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Results for “PLACENTAL HORMONES”

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At least 217 records · Page 12Linked to original sources
PubMed1978

Extremely low placental lactogen hormone (hPL) values in an otherwise uneventful pregnancy preceding delivery of a normal baby.

A case of a normal pregnancy and delivery with extremely low placental lactogen hormone (hPL) values in maternal blood is presented. The low hPL-values were due to the fact that the placenta only produced about 1/25 of the normal estimated output, calculated on the basis of the hPL-concentration in the intervillous spaces. The concentrations of progesterone, the placenta-specific beta-glycoprotein (SP1) and total estriol in serum were normal, while prolactin and chorionic gonadotropin (hCG) were considerably elevated. Glucose levels were normal. At the ultrastructural level the actual placenta under study did not differ from a normal term placenta. In spite of the very low concentrations of hPL there was a good milk secretion, and the mother was still breast-feeding her baby 11 months after the delivery. Basal level of prolactin was at this time normal.

Adult↗
PubMed1979

Endocrine factors in genetic improvement of milk production.

The endocrine role in lactation is undisputed, but attempts to correlate milk production with various endocrine products have had limited success. Recent work has suggested that placental hormones, in particular placental lactogen, may be an important regulator of lactation capacity. In addition to concentrations of hormones in blood, it is important to consider receptors in target tissue for the hormones. The concentration of receptors in a tissue may vary with genotype of the individual or under the influence of hormonal state. Other aspects of the target tissue's system for response also must be considered.

Animals↗
PubMed1982

Stress hormones and placental steroids in physical exercise during pregnancy.

The hormonal responses to exercise during later pregnancy were studied in relation to an exercise test in ten healthy women. At the end of the 10-min exercise, maternal heart rate had risen from 93 +/- 3.2 (mean +/- SEM) to 157 +/- 6.3 beats/min, and systolic blood pressure from 120 +/- 3.4 to 148 +/- 5.4 mmHg, but diastolic blood pressure was unchanged. Plasma concentrations of noradrenaline and adrenaline rose rapidly during the exercise, from 2.9 +/- 0.3 to 6.9 +/- 1.2 nmol/l and from 0.31 +/- 0.04 to 0.47 +/- 0.08 nmol/l respectively. The serum concentration of prolactin did not change during the test, but 30 min after the exercise the value had risen from 146 +/- 17 to 212 +/- 22 mg/ml, thereafter slowly declining. The serum concentration of cortisol remained unchanged. The mean concentration of oestriol rose from 31.5 +/- 2.6 to 33.9 +/- 3.0 nmol/l at least 5 min after the exercise, thereafter declining to 29 +/- 2.6 nmol/l. After the test, levels of progesterone and oestradiol also fell slightly. Mild irregular uterine activity was found in four subjects. Cardiotocography revealed a transient fetal tachycardia in two subjects.

Adult↗
PubMed1984

Treatment of ewes at different stages of pregnancy with epidermal growth factor: effects on wool growth and plasma concentrations of growth hormone, prolactin, placental lactogen and thyroxine and on foetal development.

Pregnant ewes at 57, 75 and greater than or equal to 101 days of gestation were infused with approximately 3 mg of epidermal growth factor (EGF) for a period of 24-28 h. The strength of attachment of the wool fibres to the skin became progressively reduced during the week following treatment. After 3 weeks, the mean forces required to pluck staples had declined to between 10 and 30% of the pre-infusion measurements and the fleeces were able to be removed easily by hand. Increases in growth hormone and placental lactogen occurred in plasma of ewes during EGF treatment. Prolactin was not affected by EGF but circulating levels of thyroxine declined. The concentrations of these hormones returned to approximate pretreatment values within 24 h of the end of infusion. EGF treatment at the dose levels used did not appear to significantly affect the development or viability of the foetus.

Animals↗
PubMed1976

The synthesis of human placental lactogen hormone (hPL) in a cell-free wheat germ system.

