physiology of steroids

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Physiology of steroids treatment for steroid induced hyperglycemia

Physiology of steroids

The natural steroid hormones are generally synthesized from cholesterol in the gonads and adrenal glands. These forms of hormones are lipids. They can pass through the cell membrane as they are fat-soluble, [5] and then bind to steroid hormone receptors which may be nuclear or cytosolic depending on the steroid hormone to bring about changes within the cell.

Steroid hormones are generally carried in the blood, bound to specific carrier proteins such as sex hormone-binding globulin or corticosteroid-binding globulin. Further conversions and catabolism occurs in the liver, in other "peripheral" tissues, and in the target tissues. A variety of synthetic steroids and sterols have also been contrived. Most are steroids, but some nonsteroidal molecules can interact with the steroid receptors because of a similarity of shape.

Some synthetic steroids are weaker or stronger than the natural steroids whose receptors they activate. Steroid hormones are transported through the blood by being bound to carrier proteins—serum proteins that bind them and increase the hormones' solubility in water.

Some examples are sex hormone-binding globulin SHBG , corticosteroid-binding globulin , and albumin. In order to be active, steroid hormones must free themselves from their blood-solubilizing proteins and either bind to extracellular receptors, or passively cross the cell membrane and bind to nuclear receptors. This idea is known as the free hormone hypothesis.

This idea is shown in Figure 1 to the right. One study has found that these steroid-carrier complexes are bound by megalin , a membrane receptor, and are then taken into cells via endocytosis. One possible pathway is that once inside the cell these complexes are taken to the lysosome, where the carrier protein is degraded and the steroid hormone is released into the cytoplasm of the target cell.

The hormone then follows a genomic pathway of action. This process is shown in Figure 2 to the right. In order for steroid hormones to cross the lipid bilayer of cells, they must overcome energetic barriers that would prevent their entering or exiting the membrane. Gibbs free energy is an important concept here. These hormones, which are all derived from cholesterol, have hydrophilic functional groups at either end and hydrophobic carbon backbones.

When steroid hormones are entering membranes free energy barriers exist when the functional groups are entering the hydrophobic interior of membrane, but it is energetically favorable for the hydrophobic core of these hormones to enter lipid bilayers. These energy barriers and wells are reversed for hormones exiting membranes.

Steroid hormones easily enter and exit the membrane at physiologic conditions. Though it is energetically more favorable for hormones to be in the membrane than in the ECF or ICF, they do in fact leave the membrane once they have entered it. This is an important consideration because cholesterol—the precursor to all steroid hormones—does not leave the membrane once it has embedded itself inside.

The difference between cholesterol and these hormones is that cholesterol is in a much larger negative Gibb's free energy well once inside the membrane, as compared to these hormones. This is because the aliphatic tail on cholesterol has a very favorable interaction with the interior of lipid bilayers.

There are many different mechanisms through which steroid hormones affect their target cells. All of these different pathways can be classified as having either a genomic effect or a non-genomic effect. Genomic pathways are slow and result in altering transcription levels of certain proteins in the cell; non-genomic pathways are much faster.

The first identified mechanisms of steroid hormone action were the genomic effects. Then the steroid binds to a specific steroid hormone receptor , also known as a nuclear receptor , which is a large metalloprotein. Upon steroid binding, many kinds of steroid receptors dimerize : two receptor subunits join together to form one functional DNA -binding unit that can enter the cell nucleus. Once in the nucleus, the steroid-receptor ligand complex binds to specific DNA sequences and induces transcription of its target genes.

Because non-genomic pathways include any mechanism that is not a genomic effect, there are various non-genomic pathways. However, all of these pathways are mediated by some type of steroid hormone receptor found at the plasma membrane. For more information on these proteins and pathways, visit the steroid hormone receptor page. From Wikipedia, the free encyclopedia. Substance with biological function. Estradiol , an important estrogen steroid hormone in both women and men.

Further information: Steroidogenesis. Notes and sources. Notes: "The concentration of a steroid in the circulation is determined by the rate at which it is secreted from glands, the rate of metabolism of precursor or prehormones into the steroid, and the rate at which it is extracted by tissues and metabolized.

