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EVALUATION OF HORMONAL FUNCTION IN WOMEN WITH CERVICAL INSUFFICIENCY AND INFERTILITY IN THE HISTORY.Wiadomosci Lekarskie (Warsaw, Poland :... 2021The aim: To assess the levels of hormones in women with cervical insufficiency and infertility in the history in the II trimester of gestation.
OBJECTIVE
The aim: To assess the levels of hormones in women with cervical insufficiency and infertility in the history in the II trimester of gestation.
PATIENTS AND METHODS
Materials and methods: 120 pregnant women with cervical insufficiency and anovulatory infertility in the history were examined in the II trimester of gestation: in the I group (60 persons) pregnancy occurred after hormonal treatment of infertility, in the II group (60 individuals) - after in vitro fertilization. 30 pregnant women without cervical insufficiency and a history of infertility were controls. The levels of estradiol, progesterone, placental lactogen, prolactin and cortisol were determined in the blood serum.
RESULTS
Results: The concentration of maternal progesterone was lower in the persons in the I group on 12.36 %, in the II group - on the 15.37 % (p=0.03) compared to the healthy women. Cortisol and prolactin amounts were statistically higher in I and II groups (p<0.001) than in controls. While the levels of estradiol and placental lactogen were slightly less in the subjects with cervical insufficiency and a history of anovulatory infertility compared to the healthy women.
CONCLUSION
Conclusions: In pregnant women with cervical insufficiency and a history of anovulatory infertility in the II trimester of gestation there are decrease progesterone level and high prolactin and cortisol concentrations in blood serum. The changes in estradiol and placental lactogen amounts are not significant compared to healthy women.
Topics: Estradiol; Female; Humans; Infertility, Female; Placenta; Placental Lactogen; Pregnancy; Progesterone
PubMed: 34896996
DOI: No ID Found -
Frontiers in Endocrinology 2021Adaptive changes in glucose homeostasis during pregnancy require proliferation of insulin-secreting beta-cells in the pancreas, together with increased sensitivity for...
Adaptive changes in glucose homeostasis during pregnancy require proliferation of insulin-secreting beta-cells in the pancreas, together with increased sensitivity for glucose-stimulated insulin secretion. Increased concentrations of maternal prolactin/placental lactogen contribute to these changes, but the site of action remains uncertain. Use of Cre-lox technology has generated pancreas-specific prolactin receptor (Prlr) knockouts that demonstrate the development of a gestational diabetic like state. However, many Cre-lines for the pancreas also express Cre in the hypothalamus and prolactin could act centrally to modulate glucose homeostasis. The aim of the current study was to examine the relative contribution of prolactin action in the pancreas and brain to these pregnancy-induced adaptations in glucose regulation. Deletion of prolactin receptor (Prlr) from the pancreas using Pdx-cre or Rip-cre led to impaired glucose tolerance and increased non-fasting blood glucose levels during pregnancy. Prlr /Pdx-Cre mice also had impaired glucose-stimulated insulin secretion and attenuated pregnancy-induced increase in beta-cell fraction. Varying degrees of Prlr recombination in the hypothalamus with these Cre lines left open the possibility that central actions of prolactin could contribute to the pregnancy-induced changes in glucose homeostasis. Targeted deletion of Prlr specifically from the forebrain, including areas of expression induced by Pdx-Cre and Rip-cre, had no effect on pregnancy-induced adaptations in glucose homeostasis. These data emphasize the pancreas as the direct target of prolactin/placental lactogen action in driving adaptive changes in glucose homeostasis during pregnancy.
Topics: Adaptation, Physiological; Animals; Female; Glucose; Glucose Intolerance; Homeostasis; Hypothalamus; Insulin-Secreting Cells; Male; Mice; Pancreas; Placenta; Pregnancy; Prolactin; Prosencephalon; Receptors, Prolactin; Signal Transduction
PubMed: 34867810
DOI: 10.3389/fendo.2021.765976 -
Endocrinology Feb 2022Hypothyroidism increases the incidence of gestational diabetes mellitus (GDM) but the mechanisms responsible are unknown. This study aimed to assess the...
