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Animal Reproduction Science Jul 2004Production of growth promoting substances by the placenta is regulated differently from the way production of similar compounds is regulated by maternal organs in... (Comparative Study)
Comparative Study Review
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.
Topics: Animals; Cattle; Embryonic and Fetal Development; Evolution, Molecular; Female; Gene Expression Regulation; Genomic Imprinting; Goats; Growth Hormone; Humans; Placental Hormones; Placental Lactogen; Placentation; Pregnancy; Prolactin; Receptors, Prolactin; Receptors, Somatotropin; Sheep
PubMed: 15271479
DOI: 10.1016/j.anireprosci.2004.04.008 -
Hormone Research 1994In normal and in pathological human pregnancies, a specific placental growth hormone variant, rather than placental lactogen, substitutes for the suppressed pituitary GH... (Review)
Review
In normal and in pathological human pregnancies, a specific placental growth hormone variant, rather than placental lactogen, substitutes for the suppressed pituitary GH to stimulate the maternal insulin-like growth factor I (IGF-I). In pathological pregnancies with disorders of the feto-placental unit, low levels of placental GH hormone result in relatively low levels of maternal IGF-I. In normal pregnancies, the baby birth weight is positively correlated with maternal IGF-I values.
Topics: Birth Weight; Embryonic and Fetal Development; Female; Growth Hormone; Humans; Insulin-Like Growth Factor I; Placental Hormones; Pregnancy
PubMed: 7959636
DOI: 10.1159/000184147 -
American Journal of Physiology.... Oct 2018The human (h) placental lactogenic hormone chorionic somatomammotropin (CS) is highly produced during pregnancy and acts as a metabolic adaptor in response to maternal...
The human (h) placental lactogenic hormone chorionic somatomammotropin (CS) is highly produced during pregnancy and acts as a metabolic adaptor in response to maternal insulin resistance. Maternal obesity can exacerbate this "resistance", and a >75% decrease in CS RNA levels was observed in term placentas from obese vs. lean women. The genes coding for hCS ( hCS-A and hCS-B) and placental growth hormone ( hGH-V) as well as the hCS-L pseudogene and pituitary growth hormone (GH) gene ( hGH-N) are located at a single locus on chromosome 17. Three remote hypersensitive sites (HS III-V) located >28 kb upstream of hGH-N as well as local hCS gene promoter and enhancer regions are implicated in hCS gene expression. A placenta-specific chromosomal architecture, including interaction between HS III-V and hCS but not hGH gene promoters, was detected in placentas from lean women (BMI <25 kg/m) by using the chromosome conformation capture assay. This architecture was disrupted by pre-pregnancy maternal obesity (BMI >35 kg/m), resulting in a predominant interaction between HS III and the hGH-N promoter, which was also observed in nonplacental tissues. This was accompanied by a decrease in hCS levels, which was consistent with reduced RNA polymerase II and CCAAT/enhancer-binding protein-β association with individual hCS promoter and enhancer sequences, respectively. Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.
Topics: Body Mass Index; Chromatin Immunoprecipitation; Chromosomes, Human; Female; Gene Expression; Growth Hormone; Human Growth Hormone; Humans; Immunoblotting; Insulin Resistance; Obesity; Placenta; Placental Hormones; Placental Lactogen; Pregnancy; Pregnancy Complications; Promoter Regions, Genetic; Pseudogenes; RNA, Messenger; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction
PubMed: 29763375
DOI: 10.1152/ajpendo.00042.2018 -
Acta Paediatrica (Oslo, Norway : 1992).... Apr 1994
Review
Topics: Female; Growth Hormone; Humans; Placental Hormones; Pregnancy; Pregnancy Complications
PubMed: 7949617
DOI: 10.1111/j.1651-2227.1994.tb13287.x -
International Journal of Molecular... Dec 2022Human placental lactogen (hPL) is a placental hormone which appears to have key metabolic functions in pregnancy. Preclinical studies have putatively linked hPL to... (Meta-Analysis)
Meta-Analysis Review
Human placental lactogen (hPL) is a placental hormone which appears to have key metabolic functions in pregnancy. Preclinical studies have putatively linked hPL to maternal and fetal outcomes, yet-despite human observational data spanning several decades-evidence on the role and importance of this hormone remains disparate and conflicting. We aimed to explore (via systematic review and meta-analysis) the relationship between hPL levels, maternal pre-existing and gestational metabolic conditions, and fetal growth. MEDLINE via OVID, CINAHL plus, and Embase were searched from inception through 9 May 2022. Eligible studies included women who were pregnant or up to 12 months post-partum, and reported at least one endogenous maternal serum hPL level during pregnancy in relation to pre-specified metabolic outcomes. Two independent reviewers extracted data. Meta-analysis was conducted where possible; for other outcomes narrative synthesis was performed. 35 studies met eligibility criteria. No relationship was noted between hPL and gestational diabetes status. In type 1 diabetes mellitus, hPL levels appeared lower in early pregnancy (possibly reflecting delayed placental development) and higher in late pregnancy (possibly reflecting increased placental mass). Limited data were found in other pre-existing metabolic conditions. Levels of hPL appear to be positively related to placental mass and infant birthweight in pregnancies affected by maternal diabetes. The relationship between hPL, a purported pregnancy metabolic hormone, and maternal metabolism in human pregnancy is complex and remains unclear. This antenatal biomarker may offer value, but future studies in well-defined contemporary populations are required.
