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Alcoholism, Clinical and Experimental... Aug 1993Maternal alcohol abuse during pregnancy can lead to abnormalities in fetal development, including the fetal alcohol syndrome (FAS). Although intrauterine growth...
Maternal alcohol abuse during pregnancy can lead to abnormalities in fetal development, including the fetal alcohol syndrome (FAS). Although intrauterine growth retardation is a hallmark of FAS, the pathophysiology is not fully understood. A contributing factor may be altered placental function, which could affect fetal growth and development. As a major endocrine organ during pregnancy, changes in the production of placental hormones could affect pregnancy and possibly fetal development. In this study, the effect of continued exposure to ethanol on placental hormone production was examined using cultured human placental trophoblasts. Ethanol exposure involved diffusion of ethanol from the atmosphere into the culture medium. This was refreshed daily, leading to daily peak concentrations of 280 to 300 mg/dl (60-65 mM) at 16 to 24 hr. This ethanol exposure for 2 or 4 days significantly increased the production of human chorionic gonadotropin and progesterone by the cultured trophoblasts. However, ethanol treatment had no effect on human placental lactogen production. Acute stimulation (10 min) of cultured trophoblasts with adenosine (50 microM) normally results in increased production of cyclic adenosine 3',5'-monophosphate (cAMP). With ethanol exposure, adenosine-stimulated cAMP production was significantly elevated relative to that in controls. However, the effect of ethanol on adenosine-stimulated cAMP did not appear to be secondary to chronic alterations in adenosine in the culture medium. Measurement of adenosine in the culture medium revealed no difference in concentration or production between control and ethanol treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Adenosine; Cell Differentiation; Cells, Cultured; Chorionic Gonadotropin; Cyclic AMP; DNA Replication; Dose-Response Relationship, Drug; Ethanol; Female; Fetal Alcohol Spectrum Disorders; Fetal Growth Retardation; Humans; Infant, Newborn; Placental Hormones; Placental Lactogen; Pregnancy; Progesterone; Trophoblasts
PubMed: 8214420
DOI: 10.1111/j.1530-0277.1993.tb00847.x -
Revista Chilena de Obstetricia Y... 1972
Topics: Female; Humans; Placental Hormones; Pregnancy
PubMed: 4669038
DOI: No ID Found -
Archives of Otolaryngology--head & Neck... Apr 1998To describe any relationship between pregnancy rhinitis and weight gain or serum levels of estradiol, progesterone, placental growth hormone, or insulinlike growth...
OBJECTIVE
To describe any relationship between pregnancy rhinitis and weight gain or serum levels of estradiol, progesterone, placental growth hormone, or insulinlike growth factor I.
PATIENTS
Twenty-seven nonsmoking healthy pregnant women aged 22 to 38 years (mean age, 28 years) who had no history of respiratory allergy or chronic nasal or sinus problems volunteered to enter the study. They had no nasal complaints at entry.
METHODS
Nasal patency was registered daily from early pregnancy until 1 month after delivery. Nasal and oral peak expiratory flow rates were established, and the subjective blockage was scored from 0 to 4, with 0 indicating no blockage. Serum samples were collected and weight was measured on 4 occasions during pregnancy and again at the end of the study. Pregnancy rhinitis was diagnosed if the subjective nasal obstruction score was 1 or higher every morning for at least 6 weeks immediately preceding delivery, then returned to 0 within 2 weeks and remained at 0 until the end of the study. If on any day other signs of respiratory tract infection occurred, that day was excluded.
RESULTS
Pregnancy rhinitis was diagnosed in 5 women. These 5 women showed significantly higher levels of placental growth hormone than the women without the diagnosis. No significant difference was found between the 2 groups regarding body weight or any of the other serum levels studied.
CONCLUSIONS
Serum level of placental growth hormone is raised in pregnancy rhinitis and may be involved in its pathogeny. Pregnancy rhinitis does not significantly raise weight gain or serum levels of estradiol, progesterone, or insulinlike growth factor I.
Topics: Adult; Estradiol; Female; Gestational Age; Growth Hormone; Humans; Insulin-Like Growth Factor I; Nasal Obstruction; Placenta; Placental Hormones; Pregnancy; Pregnancy Complications; Progesterone; Reference Values; Rhinitis; Weight Gain
PubMed: 9559693
DOI: 10.1001/archotol.124.4.439 -
Molecular and Cellular Endocrinology Nov 1999Diabetes is a common complication encountered during pregnancy. Earlier studies indicated that diabetic placentas bear morphological alterations consistent with modified...
Detection of placental growth hormone variant and chorionic somatomammotropin-L RNA expression in normal and diabetic pregnancy by reverse transcriptase-polymerase chain reaction.