The secretion rate of a steroid refers to the total secretion of the compound from a gland per unit time. Secretion rates have been assessed by sampling the venous effluent from a gland over time and subtracting out the arterial and peripheral venous hormone concentration.

The metabolic clearance rate of a steroid is defined as the volume of blood that has been completely cleared of the hormone per unit time. The production rate of a steroid hormone refers to entry into the blood of the compound from all possible sources, including secretion from glands and conversion of prohormones into the steroid of interest.

If there is little contribution of prohormone metabolism to the circulating pool of steroid, then the production rate will approximate the secretion rate. Recent Prog Horm Res. PMID Cortisol can diffuse across cell membranes and regulate target protein expression directly via glucocorticoid receptor GR or indirectly via other transcription factors e. Placental corticotropin-releasing hormone CRH is the major mediator of adaptive response to stressors during pregnancy.

Cortisol stimulates placental CRH expression, which regulates placental hormone levels e. Glucocorticoids coordinate many functions such as inflammatory and immune responses, metabolic homeostasis, cognitive function, reproduction, and development. At the cellular level, glucocorticoids exert their effects by binding to the GR that is almost ubiquitously expressed and induces target gene transcription.

The classical model of GR transactivation involves GR dimerization and binding at glucocorticoid response elements GREs leading to co-activator recruitment and activation of transcription from proximate promoters Pavek and Smutny, ; Whirledge and DeFranco, Increased cortisol levels in the placenta are linked to the induction of estrogen synthesis, which precedes the onset of parturition in human. CRH is the major mediator of adaptive response to stressors and is synthesized by several organs Koutmani et al.

During pregnancy, the CRH concentration in maternal plasma increases substantially and reaches levels that are 1,—10, times that of non-pregnant women. In humans and great apes CRH levels rise exponentially throughout pregnancy to peak at labor. Rodents, in contrast, do not exhibit placental CRH production Heussner et al. Placental CRH production may have evolved in primates to stimulate fetal ACTH release and adrenal steroidogenesis, in order to guarantee sufficient synthesis of DHEA, a precursor for placental sex hormone synthesis.

Concomitant stimulation of fetal cortisol and DHEA by placental CRH would couple the glucocorticoid effects on fetal organ maturation with the timing of parturition. While glucocorticoids inhibit hypothalamic CRH synthesis and secretion Frim et al. CRH operates via activation of two receptors, CRH-receptor type 1 and type 2 Grammatopoulos and Ourailidou, , which are expressed in the human placenta Florio et al.

Placental CRH exhibits many functions in pregnancy and parturition. To name a few, CRH modulates placental glucose transporter expression Gao et al. Progesterone is an inhibitor of CRH production Karalis et al. CRH is involved in the timing of birth by regulation of estrogen and progesterone levels as they control the contractile properties of the myometrium Majzoub and Karalis, ; Gangestad et al. Glucocorticoids are important during pregnancy and for fetal development.

Fetal glucocorticoid synthesis is only partially influenced by the HPA axis, but instead is primarily regulated by differential expression of the enzymes required for glucocorticoid synthesis. Moreover, maternal glucocorticoids can potentially cross the placenta. To enable pregnancy and ensure proper fetal development, glucocorticoid signaling occurs during three period of gestation: early in pregnancy to enable implantation, between week 7 and 14 to enable fetal-adrenal development, repress DHEA synthesis and enable female genital development and finally during the third trimester.

Fetal serum glucocorticoid levels must increase significantly before birth in order to ensure proper development of the lungs and several other organs Busada and Cidlowski, On the other hand, the fetus should not be exposed to excessive levels of glucocorticoids; this can suppress fetal growth and program the fetus for life-long diseases such as hypertension, glucose intolerance, diabetes, and strokes Moisiadis and Matthews, a , b ; Konstantakou et al.

CYP11B1 catalyzes deoxycorticosterone and deoxycortisol to corticosterone and cortisol, respectively. In line with this, Giannopoulos et al. Cortisol is required during early pregnancy for the establishment of gestation Michael and Papageorghiou, Cortisol levels in the maternal circulation rise toward term Goldkrand et al.