Hypothyroidism increases the incidence of gestational diabetes mellitus (GDM) but the mechanisms responsible are unknown. This study aimed to assess the pathophysiological mechanisms by which hypothyroidism leads to glucose intolerance in pregnancy. Hypothyroidism was induced in female Sprague-Dawley rats by adding methimazole (MMI) to drinking water at moderate (MOD, MMI at 0.005% w/v) and severe (SEV, MMI at 0.02% w/v) doses from 1 week before pregnancy and throughout gestation. A nonpregnant cohort received the same dose for the same duration but were not mated. On gestational day 16 (GD16), or nonpregnant day 16 (NP16), animals were subjected to an intraperitoneal glucose tolerance test. Tissues and blood samples were collected 4 days later. Hypothyroidism induced a diabetic-like phenotype by GD16 in pregnant females only. Pregnant MOD and SEV females had reduced fasting plasma insulin, less insulin following a glucose load, and altered expression of genes involved in insulin signaling within skeletal muscle and adipose tissue. Hypothyroidism reduced rat placental lactogen concentrations, which was accompanied by reduced percentage β-cell cross-sectional area (CSA) relative to total pancreas CSA, and a reduced number of large β-cell clusters in the SEV hypothyroid group. Plasma triglycerides and free fatty acids were reduced by hypothyroidism in pregnant rats, as was the expression of genes that regulate lipid homeostasis. Hypothyroidism in pregnant rats results in a diabetic-like phenotype that is likely mediated by impaired β-cell expansion in pregnancy. This pregnancy-specific phenomenon is likely due to reduced placental lactogen secretion.
Topics: Animals; Diabetes, Gestational; Disease Models, Animal; Fatty Acids, Nonesterified; Female; Glucose Intolerance; Hypothyroidism; Insulin; Placenta; Placental Lactogen; Pregnancy; Pregnancy, Animal; Rats; Rats, Sprague-Dawley; Triglycerides
PubMed: 34791119
DOI: 10.1210/endocr/bqab231 -
Biology of Sex Differences Nov 2021Current methods fail to accurately predict women at greatest risk of developing fetal growth restriction (FGR) or related adverse outcomes, including stillbirth. Sexual...
BACKGROUND
Current methods fail to accurately predict women at greatest risk of developing fetal growth restriction (FGR) or related adverse outcomes, including stillbirth. Sexual dimorphism in these adverse pregnancy outcomes is well documented as are sex-specific differences in gene and protein expression in the placenta. Circulating maternal serum microRNAs (miRNAs) offer potential as biomarkers that may also be informative of underlying pathology. We hypothesised that FGR would be associated with an altered miRNA profile and would differ depending on fetal sex.
METHODS
miRNA expression profiles were assessed in maternal serum (> 36 weeks' gestation) from women delivering a severely FGR infant (defined as an individualised birthweight centile (IBC) < 3rd) and matched control participants (AGA; IBC = 20-80th), using miRNA arrays. qPCR was performed using specific miRNA primers in an expanded cohort of patients with IBC < 5th (n = 15 males, n = 16 females/group). Maternal serum human placental lactogen (hPL) was used as a proxy to determine if serum miRNAs were related to placental dysfunction. In silico analyses were performed to predict the potential functions of altered miRNAs.
RESULTS
Initial analyses revealed 11 miRNAs were altered in maternal serum from FGR pregnancies. In silico analyses revealed all 11 altered miRNAs were located in a network of genes that regulate placental function. Subsequent analysis demonstrated four miRNAs showed sexually dimorphic patterns. miR-28-5p was reduced in FGR pregnancies (p < 0.01) only when there was a female offspring and miR-301a-3p was only reduced in FGR pregnancies with a male fetus (p < 0.05). miR-454-3p was decreased in FGR pregnancies (p < 0.05) regardless of fetal sex but was only positively correlated to hPL when the fetus was female. Conversely, miR-29c-3p was correlated to maternal hPL only when the fetus was male. Target genes for sexually dimorphic miRNAs reveal potential functional roles in the placenta including angiogenesis, placental growth, nutrient transport and apoptosis.
CONCLUSIONS
These studies have identified sexually dimorphic patterns for miRNAs in maternal serum in FGR. These miRNAs may have potential as non-invasive biomarkers for FGR and associated placental dysfunction. Further studies to determine if these miRNAs have potential functional roles in the placenta may provide greater understanding of the pathogenesis of placental dysfunction and the differing susceptibility of male and female fetuses to adverse in utero conditions.
Topics: Circulating MicroRNA; Female; Fetal Growth Retardation; Humans; Male; Placenta; Pregnancy; Pregnancy Outcome; Sex Factors
PubMed: 34789323
DOI: 10.1186/s13293-021-00405-z -
The American Journal of Case Reports Nov 2021BACKGROUND When a woman becomes pregnant, the placenta produces human placental lactogen (hPL). The anti-insulin effect of hPL raises maternal blood glucose levels,...