Diabetes is a common complication encountered during pregnancy. Earlier studies indicated that diabetic placentas bear morphological alterations consistent with modified placental differentiation, including alterations in the villous cellular content, structure, and total surface. Limited data associating the diabetic status with the expression of terminal placental differentiation markers are available. The human growth hormone/chorionic somatomammotropin (hGH/CS) family consists of five genes, one of which (GH-N) is expressed efficiently in pituitary while the other four (CS-A, B, L, and hGH-V) are expressed in placenta and represent ultimate placental differentiation markers. We developed and applied a sensitive RT-PCR method coupled with diagnostic restriction digestion to determine the relative levels of the hGH/CS family in normal pregnancies and examine whether their mRNA expression pattern is altered in pregnancies complicated by diabetes. We show that relative hCS-L content changes during placental development. Specifically, normal term placentas express higher relative levels of hCS-L, lower relative hGH-V levels and a 70-fold lower hGH-V/CS-L mRNA ratio compared to early placentas. Also, many term placentas from diabetic pregnancies express lower relative levels of hCS-L mRNA and a much higher hGH-V/CS-L mRNA ratio compared to normal term placenta, resembling more an early placenta pattern of expression. Thus, our study suggests that the expression of terminal placental differentiation markers, such as the hGH/CS genes, is altered in term placentas from these diabetics reflecting either impaired placental differentiation or post-differentiation impairment of normal placental function.
Topics: Diabetes, Gestational; Female; Genetic Variation; Gestational Age; Growth Hormone; Humans; Placenta; Placental Hormones; Placental Lactogen; Pregnancy; RNA; RNA, Messenger; Reverse Transcriptase Polymerase Chain Reaction; Time Factors
PubMed: 10619404
DOI: 10.1016/s0303-7207(99)00152-5 -
Obstetrics and Gynecology Aug 1970
Topics: Chorionic Gonadotropin; Diabetes Mellitus; Female; Glucose Tolerance Test; Growth Hormone; Humans; Hypoglycemia; Insulin; Placental Hormones; Placental Lactogen; Pregnancy; Pregnancy in Diabetics
PubMed: 5428496
DOI: No ID Found -
Molecular and Cellular Endocrinology Feb 2015Perfluorooctane sulfuric acid (PFOS) is a persistent organic pollutant, causes fetal growth retardation but the mechanism is still unclear. This study focused on...
Perfluorooctane sulfuric acid (PFOS) is a persistent organic pollutant, causes fetal growth retardation but the mechanism is still unclear. This study focused on PFOS-induced toxicity such as placental trophoblast cell histopathological changes, endocrine function (i.e., prolactin (PRL)-family hormone production) and subsequent fetal growth retardation in mice. Maternal body weight gain, placental and fetal weights were significantly decreased in proportion to PFOS dosage. Placental efficiency (fetal weight/placental weight) was significantly reduced dose-dependently. Necrotic changes were observed in PFOS-treated placental tissues, and the area of injury increased dose-dependently. Finally, mRNA levels and maternal serum concentrations of the PRL-family hormones (mPL-II, mPLP-Cα, mPLP-K) were significantly reduced dose-dependently. In addition, the changing pattern between PRL-family hormone concentrations and fetal body weight was positively correlated. These results suggest that gestational PFOS treatment induces placental histopathological changes and disruption of endocrine function, finally may lead to fetal growth retardation in mice.
Topics: Alkanesulfonic Acids; Animals; Body Weight; Embryo, Mammalian; Female; Fetal Growth Retardation; Fluorocarbons; Gene Expression Regulation, Developmental; Mice; Placental Hormones; Pregnancy; Prolactin; Transcription Factor Pit-1; Trophoblasts
PubMed: 25449418
DOI: 10.1016/j.mce.2014.10.026 -
Human Genetics Jan 1998Human placental lactogen (HPL) is produced in large amounts in normal pregnancies. We report a pregnancy with complete lack of HPL and the placental variant of the human...
Human placental lactogen (HPL) is produced in large amounts in normal pregnancies. We report a pregnancy with complete lack of HPL and the placental variant of the human growth hormone HGH-V. The pregnancy resulted in a severely growth-retarded but otherwise normal male baby. PCR analysis of DNA extracted from the placenta showed that the HPL encoding genes hPL-4 and hPL-3 were deleted along with the human growth hormone variant gene (hGH-V), which is located between these two active hPL genes and also expressed in the normal placenta. Of the five members of this multigene family, hGH-N, which is expressed in the pituitary gland, and hPL-1, a presumed pseudogene, were left intact. The latter (hPL-1) was expressed as RNA transcripts only at very low levels as is usually reported in normal pregnancies. Analysis of the parents' DNA showed that both of them carried a different heterozygous deletion at the 3' end of the hGH/hPL locus.
Topics: Adult; Female; Gene Deletion; Genotype; Growth Hormone; Humans; Infant, Newborn; Male; Parents; Placenta; Placental Hormones; Placental Lactogen; Polymerase Chain Reaction; Pregnancy; RNA, Messenger
PubMed: 9490304
DOI: 10.1007/s004390050658 -
Hormone and Metabolic Research =... Mar 2008Placental growth hormone (PGH) is secreted from the syncytiotrophoblast in increasing amounts during pregnancy. The physiology and regulation of PGH is not well known;...