As steroid hormones use free diffusion to enter target cells, maternal cortisol reaches placental cells. Overexposure of the fetus to glucocorticoids during pregnancy reduces birth weight and can be detrimental to fetal development. Furthermore, cortisol stimulates hCG production in trophoblasts Wang et al. Nevertheless, the conversion of cortisol is incomplete and a fraction of cortisol remains unmetabolized Sun et al.

The energy-dependent drug-efflux pump ABCB1 may mediate export of glucocorticoids from cells Uhr et al. Studies in BeWo cells suggested that this transporter could contribute to the placental glucocorticoid barrier Mark and Waddell, Both are expressed in the human decidua and placenta and both are related to a number of pregnancy-associated complications.

These interesting studies have been extensively reviewed in a recent publication Konstantakou et al. Many of the underlying mechanisms causing altered expression of the enzymes remain to be explored, and additionally suspected correlations between altered enzyme expression and diseases such as GDM need to be confirmed.

Cholesterol, progesterone, estrogens, and cortisol are required to establish and maintain pregnancy and ensure healthy fetal development. The human placenta, located at the interface of maternal and fetal circulation, has an active role in biosynthesis, metabolism, and transport of these molecules.

Many enzymes and transporters are involved in these processes but our knowledge concerning their function and regulation is incomplete. The placental barrier is composed of trophoblast cells and pFECs. Few studies have addressed the role of pFECs in placental steroid handling. The functional interdependence of trophoblasts, pFECs, and fetal adrenal cells is incompletely understood.

The use of co-culture systems may significantly broaden our understanding. Diseases, but also external factors such as high fat diet or smoking alter the placental steroid metabolism. We need to explore these alterations and their potential consequences for fetus or mother. It should be kept in mind that the enzymes and transporters involved are regulated at multiple levels and by many endogenous molecules. Thus, whenever possible, mRNA levels, protein levels and posttranslational modifications should be examined Hudon Thibeault et al.

Likewise, when looking for changes in the concentration levels of steroids or other substances, subcellular fractionation should be considered in order not to miss important details Lassance et al. Apart from diseases, we are facing an ever-growing number of toxic substances in the environment. As the steroid metabolism of the human placenta is crucial for life long health of fetus and mother, we should be interested to understand their influence on the function of the human placenta.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. We thank Adi Ellinger and Enna Schepelmann for careful reading of the manuscript and we gratefully acknowledge the support of Thomas Nardelli and Adi Ellinger in preparing part of the artwork. Acikgoz, S. Levels of oxidized LDL, estrogens, and progesterone in placenta tissues and serum paraoxonase activity in preeclampsia.

Mediators Inflamm. Albrecht, C. Placental ABCA1 expression is reduced in primary antiphospholipid syndrome compared to pre-eclampsia and controls. Placenta 28, — Albrecht, E. Developmental increase in low density lipoprotein receptor messenger ribonucleic acid levels in placental syncytiotrophoblasts during baboon pregnancy. Endocrinology , — Alsat, E. Low-density lipoprotein binding sites in the microvillous membranes of human placenta at different stages of gestation.

Characterization of specific low-density lipoprotein binding sites in human term placental microvillous membranes. High density lipoprotein interaction with human placenta: biochemical and ultrastructural characterization of binding to microvillous receptor and lack of internalization. Arabin, B.

Pregnancy: an underutilized window of opportunity to improve long-term maternal and infant health-an appeal for continuous family care and interdisciplinary communication. Aye, I. Transport of lipids by ABC proteins: interactions and implications for cellular toxicity, viability and function. Acta , — Oxysterols inhibit differentiation and fusion of term primary trophoblasts by activating liver X receptors. Placenta 32, — Oxysterols exert proinflammatory effects in placental trophoblasts via TLR4-dependent, cholesterol-sensitive activation of NF-kappaB.

Baardman, M. The origin of fetal sterols in second-trimester amniotic fluid: endogenous synthesis or maternal-fetal transport? The role of maternal-fetal cholesterol transport in early fetal life: current insights. Babischkin, J. Estrogen stimulation of P cholesterol side-chain cleavage activity in cultures of human placental syncytiotrophoblasts.