BACKGROUND When a woman becomes pregnant, the placenta produces human placental lactogen (hPL). The anti-insulin effect of hPL raises maternal blood glucose levels, allowing the fetus to use glucose as a nutrient. Because hPL is produced by the placenta until delivery, insulin requirements in patients with gestational diabetes mellitus (GDM) typically increase, but in some cases, they may decrease. We retrospectively examined data from women with GDM who received insulin and delivered at our hospital. CASE REPORT From April 2019 to March 2020, we targeted patients who were diagnosed with GDM, received insulin, and delivered at our hospital. GDM was diagnosed based on the guidelines from the Japanese Society of Obstetrics and Gynecology. The rate of change in insulin dosage was calculated as: (insulin dosage at delivery - insulin dosage 14 days before delivery) divided by 14. Two patients whose insulin dosage was significantly reduced developed a syndrome of hemolysis, elevated liver enzymes, and low platelet count or acute fatty liver of pregnancy and underwent emergency cesarean section. CONCLUSIONS The present case report suggests that a decrease in insulin requirement in pregnant patients with GDM can predict maternal abnormalities due to placental dysfunction.
Topics: Blood Glucose; Cesarean Section; Diabetes, Gestational; Female; Hemolysis; Humans; Insulin; Liver; Placenta; Platelet Count; Pregnancy; Retrospective Studies
PubMed: 34744160
DOI: 10.12659/AJCR.933460 -
Advances in Anatomy, Embryology, and... 2021The female elephant shows a 3-week "follicular phase" to commence her 16-week estrous cycle at the end of which a second surge in pituitary luteinizing hormone (LH)...
The female elephant shows a 3-week "follicular phase" to commence her 16-week estrous cycle at the end of which a second surge in pituitary luteinizing hormone (LH) release matures and ovulates an ovarian follicle in association with estrous behavior and mating, whereas the first LH surge at the start of the follicular phase causes luteinization of 3-5 partially developed follicles. The prolonged pregnancy of 22 months is supported by a zonary endotheliochorial placenta which secretes placental lactogen (ePL) from around 40 days of gestation in association with replacement of the lumenal epithelium of the endometrium by trophoblast and the development of large corpora lutea (CLs) in the maternal ovaries from the previously formed luteinized follicles in response to the first LH peak early in the follicular phase. The zonary placenta develops above, rather than within, the endometrium. The elephant placenta secretes neither estrogens nor progestagens throughout gestation, as pregnancy maintenance relies on 5α-dihyroprogesterone and other 5α reduced progestagens secreted by secondary CLs stimulated by ePL and the stromal tissue of the fetal gonads, which become extremely enlarged during the second half of the 22-month pregnancy. In female fetuses, this ovarian enlargement includes the development and subsequent regression of multiple primary and secondary follicles with a consequent substantial decline in primary follicle numbers at birth. During the next 8-9 years of pre-pubertal life, however, oocyte and primary follicle numbers recover to levels near those found in late gestation, which may be evidence of postnatal oogenesis occurring in the elephant.
Topics: Animals; Corpus Luteum; Elephants; Female; Ovary; Placenta; Placentation; Pregnancy
PubMed: 34694482
DOI: 10.1007/978-3-030-77360-1_9 -
Journal of Medicine and Life 2021The purpose of the study was TO analyze the fetoplacental complex hormone levels and changes in their dynamics in pregnant women with miscarriage and the impact of these...
The purpose of the study was TO analyze the fetoplacental complex hormone levels and changes in their dynamics in pregnant women with miscarriage and the impact of these features on the subsequent course of pregnancy. Hormone levels were determined at different stages of gestation in 50 healthy women with a physiological course of pregnancy (control group) and 50 pregnant women with a history of miscarriage (main group). The women of the main group had a significantly slower rate of increase in hormones and a lag in quantitative indicators than the control group. The estradiol level indicators were 4.1 times (76.0%) and 2.89 times (65.5%) lower in women with miscarriage in the embryonic and late fetal period, respectively, compared to healthy women. Indicators of the level of placental lactogen and chorionic gonadotropin in the embryonic period in women with miscarriage were lower by 39.1% and 50.9%, respectively, compared to healthy women. In the late fetal period, the level of these hormones was lower by 72.9% and 35.4%, respectively. In the embryonic and late fetal periods, progesterone levels were lower by 67.4% and 68.4%, respectively, compared to the control group. The data obtained are evidence of a pronounced hormonal abnormality of the placenta, and hence a marker of fetoplacental dysfunction, which on the background of miscarriage develops at the early stages and continues to progress with the course of pregnancy.
Topics: Abortion, Spontaneous; Female; Hormones; Humans; Placenta; Placental Lactogen; Pregnancy; Pregnant Women; Progesterone
PubMed: 34621371
DOI: 10.25122/jml-2021-0089 -
Journal of Obstetrics and Gynaecology... Oct 2021Pregnancy is characterized by a series of metabolic changes that promote insulin resistance. This could be due to increase in the plasma levels of one or more...