Placental growth hormone (PGH) is secreted from the syncytiotrophoblast in increasing amounts during pregnancy. The physiology and regulation of PGH is not well known; however, low glucose levels appear to stimulate PGH liberation IN VITRO and IN VIVO. PGH appears to have lipolytic effects, and inverse correlations between maternal body mass index and serum PGH levels have been reported. Therefore, substances related to maternal adipose tissue metabolism could influence PGH secretion. The effect of insulin, glycerol, 3-hydroxybutyrate (3-OHB), and leptin on PGH and human placental lactogen (hPL) secretion from cultured placental explants was studied. In glucose-free media, PGH content increased upto 237.5+/-28.4% of control media (p<0.001, ANOVA). Insulin levels were without effect on PGH secretion, as were 3-OHB, leptin, and glycerol at 0.02 mmol/l. Glycerol at 0.2 mmol/l increased PGH in all of the placental explants studied (n=8; mean increase 27.3+/-7.1%), and this difference was significantly different from the control explants (p=0.004). The liberation of hPL to culture media was different from PGH and was influenced by glucose and insulin. In conclusion, the absence of glucose profoundly increased PGH secretion in cultured placental explants. Addition of glycerol in physiologically relatively high concentrations showed a less pronounced stimulatory effect.
Topics: 3-Hydroxybutyric Acid; Female; Glucose; Glycerol; Growth Hormone; Humans; Insulin; Leptin; Organ Culture Techniques; Placenta; Placental Hormones; Pregnancy
PubMed: 18246527
DOI: 10.1055/s-2007-1004575 -
Federation Proceedings Feb 1980The human placenta is an organ with a long period of growth in cell number later succeeded by cessation of cell division but some continued growth in cell size. The RNA... (Comparative Study)
Comparative Study
The human placenta is an organ with a long period of growth in cell number later succeeded by cessation of cell division but some continued growth in cell size. The RNA concentration and content per cell (RNA/DNA ratio) are reduced between the end of the first trimester and the end of pregnancy, and there is a change in availability of placental chromatin for transcription when incubated in vitro with RNA polymerase II. Synthesis and secretion of placental peptide hormones on membrane-bound polyribosomes also undergo changes during pregnancy. During early pregnancy, levels of human chorionic gonadotropin are maximal, declining in later pregnancy, levels of human chorionic gonadotropin are maximal, declining in later pregnancy. The messenger RNA for this hormone undergoes similar changes in relative amount in the placenta. In contrast, the plasma level of placenta lactogen increases progressively during pregnancy, and in parallel with this, the placenta content of mRNA for this hormone increases throughout later pregnancy. It is concluded that placental programing regulates the relative amounts of mRNA for each hormone, and this in turn determines the amounts secreted at any stage of pregnancy. Nutritional status of the mother can affect placental RNA content, most clearly established in studies on rats in which a diet low in protein or with added alcohol results in a reduced capacity to form and secrete placental lactogen. The extent of this depression parallels the reduction in placental RNA content. It is suggested that underproduction of placental lactogen may be a factor in reducing flow of nutrients from the maternal tissues to the fetus in later pregnancy, under conditions of malnutrition.
Topics: Animals; DNA; Female; Humans; Maternal-Fetal Exchange; Nutritional Physiological Phenomena; Placenta; Placental Hormones; Pregnancy; Pregnancy Proteins; Protein Biosynthesis; RNA; RNA, Messenger; Rats
PubMed: 7353683
DOI: No ID Found -
The Journal of Maternal-fetal &... Sep 2012To investigate whether the maternal serum concentration of human placental growth hormone (PGH) at 11-13 weeks' gestation is altered in pregnancies that deliver small...
OBJECTIVE
To investigate whether the maternal serum concentration of human placental growth hormone (PGH) at 11-13 weeks' gestation is altered in pregnancies that deliver small for gestational age (SGA) neonates.
METHODS
Maternal serum concentration of PGH was measured in 60 cases that subsequently delivered SGA neonates in the absence of preeclampsia and compared to 120 non-SGA controls.
RESULTS
In the SGA group, compared to the non-SGA group, there was no significant difference in the median PGH MoM (0.95 MoM, IQR 0.60-1.30 vs. 1.00 MoM, IQR 0.70-1.30, p = 0.97). There was no significant association between PGH MoM and birth weight percentile in either the SGA (p = 0.72) or in the non-SGA group (p = 0.63).
CONCLUSION
Maternal serum PGH at 11-13 weeks' gestation is unlikely to be a useful biochemical marker for early prediction of SGA.
Topics: Adult; Biomarkers; Birth Weight; Case-Control Studies; Delivery, Obstetric; Female; Fetal Growth Retardation; Gestational Age; Growth Hormone; Humans; Infant, Newborn; Infant, Small for Gestational Age; Mothers; Placental Hormones; Pregnancy; Pregnancy Trimester, First; Prognosis
PubMed: 22489624
DOI: 10.3109/14767058.2012.663834