Estrogen regulation of placental P cholesterol side-chain cleavage enzyme messenger ribonucleic acid levels and activity during baboon pregnancy. Bahn, R. Characterization of steroid production in cultured human choriocarcinoma cells. Baird, D. Formation of progesterone and pregnenolone from 4- 14 C cholesterol by the intact mid-term human foeto-placental unit perfused in vitro. Bansal, N. Cord blood lipoproteins and prenatal influences. Barker, D.

Placental programming of chronic diseases, cancer and lifespan: a review. Placenta 34, — Bartel, D. MicroRNAs: target recognition and regulatory functions. Cell , — Baumann, M. Belknap, W. Sterol synthesis and low density lipoprotein clearance in vivo in the pregnant rat, placenta, and fetus. Sources for tissue cholesterol during fetal development. Belo, L. Atherosclerosis , — Benirschke, K. Pathology of the Human Placenta. Benirschke, Heidelberg: Springer.

Bhattacharjee, J. Placenta 31, — Bicknell, A. The tissue-specific processing of pro-opiomelanocortin. Bilban, M. Trophoblast invasion: assessment of cellular models using gene expression signatures. Bjorkhem, I. Do oxysterols control cholesterol homeostasis? Blassberg, R. Lipid metabolism fattens up hedgehog signaling. BMC Biol. Bloch, K. The biological synthesis of cholesterol. Science , 19— Bloise, E. ATP-binding cassette transporters in reproduction: a new frontier. Update 22, — Blundell, C.

A microphysiological model of the human placental barrier. Lab Chip 16, — Placental drug transport-on-a-chip: a microengineered in vitro model of transporter-mediated drug efflux in the human placental barrier. Bodzek, P. Concentration of chosen oxycholesterols in plasma of pregnant women with pregnancy-induced hypertension. Wiad Lek 55 Suppl. PubMed Abstract Google Scholar. Boguslawski, W. HMG-CoA reductase activity in the microsomal fraction from human placenta in early and term pregnancy.

Bokslag, A. Preeclampsia; short and long-term consequences for mother and neonate. Early Hum. Bonenfant, M. Localization of type 1 17beta-hydroxysteroid dehydrogenase mRNA and protein in syncytiotrophoblasts and invasive cytotrophoblasts in the human term villi. Bonet, B. Metabolism of very-low-density lipoprotein triglyceride by human placental cells: the role of lipoprotein lipase. Metabolism 41, — Bose, H. Biochemistry 39, — Bose, P. High viral load and deregulation of the progesterone receptor signaling pathway: association with hepatitis E-related poor pregnancy outcome.

Brett, K. Maternal-fetal nutrient transport in pregnancy pathologies: the role of the placenta. Brownfoot, F. Soluble endoglin production is upregulated by oxysterols but not quenched by pravastatin in primary placental and endothelial cells. Placenta 35, — Burke, K. Expression and immunolocalisation of the endocytic receptors megalin and cubilin in the human yolk sac and placenta across gestation. Transport of maternal cholesterol to the fetus is affected by maternal plasma cholesterol concentrations in the golden Syrian hamster.

Lipid Res. Burton, G. Regulation of vascular growth and function in the human placenta. Reproduction , — Placental origins of Chronic disease. Nutrition of the human fetus during the first trimester—a review. Placenta 22 Suppl. A , S70—S Busada, J. Mechanisms of glucocorticoid action during development. Bussen, S. Influence of the vascular endothelial growth factor on the development of severe pre-eclampsia or HELLP syndrome.

Cao, C. Cao, G. Evidence for transcriptional control by steroidogenic factor 1. Cao, S. The effects of fungicides on human 3beta-Hydroxysteroid Dehydrogenase 1 and aromatase in human placental cell line JEG Pharmacology , — Cardoso, R. Steroidogenic versus metabolic programming of reproductive neuroendocrine, ovarian and metabolic dysfunctions. Neuroendocrinology , — Carter, A. Animal models of human placentation—a review. Placenta 28 Suppl. A , S41—S Placentation in mammals: definitive placenta, yolk sac, and paraplacenta.

