Estrogens in Pregnancy

doi:10.1016/S0083-6729(08)60522-1

Vitamins & Hormones

Volume 35, 1978, Pages 109-147

https://doi.org/10.1016/S0083-6729(08)60522-1 Get rights and content

Publisher Summary

This chapter discusses the estrogens in pregnancy. A notable characteristic of normal human pregnancy is the extensive production of a variety of biologically active substances. These include (1) the protein hormones human chorionic gonadotropin and human placental lactogen, (2) the enzymes heat-stable alkaline phosphatase and diamine oxidase, and (3) the progestational and estrogenic steroid hormones. Considerable interest has been generated in the biosynthesis, production rate, metabolic clearance, and relationship to the status of the pregnancy of each of these substances. However, the estrogens have evoked the greatest interest. Estrogen synthesis in pregnancy is highly complex, involving interaction with the placenta of precursors made by specific organs of the fetus and mother. A deeper appreciation of the qualitative and quantitative aspects of estrogen synthesis in pregnancy may be gained from comparison with the nonpregnant state. Because the placenta is particularly rich in the enzyme activities responsible for estrogen synthesis and a limitless supply of fresh tissue is available to interested investigators, it is not unexpected that there is a copious literature on the isolation and purification of these enzymes.

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Does exercise during pregnancy impact organs or structures of the maternal-fetal interface?
2021, Tissue and Cell
Citation Excerpt :
A coordinated interdependence of maternal, placental and fetal circulation is necessary for oestrogen synthesis from its precursor, cholesterol. The placenta is devoid of the enzyme dehydroepiandrosterone sulphate and 16 alpha-hydroxy-dehydroepiandrosterone sulphate necessary for the synthesis of different kinds of oestrogens (Levitz and Young, 1978). Instead, the placenta benefits from the availability of these enzymes within fetal and maternal circulation (Levitz and Young, 1978).
Exercise during pregnancy has been shown to be associated with improved health outcomes both during and after pregnancy for mother and fetus across the lifespan. Increasing physical activity and reducing sedentary behaviour during pregnancy have been recommended by many researchers and clinicians-alike. It is thought that the placenta plays a central role in mediating any positive or negative pregnancy outcomes. The positive outcomes obtained through prenatal exercise are postulated to result from exercise-induced regulation of maternal physiology and placental development. Considerable research has been performed to understand the placenta's role in pregnancy-related diseases, such as preeclampsia, fetal growth restriction, and gestational diabetes mellitus. However, little research has examined the potential for healthy lifestyle and behavioural changes to improve placental growth, development, and function. While the placenta represents the critical maternal-fetal interface responsible for all gas, nutrient, and waste exchange between the mother and fetus, the impact of exercise during pregnancy on placental biology and function is not well known. This review will focus on prenatal exercise and its promising influence on the structures of the maternal-fetal interface, with particular emphasis on the placenta. Potential molecular mechanistic hypotheses are presented to aid future investigations of prenatal exercise and placental health.
Passively acquired lupus in the fetus and neonate
2021, Lahita’s Systemic Lupus Erythematosus
In 1%–18% of pregnancies, fetal exposure to maternal anti-SSA/Ro and anti-SSB/La autoantibodies transported across the placenta via FcγRn can result in a spectrum of injury referred to as neonatal lupus. Disease in the offspring may be independent of the maternal health status as often the mother has no previous history of any autoimmune or rheumatic disorder. The classic manifestations include cardiac injury in utero and a cutaneous rash in the neonatal period though other organ systems may be affected as well. The antibodies associating with injury are reactive with an intracellular target, providing a rare opportunity to evaluate pathways leading to autoimmune-mediated tissue injury and to translate these findings to management. This chapter extensively covers the epidemiology, clinical spectrum, proposed pathogenesis, biomarkers, and guidelines for prevention and therapy, taking into account new advances from the bench and bedside, including the introduction of home monitoring.