Topics: Pregnancy; Female; Humans; Placental Lactogen; Placenta; Placental Hormones; Fetal Development; Biomarkers
PubMed: 36555258
DOI: 10.3390/ijms232415621 -
The Journal of Endocrinology Aug 1993
Topics: Chorionic Villi; Female; Humans; Placenta; Placental Hormones; Pregnancy; Trophoblasts
PubMed: 8228725
DOI: 10.1677/joe.0.1380177 -
Growth Factors (Chur, Switzerland) Dec 2016To investigate the relationship between maternal serum concentrations of placental growth hormone (GH-V), insulin-like growth factor (IGF)-1 and 2, IGF binding proteins...
To investigate the relationship between maternal serum concentrations of placental growth hormone (GH-V), insulin-like growth factor (IGF)-1 and 2, IGF binding proteins (IGFBP)-1 and 3 and birth weight in appropriate-for-gestational-age (AGA), large-for-gestational-age (LGA) and small-for-gestational-age (SGA) cases in a nested case-control study. Maternal serum samples were selected from the Screening for Pregnancy Endpoints (SCOPE) biobank in Auckland, New Zealand. Serum hormone concentrations were determined by ELISA. We found that maternal serum GH-V concentrations at 20 weeks of gestation in LGA pregnancies were significantly higher than in AGA and SGA pregnancies. Maternal GH-V concentrations were positively correlated to birth weights and customized birth weight centiles, while IGFBP-1 concentrations were inversely related to birth weights and customized birth weight centiles. Our findings suggest that maternal serum GH-V and IGFBP-1 concentrations at 20 weeks' gestation are associated with fetal growth.
Topics: Adult; Birth Weight; Case-Control Studies; Female; Fetal Development; Growth Hormone; Humans; Infant, Low Birth Weight; Infant, Newborn; Insulin-Like Growth Factor Binding Protein 1; Insulin-Like Growth Factor I; Placental Hormones; Pregnancy
PubMed: 28122472
DOI: 10.1080/08977194.2016.1273223 -
American Journal of Obstetrics and... Jan 2003The purpose of this study was to evaluate placental growth hormone levels in maternal circulation throughout pregnancy in normal and growth hormone-deficient women with...
OBJECTIVE
The purpose of this study was to evaluate placental growth hormone levels in maternal circulation throughout pregnancy in normal and growth hormone-deficient women with the use of a specific assay and to determine the clearance of placental growth hormone from maternal circulation after birth.
STUDY DESIGN
Seventeen healthy pregnant women and 1 patient with growth hormone deficiency substituted with recombinant growth hormone during pregnancy participated in a longitudinal study from early pregnancy until birth with repetitive blood sampling and measurement of placental growth hormone levels throughout pregnancy. Furthermore, serial blood samples were drawn before, during, and after elective caesarean deliveries in 5 healthy women to calculate the half-life of placental growth hormone. Placental growth hormone was measured with the use of two monoclonal antibodies in a commercially available solid-phase iodine 125-labeled immunoradiometric assay (Biocode, Liège, Belgium).
