast cell development, specifically trophoblast migration. Furthermore, the impact of heat exposure during maximal placental growth is great enough to restrict early fetal development, even before the fetal maximal growth phase (100 dpc-term). These data highlight that intrauterine growth retardation (IUGR) may result primarily from placental trophoblast cell dysfunction, and secondarily from later reduced placental size.

Animals↗
PubMed1986

Gonadotropin-releasing hormone effects on placental hormones during gestation: II. Progesterone, estrone, estradiol and estriol.

The release of progesterone (P), estrone (E1), estradiol (E2) and estriol (E3) from human placental tissue in vitro was found to be related to the gestational age of the placenta. The basal release of P, E1 and E2 on Day 1 of culture was highest from placentas of early gestation (9-13 wk). The release of P then declined, reaching a nadir by 15 wk, and continued at that level. The release of E1 and E2, reached a nadir at 17 weeks, and then again increased by term. In contrast, the basal release of E3 increased with increasing gestational age of the placenta. Thus, it appears that differing factors may influence placental P, E1, E2 and E3 production. In addition, the effect of synthetic gonadotropin-releasing hormone (GnRH) on these hormonal releases was studied. The stimulation of P by GnRH was greatest in placentas of 16 and 17 wk of gestation after extended culture when the basal release of P had declined. As much as a 240-fold increase was observed on the eighth day of culture. A large stimulation of P (32-fold) was also observed in the term placental cultures. A stimulation of E1 and E2 by GnRH was observed during the initial days of culture and in mid-gestational placental cultures (16-17 wk). A stimulation of E2 only was also observed at 13-15 wk and at term. A stimulation of E3 was observed in certain individual placentas. A correlation of the P and human chorionic gonadotropin (hCG) response to GnRH stimulation was noted, as well as an inverse relation of estrogens and hCG stimulation by GnRH. These data demonstrate that steroidogenic competence of the placenta differs with gestational age and that GnRH can influence steroid release. The degree and pattern of response to GnRH varied with the gestational age of the placenta and its endocrine milieu.

Estradiol↗
PubMed2004

Placental hormones and fetal-placental development.

Production of growth promoting substances by the placenta is regulated differently from the way production of similar compounds is regulated by maternal organs in various cases. Gene duplication is one of the mechanisms that facilitated the evolution of placental specific endocrine activity. Cattle, sheep and goats, although evolutionarily related, differ significantly from each other in the way their placental growth hormone (GH) and prolactin (PRL)-like hormones have evolved. Cattle carry one copy of the GH gene and there is no evidence yet for expression of that single GH gene copy in the placenta. On the other hand, the ovine GH gene has been duplicated and both oGH copies are expressed in the placenta during early stages of gestation. Prolactin gene duplication in ruminants resulted in the formation of specific placental-expressed prolactin-related genes including the placental lactogen (PL) gene. In homologous state, ovine PL manifests PRL activity, but antagonizes GH activity. Ovine PL activity which can be mediated by PRL receptors or by hetero-dimerization of GH and PRL receptors, provide a novel regulatory mechanism for somatogenic activity dependent on the coexistence of both GH and PRL receptors in the same cells. Another mechanism for specific placental endocrine activity is silencing of the alleles through genetic imprinting. Disruption of genetic imprinting of placental genes has been proposed as one of the explanations for the loss of cloned fetuses generated by somatic cell nuclear transfer.

Animals↗
PubMed1986

Gonadotropin-releasing hormone effects on placental hormones during gestation: I. Alpha-human chorionic gonadotropin, human chorionic gonadotropin and human chorionic somatomammotropin.

The release of alpha-human chorionic gonadotropin (alpha hCG), gonadotropin human chorionic gonadotropin (hCG) and human chorionic somatomammotropin (hCS) in vitro from placentas of different gestational ages was studied. In addition, the effect of gonadotropin-releasing hormone (GnRH) on these hormonal releases, as related to the gestational age of the placenta cultured and the dose of GnRH, was determined. The basal release of alpha hCG and hCG was greatest at 9-13 wk of gestation (1000-1500 ng/mg and 250-350 ng/mg, respectively). Lowest release rates were at term (28 ng/mg and 20 ng/mg, respectively). Hormonal release declined with extended culture, except from the cultures of 13- and 15-wk placentas, in which the initially high release continued throughout the 8 days of culture. The initial release of hCS was low at 6 wk, increased to maximum rates by 15 wk, and was similar to the initial rate of release at term. Gonadotropin-releasing hormone stimulated the release of alpha hCG and hCG most dramatically in cultures of 16-wk and 17-wk placentas, where as much as a 400- and 250-fold increase, respectively, on Day 6 of culture was observed (p less than 0.0001). In term placenta cultures after 6 days in vitro, a 20-fold stimulation of alpha hCG and a 10-fold increase of hCG was effected by GnRH (p less than 0.001). The largest responses of alpha hCG and hCG to GnRH were observed when estrogen levels were low. Dose-related responses were observed in some placentas, yet in some instances, maximal effects were attained with all doses utilized in these studies (0.2 to 50 micrograms/ml). These data demonstrate that human placentas of different gestational ages have varying hormonogenic capabilities in vitro. The data also establish that synthetic GnRH is capable of stimulating alpha hCG and hCG production, but the degree and pattern of response to GnRH stimulation are related to the gestational age of the placental tissue and its time in culture. The most responsive period to exogenous GnRH stimulation of alpha hCG and hCG release was on Days 5 and 6 of culture, when basal estrogen release was very low. These data support the hypothesis that hCG release might be controlled by a chorionic GnRH stimulation and suggest that local steroid levels may modulate the hCG response to GnRH stimulation.