The association between maternal lipid profile after birth and offspring risk of autism spectrum disorder
2021, Annals of Epidemiology
Citation Excerpt :
This observed inverse association between LDL concentration and ASD may be a result of abnormal maternal lipid regulation in obese gravidas. Under physiologic pregnancy conditions, the placental production of estrogen progressively increases with gestational age [25]. The rise in estrogen suppresses peripheral lipoprotein lipase activities [15].
Maternal obesity has been consistently associated with offspring risk for ASD, as well as lipid metabolism derangements. However, few ASD studies have examined maternal lipids in conjunction with maternal prepregnancy body mass index (BMI).
This nested case-control study was based on the Boston Birth Cohort, a prospective cohort study of mother-child dyads recruited at the Boston Medical Center. Maternal blood samples were collected shortly after delivery and analyzed for total plasma cholesterol, HDL, and triglyceride (TG) concentrations. Low-density lipoprotein (LDL) was subsequently calculated by the Friedewald equation. Cases were identified using ASD diagnoses in children’s medical records. The odds of ASD were estimated with continuous lipid levels for a linear relationship, and we further explored the nonlinear relationship using the tertile of each lipid analyte with the highest tertile as the reference group. Logistic regression was used to estimate the risk of ASD adjusting for potential confounders. The analyses were performed separately for mothers with normal weight and overweight/obese based on maternal prepregnancy BMI.
One standard deviation decrease in postpartum maternal LDL was associated with increased odds of ASD aOR 1.35 [1.04–1.75]. There was no association between postpartum maternal HDL and TG levels and ASD risk. Decreasing levels of LDL were not associated with ASD risk in normal-weight mothers (aOR 1.2 [0.83–1.75]), but the ASD risk was more pronounced in overweight and obese mothers (aOR 1.54 [1.03–2.27]). Follow-up analysis of nonlinear association models showed that, when compared to the highest tertile, lower maternal LDL concentrations were associated with approximately two times increased risk of ASD (first tertile: aOR 2.49 [1.27–4.87] and second tertile: aOR 2.79 [1.42–5.48]). A similar pattern was observed with overweight/obese mothers but not in normal-weight mothers.
Lower maternal postpartum plasma LDL concentration was associated with increased odds of ASD in offspring among children born to overweight and obese mothers. Our findings suggest that both maternal BMI and lipids should be considered in assessing their role in offspring ASD risk, and additional longitudinal studies are needed to better understand maternal lipid dynamics during pregnancy among normal-weight and overweight/obese mothers.
Functional significance of lymphocytes in pregnancy and lymphocyte immunotherapy in infertility: A comprehensive review and update
2020, International Immunopharmacology
During pregnancy, the fetal-maternal interface underlies several dynamic alterations to permit the fetus to be cultivated and developed in the uterus, in spite of being identifies by the maternal immune system. A large variety of decidual leukocyte populations, including natural killer cells, NKT cells, innate lymphoid cells, dendritic cells, B cells, T cells, subpopulations of helper T cells play a vital role in controlling the trophoblast invasion, angiogenesis as well as vascular remodeling. In contrast, several regulatory immunosuppressive mechanisms, including regulatory T cells, regulatory B cells, several cytokines and mediators are involved in maintain the homeostasis of immune system in the fetal-maternal interface. Nonetheless, aberrant alterations in the balance of immune inflammatory or immunosuppressive arms have been associated with various pregnancy losses and infertilities. As a result, numerous strategies have been developed to revers dysregulated balance of immune players to increase the chance of successful pregnancy. Lymphocyte immunotherapy has been developed through utilization of peripheral white blood cells of the husband or others and administered into the mother to confer an immune tolerance for embryo’s antigens. However, the results have not always been promising, implying to further investigations to improve the approach. This review attempts to clarify the involvement of lymphocytes in contributing to the pregnancy outcome and the potential of lymphocyte immunotherapy in treatment of infertilities with dysregulated immune system basis.