Theriogenology 86, — Castro, M. Google Scholar. Catov, J. Early pregnancy lipid concentrations and spontaneous preterm birth. Cavender, C. Sterol metabolism in fetal, newborn, and suckled lambs and their response to cholesterol after weaning. Cerqueira, N. Cholesterol biosynthesis: a mechanistic overview. Biochemistry 55, — Cha, S. Molecular cloning and characterization of multispecific organic anion transporter 4 expressed in the placenta.

Challis, J. Current topic: the placental corticotrophin-releasing hormone-adrenocorticotrophin axis. Placenta 16, — Chigusa, Y. ATP-binding cassette transporter A1 expression is decreased in preeclamptic placentas. Collier, A. Assisted reproduction technologies impair placental steroid metabolism. Steroid Biochem. Connor, W. Placental transfer of cholesterolC into rabbit and guinea pig fetus. Costa, M. The endocrine function of human placenta: an overview. Online 32, 14— Coukos, G. Potential roles for the low-density-lipoprotein receptor family of proteins in implantation and placentation.

Cox, B. Placental transcriptome in development and pathology: expression, function, and methods of analysis. Cvitic, S. The human placental sexome differs between trophoblast epithelium and villous vessel endothelium.

PLoS One 8:e Desforges, M. Placental nutrient supply and fetal growth. Di Renzo, G. Progesterone in normal and pathological pregnancy. The role of progesterone in maternal and fetal medicine. Drolet, R. Human type 2 17 beta-hydroxysteroid dehydrogenase mRNA and protein distribution in placental villi at mid and term pregnancy.

Drwal, E. Co-culture of JEG-3, BeWo and syncBeWo cell lines with adrenal HR cell line: an alternative model for examining endocrine and metabolic properties of the fetoplacental unit. Cytotechnology 70, — Dube, E. Modulation of cholesterol transport by insulin-treated gestational diabetes mellitus in human full-term placenta. Duttaroy, A. Eades, C. Prevalence of gestational diabetes mellitus in Europe: a meta-analysis.

Diabetes Res. Edison, R. Adverse birth outcome among mothers with low serum cholesterol. Pediatrics , — Elustondo, P. Mitochondrial cholesterol import. Acta , 90— Enquobahrie, D. Differential placental gene expression in preeclampsia. Ermini, L. Statins, mevalonate pathway and its intermediate products in placental development and preeclampsia. Escobar, J. The protein kinase a pathway regulates CYP17 expression and androgen production in the human placenta.

The human placenta expresses CYP17 and generates androgens de novo. Esparza-Perusquia, M. Mitochondrial proteases act on STARD3 to activate progesterone synthesis in human syncytiotrophoblast. Esteve-Valverde, E.

Pravastatin for preventing and treating preeclampsia: a systematic review. Ethier-Chiasson, M. Evain-Brion, D. Human placenta as an endocrine organ. Growth Horm. IGF Res. A , S34—S Fahlbusch, F. Corticotropin-releasing hormone stimulates expression of leptin, 11beta-HSD2 and syncytin-1 in primary human trophoblasts.

Favari, E. Cholesterol efflux and reverse cholesterol transport. Florio, P. Human placenta, chorion, amnion and decidua express different variants of corticotropin-releasing factor receptor messenger RNA. Placenta 21, 32— Forbes, K. Statins are detrimental to human placental development and function; use of statins during early pregnancy is inadvisable. Cell Mol. Statins inhibit insulin-like growth factor action in first trimester placenta by altering insulin-like growth factor 1 receptor glycosylation.

Fournier, T. Role of nuclear receptors and their ligands in human trophoblast invasion. Fowden, A. Review: endocrine regulation of placental phenotype. Placenta 36 Suppl. French, A. Steroidbeta-sulfatase in fetal and placental tissues. Steroids 6, — Frim, D.

Differential regulation of corticotropin-releasing hormone mRNA in rat brain. Fukata, Y. Endocrine 46, — Furuhashi, M. Expression of low density lipoprotein receptor gene in human placenta during pregnancy. Gafvels, M. III Gallo, L. Review: placental transport and metabolism of energy substrates in maternal obesity and diabetes. Placenta 54, 59—67 doi: Gangestad, S. On the function of placental corticotropin-releasing hormone: a role in maternal-fetal conflicts over blood glucose concentrations.