INTRODUCTION
Pregnancy is characterized by a series of metabolic changes that promote insulin resistance. This could be due to increase in the plasma levels of one or more pregnancy-related hormones such as oestrogen, progesterone, prolactin, cortisol, and human placental lactogen (HPL). The increased insulin resistance in pregnancy is associated with development of diabetes which has implications for the future gestations also.
AIMS AND OBJECTIVES
To determine status of insulin resistance in pregnant women and correlate the presence of insulin resistance with obstetric outcome.
MATERIAL AND METHOD
A prospective cohort study was conducted in the Department of Obstetrics and Gynaecology, KGMU, Lucknow, over a period of one year. Total 150 pregnant women were enrolled from OPD, out of which 136 women were followed up till delivery. Insulin resistance was calculated by HOMA IR index, twice in whole antenatal period (first in early pregnancy and second in late pregnancy). All women were also tested for GDM by DIPSI test (plasma glucose value after 2 h of 75 gm glucose load irrespective of last meal) as per protocol.
RESULTS
In our study, we found 71 women out of 136 (52.2%) were GDM. Total 30 women out of 136 (22.05%) were GGI (Gestational Glucose Intolerance), and total 38 out of 136 (27.9%) women were found to have insulin resistance using HOMA IR ≥ 2 as cut off. Significant correlation was found in between BMI and insulin resistance ( = 0.001) and between GDM and insulin resistance ( = 0.001). Relative risk of development of complications like Preeclampsia, neonatal hypoglycemia, and respiratory distress syndrome was higher in women having insulin resistance and GDM.
CONCLUSION
Obstetric complications like preeclampsia, neonatal hypoglycemia, and respiratory distress syndrome are more likely to occur in women with insulin resistance, but larger studies are required to delineate whether insulin resistance alone without development of GDM will have the same implication.
PubMed: 34602761
DOI: 10.1007/s13224-021-01426-9 -
Molecular and Cellular Endocrinology Dec 2021Vasoinhibin is an antiangiogenic, profibrinolytic peptide generated by the proteolytic cleavage of the pituitary hormone prolactin by cathepsin D, matrix...
Vasoinhibin is an antiangiogenic, profibrinolytic peptide generated by the proteolytic cleavage of the pituitary hormone prolactin by cathepsin D, matrix metalloproteinases, and bone morphogenetic protein-1. Vasoinhibin can also be generated when placental lactogen or growth hormone are enzymatically cleaved. Here, it is investigated whether plasmin cleaves human prolactin and placental lactogen to generate vasoinhibin-like peptides. Co-incubation of prolactin and placental lactogen with plasmin was performed and analyzed by gel electrophoresis and Western blotting. Mass spectrometric analyses were carried out for sequence validation and precise cleavage site identification. The cleavage sites responsible for the generation of the vasoinhibin-like peptides were located at K170-E171 in prolactin and R160-T161 in placental lactogen. Various genetic variants of the human prolactin and placental lactogen genes are projected to affect proteolytic generation of the vasoinhibin-like peptides. The endogenous counterparts of the vasoinhibin-like peptides generated by plasmin may represent vasoinhibin-isoforms with inhibitory effects on vasculature and coagulation.
Topics: Cell Cycle Proteins; Fibrinolysin; Genetic Variation; HEK293 Cells; Humans; Mass Spectrometry; Peptides; Placental Lactogen; Prolactin; Proteolysis
PubMed: 34601001
DOI: 10.1016/j.mce.2021.111471 -
Biochemical and Biophysical Research... Nov 2021The liver increases its size during pregnancy to adapt to metabolic demand associated with pregnancy. Our previous study showed that proliferation of maternal...
The liver increases its size during pregnancy to adapt to metabolic demand associated with pregnancy. Our previous study showed that proliferation of maternal hepatocytes are increased during pregnancy in mice and that estradiol (E2) is one of the candidate hormones responsible for maternal hepatocyte proliferation. Here, we discovered that chorionic gonadotropin (CG) induces maternal hepatocyte proliferation during pregnancy. CG administration was sufficient to stimulate hepatocyte proliferation in non-pregnant mice as well as in cell culture system. We conclude that CG stimulates proliferation in the early pregnancy of maternal hepatocytes. In contrast, estrogen stimulates hepatocyte proliferation in the late pregnancy.
Topics: Aging; Animals; Cell Proliferation; Cells, Cultured; Chorionic Gonadotropin; Estradiol; Estrogens; Female; HEK293 Cells; Hep G2 Cells; Hepatocytes; Humans; Luteinizing Hormone; Mice; Mice, Inbred C57BL; Placenta; Pregnancy; Pregnancy, Animal; Protein Binding; Time Factors
PubMed: 34597993
DOI: 10.1016/j.bbrc.2021.09.039