Total polysomes from human term placenta were incubated in a wheat germ cell-free system during 1 hr at 25 degrees C. Human placental lactogen hormone was identified among the proteins synthesized in vitro by immune precipitation and subsequent sodium dodecylsulphate electrophoresis of the immunoprecipitate. The zone containing the radioactivity from the immunoprecipitate [3H]-labelled lactogen hormone comigrated exactly with the radioactivity zone from added [14C]-labelled marker hormone. This result indicates that the molecular weight of the synthesized product must be equal or very similar to that of the native protein hormone.

Carbon Radioisotopes↗
PubMed2005

Stimulation of human trophoblast invasion by placental growth hormone.

A critical step in establishment of human pregnancy is the invasion of the uterus wall by the extravillous cytotrophoblast (EVCT), a process regulated by multiple autocrine and paracrine factors. Hormones belonging to the GH/prolactin family are expressed at the maternofetal interface. Because they are involved in cell motility in various models, we examined the possible regulatory role of human placental GH (hPGH) in EVCT invasiveness. By using an in vitro invasion model, we found that EVCT isolated from first-trimester chorionic villi and cultured on Matrigel secreted hPGH and expressed human GH receptor (hGHR). These data were confirmed by in situ immunohistochemistry. EVCT expressed the full-length and truncated forms of hGHR, and the Janus kinase-2/signal transducer and activator of transcription factor-5 signaling pathway was activated in EVCT by hPGH treatment. Strong hPGH and hGHR expression was observed when EVCT invaded Matrigel and moved through the pores of the filter on which they were cultured. hPGH stimulated EVCT invasiveness, and this effect was inhibited by a Janus kinase-2 inhibitor. Interestingly, hPGH was more efficient than pituitary GH in stimulating EVCT invasiveness. These results offer the first evidence for a placental role of hPGH and suggest an autocrine/paracrine role of hPGH in the regulation of trophoblast invasion.

Cells, Cultured↗
PubMed1986

[Management of pregnancy at risk: evaluation of fetal movements, determination of total plasma estriol and placental lactogen hormone in relation to fetal heart rhythm].

The authors studied 50 at-risk pregnancies to decide how useful fetal movements were prognostically. They compared this method with electronic measurements of fetal cardiac rhythm. The results show that it is both sensitive and specific. The levels of total oestriols and of plasma placental lactogen hormone when compared with the fetal heart rhythm are just as specific and sensitive.

Estriol↗
PubMed1985

Binding of the human glucocorticoid receptor to defined regions in the human growth hormone and placental lactogen genes.

An in vitro competition assay was used to investigate whether binding sites for the human glucocorticoid receptor occur in the human genes for growth hormone (hGH) and placental lactogen (chorionic somatomammotropin, hCS). These genes display 95% sequence homology. Two receptor-binding regions were found in the hGH gene, one of which is located within 290 bp upstream, and one within 251 bp downstream from the transcription initiation site. Two binding regions homologous to those in the hGH gene were found in the hCS gene. The receptor-binding DNA fragment from the structural part of the genes, but not that from their promoter area, contained a sequence homologous to a 15-bp consensus sequence proposed earlier for the glucocorticoid receptor binding site. It is unlikely that the putative difference in glucocorticoid sensitivity between the hGH and hCS genes is accounted for by major differences in glucocorticoid receptor binding pattern.

Base Sequence↗
PubMed1975

Fertility control through active immunization using placenta proteins.