RESULTS
Placental growth hormone levels were detectable from as early as 8 weeks of gestation in some of the women and increased throughout gestation, with a maximum at approximately 35 to 36 weeks of gestation (13.7 ng/mL; range, 5.9-24.4 ng/mL) and large interindividual variations. Placental growth hormone levels did not correlate with birth weight or placental weight. In the patient with isolated growth hormone deficiency, placental growth hormone levels were detectable from 11 weeks of gestation (3.4 ng/mL) and increased throughout pregnancy to 13.9 ng/mL, which is similar to values that are obtained in the healthy pregnant women. Substitution therapy with recombinant human growth hormone did not suppress the increase in placental growth hormone. We found a mean half-life of placental growth hormone of 13.8 minutes (range, 11.5-15.2 minutes) in healthy pregnant women and an apparently similar half-life of placental growth hormone (15.8 minutes) in the growth hormone-deficient patient, assuming a monoexponential disappearance of placental growth hormone during the first 30 minutes after the delivery. After the initial 30 minutes, approximately 75% (range, 65%-89%) of the placental growth hormone had been cleared from the maternal circulation.
CONCLUSION
Levels of placental growth hormone in maternal circulation increase throughout pregnancy from as early as 8 weeks of pregnancy, with maximum levels around the week 35 of gestation. The pregnancy-induced rise in placental growth hormone levels in the growth hormone-deficient patient was comparable to the rise seen during normal pregnancies and was not suppressed by the concurrent human growth hormone treatment. We speculate that maternal serum levels of placental growth hormone reflect placental function and fetal growth. However, further studies are needed to evaluate the potential clinical use of placental growth hormone determinations.
Topics: Adult; Birth Weight; Body Height; Female; Gestational Age; Growth Hormone; Half-Life; Human Growth Hormone; Humans; Infant, Newborn; Kinetics; Labor, Obstetric; Longitudinal Studies; Organ Size; Placenta; Placental Hormones; Pregnancy
PubMed: 12548225
DOI: 10.1067/mob.2003.82 -
Ciba Foundation Symposium 1981Hormone production in the human feto-placental unit has been studied extensively yet relatively little is known about the regulatory mechanisms involved. A tissue...
Hormone production in the human feto-placental unit has been studied extensively yet relatively little is known about the regulatory mechanisms involved. A tissue culture approach has been used to examine the effect of potential controlling factors on steroid production by the human mid-term fetal adrenal and mid-term and term placenta. Adrenal. The pituitary peptides corticotropin (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) had the most significant influence on adrenal steroidogenesis in both the fetal and definitive zones. Their effects were not identical: they enhanced dehydroepiandrosterone sulphate (DHA-S) production in a comparable manner but alpha-MSH had much less of a stimulatory effect on cortisol biosynthesis. Medium from homologous fetal pituitary cultures mimicked the effects of alpha-MSH rather than ACTH. Homologous placental culture medium and progesterone enhanced only cortisol production and only in the fetal zone cells. These results demonstrate that specific fetal pituitary and placental factors influence fetal adrenal activity and suggest a functional zonation of the fetal adrenal. Placenta. DHA, DHA-S and 16-hydroxy-DHA stimulated oestrogen biosynthesis while high concentrations of DHA and DHA-S (but not 16-hydroxy-DHA) inhibited progesterone production. Luteinizing hormone-releasing hormone (LRH) inhibited both oestrogen and progesterone biosynthesis. Placental steroidogenesis can therefore be influenced not only by the fetus, through its increasing adrenal output of oestrogen precursors, but also by factors originating within the placenta itself.
Topics: Adrenal Glands; Adrenocorticotropic Hormone; Chorionic Gonadotropin; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Estrogens; Female; Fetus; Gonadotropin-Releasing Hormone; Hormones; Humans; Hydrocortisone; Melanocyte-Stimulating Hormones; Placental Hormones; Pregnancy; Progesterone
PubMed: 6279368
DOI: 10.1002/9780470720684.ch5 -
Biology of Reproduction Feb 1982
Review
Topics: Amino Acid Sequence; Base Sequence; Cell-Free System; Centrifugation, Density Gradient; Chorionic Gonadotropin; DNA Restriction Enzymes; DNA, Neoplasm; DNA, Recombinant; Female; Humans; Magnesium; Nucleic Acid Hybridization; Placenta; Placental Hormones; Placental Lactogen; Pregnancy; Protein Biosynthesis; RNA, Messenger; Trophoblasts
PubMed: 6279188
DOI: 10.1095/biolreprod26.1.73