Essential oils disrupt steroidogenesis in a feto-placental co-culture model
2019, Reproductive Toxicology
Citation Excerpt :
Moreover, it has been recently reported that neonicotinoids thiaclopid and thiamethoxam also possesses this non-monotonic effect in H295R cells [31]. During pregnancy, estriol is a unique estrogen that is produced by the placenta from a fetal androgen precursor, 16α-DHEA-sulfate, which is produced by the fetal liver [67,68]. Fetal hepatic 16α-hydroxylation is mediated by the cytochrome P450 enzyme CYP3A7.
We determined whether 5 common essential oils (basil, fennel seed, orange, black pepper and sage) interfered with feto-placental steroidogenesis in a co-culture model composed of fetal-like adrenocortical (H295R) and placental trophoblast-like (BeWo) cells. After a 24 h exposure, only basil and fennel seed oil significantly increased hormone concentrations of estradiol, estrone, dehydroepiandrosterone (DHEA), androstenedione, progesterone, and estriol. Basil and fennel seed oil were shown to significantly alter the expression of steroidogenic enzymes involved in cholesterol transport and steroid hormone biosynthesis, including StAR, CYP11A1, 3β-HSD1/2, SULT2A1, and HSD17β1, -4, and -5. Also, basil and fennel seed oil stimulated placental-specific promoter I.1 and pII-derived CYP19 mRNA in BeWo and H295R cells, respectively, as well as, increased CYP19 enzyme activity. Our results indicate that further study is necessary to determine the potential risks of using basil and fennel seed oils during pregnancy considering their potential to disrupt steroidogenic enzyme activity and expression in vitro.
Serotonin-estrogen interactions: What can we learn from pregnancy?
2019, Biochimie
Citation Excerpt :
In the former, which compose the chorionic villi, cells fuse and form an endocrine–active multinucleated syncytium, the syncytiotrophoblast cells while in the latter, cells invade the maternal decidua to regulate blood flow [285–288]. The human villous trophoblasts produce a large quantity of estrogens, as well as 5-HT, making it an interesting model to study 5-HT-estrogen interaction [289–291]. Pregnancy has been known for a long time to be a hyperestrogenic state [289].
We have reviewed the scientific literature related to four diseases in which to serotonin (5-HT) is involved in the etiology, herein named 5-HT-linked diseases, and whose prevalence is influenced by estrogenic status: depression, migraine, irritable bowel syndrome and eating disorders. These diseases all have in common a sex-dimorphic prevalence, with women more frequently affected than men. The co-occurrence between these 5-HT-linked diseases suggests that they have common physiopathological mechanisms. In most 5-HT-linked diseases (except for anorexia nervosa and irritable bowel syndrome), a decrease in the serotonergic tone is observed and estrogens are thought to contribute to the improvement of symptoms by stimulating the serotonergic system. Human pregnancy is characterized by a unique 5-HT and estrogen synthesis by the placenta. Pregnancy-specific disorders, such as hyperemesis gravidarum, gestational diabetes mellitus and pre-eclampsia, are associated with a hyperserotonergic state and decreased estrogen levels. Fetal programming of 5-HT-linked diseases is a complex phenomenon that involves notably fetal-sex differences, which suggest the implication of sex steroids. From a mechanistic point of view, we hypothesize that estrogens regulate the serotonergic system, resulting in a protective effect against 5-HT-linked diseases, but that, in turn, 5-HT affects estrogen synthesis in an attempt to retrieve homeostasis. These two processes (5-HT and estrogen biosynthesis) are crucial for successful pregnancy outcomes, and thus, a disruption of this 5-HT-estrogen relationship may explain pregnancy-specific pathologies or pregnancy complications associated with 5-HT-linked diseases.

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Estrogens in Pregnancy

Publisher Summary

Steroids

Am. J. Obstet. Gynecol.

J. Biol. Chem.

Lancet

Am. J. Obstet. Gynecol.

J. Biol. Chem.

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J. Steroid Biochem.

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