Numerous studies have demonstrated that antibodies to placental proteins in a variety of species are capable of preventing or disrupting gestation. Early work in this area was primarily directed towards the passive immunization of rodents with heterologous antisera to whole placental extracts. Toxicity and renal damage often accompanied fertility inhibition. More recent studies reported less toxicity and a higher specificity of antibodies to reproductive function when anti-placental antibodies were absorbed with serum and extracts of non-reproductive organs. Few studies have been reported in which active immunization with placental proteins was employed. The most detailed studies of active immunization have employed highly purified placental hormones. Immunizations of rats and rabbits with human placental lactogen have resulted in marked reduction in reproductive function. Immunization of human females with chemically altered (hapten-coupled/ HCG resulted in the production of antibodies reacting with unaltered HCG and pituitary LH. These antibodies were capable of reducing the level of endogenous serum LH in pre- and post-menopausal women. The also altered the events of the menstrual cycle in premenopausal women. More specific inhibition of chorionic gonadotrophin has been obtained by immunization of baboons with the beta subunit of HCG. Antifertility effects without alterations in the menstrual cycle of female baboons immunized with the beta subunit of HCG have been reported. The antibodies produced in these animals reacted significantly with human LH in vitro. The possibility of using hormonal and non-hormonal placental proteins as antigens for the specific immunological inhibition of fertility remains.

Abortion, Spontaneous↗
PubMed1995

Increases in gill cytosolic corticosteroid receptor abundance and saltwater tolerance in juvenile coho salmon (Oncorhynchus kisutch) treated with growth hormone and placental lactogen.

Juvenile coho salmon (Oncorhynchus kisutch) were injected with one of two recombinant bovine hormones, growth hormone (bGH; 5.0 and 0.5 micrograms.g-1 body wt) or placental lactogen (bPL; 5.0, 0.5, and 0.05 micrograms.g-1 body wt) to determine the effect on growth, plasma cortisol concentration, cytosolic corticosteroid receptors (CR) in the gills, and the development of hypoosmoregulatory ability. One week following a single injection or six weekly injections of bGH or bPL, the fish were measured and sampled for CR concentration and Na+,K(+)-ATPase activity in the gills. Fish were also challenged with salt water (salinity 25%) for 24 hr to determine saltwater tolerance at the end of the 6-week treatment. Treatment with bPL and bGH significantly increased weight and length of the fish. The 0.05-micrograms bPL dose significantly elevated plasma cortisol concentration, whereas all other hormone treatments did not affect cortisol levels. bPL and bGH also significantly increased CR concentration and Na+,K(+)-ATPase activity in the gills. The perturbation in plasma sodium concentration was least in animals receiving the highest dose of bPL and the bGH-treated animals following transfer to seawater. An increase in cytosolic CR by bGH and bPL may increase responsiveness of the gills to cortisol and partially account for the increase in Na+,K(+)-ATPase activity and greater ability to regulate plasma sodium in seawater as exhibited by the experimental groups.

Animals↗
PubMed1995

Placental-fetal hormonal interactions: impact on fetal growth.

The placenta plays a critical role in providing an environment that supports optimal fetal growth. It does this by providing the site of nutrient transfer from the mother to the fetus and waste secretion from the fetus to the mother, acting as a barrier against pathogens and the maternal immune system, and as an active endocrine organ capable of secreting hormones, growth factors, cytokines, and other bioactive products. Among the hormones produced by the placenta are members of the growth hormone/prolactin gene family, the placental lactogens (PL) and prolactin-related proteins. Although the exact functions of the placental members of this gene family have not been entirely elucidated, the available evidence supports a role for some in modulating maternal and fetal metabolism. The PL are secreted into the maternal and fetal circulations and, at least in ruminants, seem to mediate their effects through unique receptors, although this remains controversial. One action of the PL may be to modulate fetal IGF production. Research with mice, using gene ablation techniques, indicates the importance of the IGF for maintaining normal fetal growth rate. This research provided data on the timing of the onset of IGF effects on fetal growth and the receptors through which these effects are mediated. This review is about the structure, mechanism of action, and potential function of the placental members of the growth hormone/prolactin gene family and the recent evidence on the role of IGF in fetal growth regulation.

Animals↗
PubMed2003

Human placental growth hormone, insulin-like growth factor I and -II, and insulin requirements during pregnancy in type 1 diabetes.