Gao, L. Differential regulation of prostaglandin production mediated by corticotropin-releasing hormone receptor type 1 and type 2 in cultured human placental trophoblasts. Differential regulation of glucose transporters mediated by CRH receptor type 1 and type 2 in human placental trophoblasts. Endocrinology 3 , Geyer, J. The role of sulfated steroid hormones in reproductive processes.

Ghorashi, V. The relationship between serum concentration of free testosterone and pre-eclampsia. Giannopoulos, G. Glucocorticoid metabolism in human placenta, decidua, myometrium and fetal membranes. Go, G. Low-density lipoprotein receptor LDLR family orchestrates cholesterol homeostasis. Yale J. Gohner, C. The placenta in toxicology. Part IV: battery of toxicological test systems based on human placenta. Goldkrand, J. Maternal and fetal plasma cortisol levels at parturition.

Goodarzi, M. Polycystic ovary syndrome: etiology, pathogenesis and diagnosis. Grammatopoulos, D. CRH receptor signalling: potential roles in pathophysiology. Gratton, A. Steroid sulfatase is increased in the placentas and whole blood of women with early-onset preeclampsia. Placenta 48 Suppl. C , 72— Grigsby, P. Animal models to study placental development and function throughout normal and dysfunctional human pregnancy.

Grimes, R. Regulation of human placental trophoblast low-density lipoprotein uptake in vitro by estrogen. Grube, M. Organic anion transporting polypeptide 2B1 and breast cancer resistance protein interact in the transepithelial transport of steroid sulfates in human placenta.

Drug Metab. Hafez, S. Comparative placental anatomy: divergent structures serving a common purpose. Hahnova-Cygalova, L. Hakkola, J. Detection of cytochrome P gene expression in human placenta in first trimester of pregnancy. Halasz, M.

The role of progesterone in implantation and trophoblast invasion. Hanukoglu, I. Steroidogenic enzymes: structure, function, and role in regulation of steroid hormone biosynthesis. He, D. Different subcellular localization of sulphotransferase 2B1b in human placenta and prostate. He, G. Abnormal apoptosis of trophoblastic cells is related to the up-regulation of CYP11A gene in placenta of preeclampsia patients.

Hellig, H. Steroid production from plasma cholesterol. Conversion of plasma cholesterol to placental progesterone in humans. Henderson, Y. DNA Cell Biol. Henson, M. Pregnancy maintenance and the regulation of placental progesterone biosynthesis in the baboon. Update 4, — Effects of reduced maternal lipoprotein-cholesterol availability on placental progesterone biosynthesis in the baboon.

Regulation of placental low-density lipoprotein uptake in baboons by estrogen: dose-dependent effects of the anti-estrogen ethamoxytriphetol MER Hentschke, M. Is the atherosclerotic phenotype of preeclamptic placentas due to altered lipoprotein concentrations and placental lipoprotein receptors?

Role of a small-for-gestational-age phenotype. Herman, B. Enzyme Inhib. Herrera, E. Lipid metabolism in pregnancy and its consequences in the fetus and newborn. Endocrine 19, 43— Maternal lipid metabolism and placental lipid transfer. Hertig, A. Steroid profiling in preeclamptic women: evidence for aromatase deficiency.

Heussner, K. Placenta 37, 79— Hochberg, R. Simple and precise assay of the enzymic conversion of cholesterol into pregnenolone. Biochemistry 13, — Hu, Y. Differential expression of microRNAs in the placentae of Chinese patients with severe pre-eclampsia. Huang, X. Identification of placental nutrient transporters associated with intrauterine growth restriction and pre-eclampsia. BMC Genomics Hudon Thibeault, A. Fluoxetine and its active metabolite norfluoxetine disrupt estrogen synthesis in a co-culture model of the feto-placental unit.

Biochimie , 12— Huynh, J. A systematic review of placental pathology in maternal diabetes mellitus. Placenta 36, — Ian Mason, J. The 3beta-hydroxysteroid dehydrogenase gene family of enzymes. Trends Endocrinol. Ikonen, E. Mechanisms for cellular cholesterol transport: defects and human disease.