Chorionic Gonadotropin↗
PubMed2006

Large-scale preparation and in vitro characterization of biologically active human placental (20 and 22K) and pituitary (20K) growth hormones: placental growth hormones have no lactogenic activity in humans.

Expression plasmids containing DNA sequences optimized for expression in Escherichia coli were prepared encoding human pituitary (hGH-N 20K) and placental (hGH-V 20 and 22K) growth hormones. The proteins were expressed in bacteria, refolded and purified to homogeneity by anion-exchange chromatography on Q-Sepharose according to a unique protocol developed for each protein. The yields from 5l of fermentation culture varied between 400 and 700mg of electrophoretically pure, over 95% monomeric protein. Circular dichroism (CD) analysis revealed similarity of the purified hGHs' secondary structure to that of the pituitary hGH-N 22K, except for hGH-V 20K, in which the alpha-helix content was lower. The purified proteins were stable as a 0.1% sterile solution held at pH 10-11 at 4 degrees C for at least one month. All three purified hGH molecules formed a 1:2 complex with hGH receptor extracellular domain (hGHR-ECD), similar to hGH-N 22K. Binding experiments using hGHR-ECD revealed that the differences between the two 22K variants or between the two 20K variants were not significant, except that hGH-V 20K exhibited slightly lower affinity. Somatogenic activity was tested in vitro using FDC-P1 cell lines. Whereas the bioactivity of 22K hGHs and hGH-N 20K in FDC-P1-9D11 cells stably transfected with hGHR was almost equal and two to threefold higher than that of hGH-V 20K, in FDC-P1 3B9 cells stably transfected with rabbit (rb) GHR, the bioactivity of both 20K analogues was significantly (five to ninefold) lower than that of the 22K hormones. The lactogenic activity measured in heterologous assays (Nb2-11C cells and Baf/3 cells stably transfected with the long form of rabbit prolactin receptor) revealed that the activity of hGH-N 20K was close to that of hGH-N 22K in the Baf/3 cells, but 4.5-fold lower in the Nb2 cells. The activity of hGH-V 22K was ninefold less in Nb2 cells and 55-fold less in Baf/3 cells, whereas hGH-V 20K had no lactogenic activity in either bioassay. In contrast, in a homologous lactogenic assay using Baf/3 LP cells stably transfected with hPRLR, the activity of both placental hGHs was nil and the activity of hGH-N 20K was 4.3-fold lower than that of hGH-N 22K. The latter finding raises the question of whether the lack of intrinsic lactogenic activity in the placental hGHs that dominate during pregnancy has any physiological relevance.

Animals↗
PubMed2006

Effect of leptin on the regulation of placental hormone secretion in cultured human placental cells.

Placenta is an important source of leptin during pregnancy that contributes to the high plasma leptin levels in pregnant women. Leptin and its functional receptors are synthesized in trophoblast cells that, in turn, secrete gestational hormones supporting a paracrine or autocrine role for leptin in the endocrine activity of the placenta. In the present study we examined the effect of leptin on in vitro release of gestational hormones (human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone, estrogens and testosterone) by human term placental cells in culture. Placentas at term were obtained immediately after delivery from mothers with uncomplicated pregnancies. Progesterone, hCG, hPL, estradiol, estrone, estriol and testosterone levels were measured by different assays in culture media of cells maintained in monolayer culture after incubation for 12, 24, 48 or 72 h with leptin or placebo. Incubation with leptin did not modify hCG, hPL, progesterone, estriol and estrone secretion for any of the doses and times assayed. However, leptin led to a dose-dependent decrease in estradiol release. This effect was observed when treatment with recombinant human leptin spanned from 12 to 72 h. At this time an increase in testosterone levels was observed in leptin-treated cells versus placebo. These results indicate that leptin can be considered a gestational hormone implied in the endocrine function of the placenta, with an important role in control of the production of steroid reproductive hormones in placental cells in vitro.