Human placental GH (hPGH) replaces pituitary GH during pregnancy. hPGH is correlated to serum IGF-I in normal pregnancies and in pregnancies complicated by fetoplacental disorders. In gestational diabetes and type 2 diabetes no correlation between hPGH and IGF-I has been found. The relationship between hPGH and IGF-I in type 1 diabetes mellitus has not been investigated thoroughly. Furthermore, hPGH may be involved in the development of insulin resistance during pregnancy. In this prospective, longitudinal study, 51 type 1 diabetic subjects were followed with repeated blood sampling during pregnancy (median, 14 blood samples/subject; range, 8-26). Maternal concentrations of serum hPGH, IGF-I, and IGF-II were measured and compared with insulin requirements and birth characteristics. hPGH was detected from as early as 6 wk gestation. In all subjects, a rise in serum hPGH was observed during pregnancy, and the rise between wk 16 and 25 was correlated to the rise between wk 26 and 35 (P < 0.001). From wk 26 onward, the increase in hPGH values was significantly correlated to the birth weight, expressed as a z-score (r(s) = 0.54; P < 0.001), as were the absolute hPGH values. Also, a positive influence of hPGH on placental weight was found. Serum IGF-I values decreased significantly from the first to the second trimester (P </= 0.021). Serum hPGH correlated to serum IGF-I from wk 24-35, and changes in IGF-I followed the increase in hPGH between wk 26 and 35 (r(s) = 0.53; P < 0.001), as did IGF-II (r(s) = 0.37; P = 0.008). Changes in IGF-I and IGF-II between wk 26 and 35 also correlated to the birth weight z-score (P </= 0.020), but only hPGH remained significant in multiple regression analysis. Similar results were found in the subgroup delivering at term. Interestingly, the increase in hPGH was not correlated to the increase in insulin requirements, nor was any consistent relationship revealed during each gestational period. In conclusion, our study suggests a role for hPGH in the regulation of both IGFs and fetal growth in type 1 diabetes. In contrast, the increase in insulin requirements during pregnancy in type 1 diabetic subjects could not be related to hPGH levels.

Adult↗
PubMed1989

Rabbit placental-conditioned medium stimulates progesterone accumulation by granulosa-lutein cells in culture: preliminary characterization of a placental luteotropic hormone.

The rabbit fetal placenta plays an important physiological role in luteal maintenance in pregnancy, probably via the secretion of an unidentified placental "luteotropin." The objective of these studies was to examine conditioned medium from fetal placental-tissue incubations (FPI) for the presence of placental luteotropic hormones/factors, using the stimulation of progesterone accumulation by rabbit granulosa-lutein cells in culture, as an in vitro luteotropic bioassay. Progesterone accumulation by rabbit granulosa-lutein cells (during 5 days of culture) was increased (compared with controls), 1.5-fold by 10(-8) M estradiol-17 beta (E2) and 11.5-fold by 100 ng/ml luteinizing hormone (oLH). FPI stimulated progesterone accumulation (approximately 3-fold) and this was further increased in the presence of E2 (FPI + E2; approximately 6-fold). Luteotropic bioactivity in FPI (+ E2) was retained after dialysis (6000-8000 MW cutoff; 7.8-fold) and heating (90-95 degrees C for 1 h; 7.5-fold), but was destroyed after incubation with trypsin (1 mg/ml, 1 h at 37 degrees C; 0.9-fold). Media conditioned with skeletal muscle (1.2-fold), heart (1.6-fold), liver (1.5-fold), and uterus (0.5-fold) and 5-10% serum (less than 1-fold), from pseudopregnant rabbits, had little or no luteotropic bioactivity. These data indicate that FPI contains a luteotropic hormone/factor that is probably a heat-stable, trypsin-sensitive, protein/peptide of greater than 6000-8000 MW that acts in synergy with E2 to promote granulosa-lutein cell steroidogenesis. This placental hormone/factor is a good candidate for the elusive rabbit placental luteotropin.

Animals↗