Cells, Cultured↗
PubMed1981

Prolactin and placental hormone levels during pregnancy in prolactinomas.

Prolactin (PRL) and the placental hormones, estradiol (E2), estriol (E3), progesterone (PG), chorionic gonadotropin (HCG), and placental lactogen (HPL) were serially measured throughout pregnancy and early postpartum in three patients with prolactinomas in whom pregnancy was achieved by one of the three modalities of treatment: bromocriptine administration (patient I), irradiation of the pituitary (patient II), and human gonadotropin administration after excision of the adenoma (patient III). It was found that PRL in patient I reached the high pretreatment levels in the 2nd month of pregnancy and increased to further abnormal concentrations in the last 2 months, but fell at the onset of labor 1 week after an episode of severe headache. The PRL changes in this patient were attributed successively to tumor expansion and apoplexy. In patient II PRL decreased after irradiation, but was not normalized. During pregnancy it remained moderately increased presenting minor fluctuations. The third patient with postoperative GH and TSH pituitary insufficiency had low pretreatment PRL levels which remained practically unchanged throughout pregnancy. The two last patients gave birth to identical twins. The placental hormones were found normal in all three patients but E2 and PG were relatively increased during the last weeks of pregnancy in the twin pregnancies. Amniotic fluid and umbilical cord PRL and E2 concentrations were normal. The patients presented agalactia and suckling did not induce a PRL increase. We conclude that a) serial PRL measurements during pregnancy reflect the changes occurring in the prolactinomas and are essential in monitoring the patients bearing these tumors; b) maternal hyperprolactinemia or failure of PRL to increase during pregnancy do not influence either the secretion of placental hormones or PRL concentration in amniotic fluid and the newborn; and c) hyperprolactinemia during pregnancy is of maternal pituitary origin.

Adenoma↗
PubMed1981

Pituitary and placental hormone levels in pseudocyesis.

Twelve patients with clinical features of pseudocyesis were divided into two groups according to the presence or absence of galactorrhea. The mean serum prolactin level of patients with galactorrhea was significantly higher than the normal values of the patients without galactorrhea. The mean serum levels of luteinizing hormone and follicle-stimulating hormone were markedly elevated in patients without galactorrhea. This was especially true of luteinizing hormone. Serum levels of human chorionic gonadotropin were undetectable in all patients. The significance of these observations is discussed.

Adolescent↗
PubMed1998

Placental hormones during induced hypoglycaemia in pregnant women with insulin-dependent diabetes mellitus: evidence of an active role for placenta in hormonal counter-regulation.

OBJECTIVE: To study the effect of induced hypoglycaemia on serum levels of the placental hormones oestriol, human placental lactogen, placental growth hormone and progesterone in the third trimester of pregnancy. DESIGN: A prospective experimental investigation. SETTING: High risk pregnancy unit and diabetes research unit at Karolinska Institutet Danderyd Hospital, a university hospital. PARTICIPANTS: Ten women with insulin-dependent diabetes mellitus in the third trimester of pregnancy. METHODS: Venous blood samples were collected every 15 minutes for analyses of oestriol, progesterone, human placental lactogen and placental growth hormone, during the 150 min of a hyperinsulinaemic hypoglycaemic clamp, which maintained arterial blood-glucose level of about 2.2 mmol/l. MAIN OUTCOME MEASURES: Levels of analysed placental hormones during hypoglycaemia. RESULTS: A statistically significant increase was observed in placental growth hormone during hypoglycaemia (P < 0.0001), whereas the placental hormones progesterone, human placental lactogen and oestriol did not show changes of clinical significance. CONCLUSIONS: The increase in placental growth hormone indicates that the placenta is an endocrine organ which may take an active part in acute metabolic processes, such as here in the hormonal counterregulation of hypoglycaemia.

Adult↗
PubMed1989

Placental hormones and maternal glucose metabolism. A study of fetal growth in normal pregnancy.

The interrelations between three placental hormones (oestradiol, progesterone and hPL), maternal glucose metabolism, maternal anthropometry and fetal growth were studied in a sample of 52 carefully selected pregnant women. A relation was found between infant birthweight and both fasting blood glucose and t1/2 of glucose of an intravenous glucose tolerance test at week 37 of pregnancy. The serum concentrations of the placental hormones were not significantly related to the glucose variables. The correlation between birthweight and the maternal levels of hPL in late pregnancy (r = 0.60) persisted when fasting blood glucose and t1/2 of glucose were taken into account. Maternal fat mass was found to explain more of the variation in basal insulin levels around week 37 than did the placental hormones.

Adipose Tissue↗