Ishibashi, O. Hydroxysteroid beta dehydrogenase 1 is dysregulated by miR and miRc that are aberrantly expressed in preeclamptic placentas: a novel marker for predicting preeclampsia. Hypertension 59, — Jeschke, U. Jetten, A. Retinoic acid-related Orphan Receptor gamma RORgamma : connecting sterol metabolism to regulation of the immune system and autoimmune disease.

Jira, P. Cholesterol metabolism deficiency. Jolibois, L. Effects of cadmium cell viability, trophoblastic development, and expression of low density lipoprotein receptor transcripts in cultured human placental cells. Jones, C. Ultrastructure of the normal human placenta. A re-appraisal of the morphophenotype and basal lamina coverage of cytotrophoblasts in human term placenta. Placenta 29, — Jones, S. Steroids modulate corticotropin-releasing hormone production in human fetal membranes and placenta.

Joshi, A. Placental ABC transporters: biological impact and pharmaceutical significance. Jurevics, H. Sources of cholesterol during development of the rat fetus and fetal organs. Kallen, C. Steroid hormone synthesis in pregnancy. Kamper, M. Estrogen-enhanced apical and basolateral secretion of apolipoprotein B by polarized trophoblast-derived BeWo cells.

Biochimie , — Kandutsch, A. Preputial gland tumor sterols. A metabolic pathway from lanosterol to cholesterol. Kang, J. Chemosphere , — Kantarci, S. Mutations in LRP2, which encodes the multiligand receptor megalin, cause Donnai-Barrow and facio-oculo-acoustico-renal syndromes. Kanungo, S. Sterol metabolism disorders and neurodevelopment-an update. Karalis, K. Cortisol blockade of progesterone: a possible molecular mechanism involved in the initiation of human labor.

Kawai, M. Placental endocrine disruption induced by cadmium: effects on P cholesterol side-chain cleavage and 3beta-hydroxysteroid dehydrogenase enzymes in cultured human trophoblasts. Keelan, J. ABCA1 and placental cholesterol efflux.

Kenis, I. Simvastatin has deleterious effects on human first trimester placental explants. Khamsi, F. The conversion of acetate to cholesterol in the fetus of the baboon and the transfer of cholesterol from mother to fetus. Endocrinology 91, 6— Kim, D. Human apolipoprotein E receptor 2. A novel lipoprotein receptor of the low density lipoprotein receptor family predominantly expressed in brain.

Kim, Y. Paraoxonase gene polymorphism, serum lipid, and oxidized low-density lipoprotein in preeclampsia. Kingdom, J. Development of the placental villous tree and its consequences for fetal growth. Knazicka, Z. Endocrine disruptive effects of cadmium on steroidogenesis: human adrenocortical carcinoma cell line NCI-HR as a cellular model for reproductive toxicity testing. Health A Tox. Knopp, R. Metabolic adjustments in normal and diabetic pregnancy. Konstantakou, P.

Dysregulation of 11beta-hydroxysteroid dehydrogenases: implications during pregnancy and beyond. Fetal Neonatal Med. Korber, M. Steryl ester synthesis, storage and hydrolysis: a contribution to sterol homeostasis. Korner, M. Pregnancy Hypertens. Koutmani, Y. Corticotropin-releasing hormone exerts direct effects on neuronal progenitor cells: implications for neuroprotection. Psychiatry 18, — Krazeisen, A. Determination of cDNA, gene structure and chromosomal localization of the novel human 17beta-hydroxysteroid dehydrogenase type 7 1.

FEBS Lett. Labrie, F. Lafond, J. Presence of CLA-1 and HDL binding sites on syncytiotrophoblast brush border and basal plasma membranes of human placenta. Placenta 20, — Lamon-Fava, S. Statins and lipid metabolism: an update. Landers, K. Transthyretin uptake in placental cells is regulated by the high-density lipoprotein receptor, scavenger receptor class B member 1.

Landschulz, K. Regulation of scavenger receptor, class B, type I, a high density lipoprotein receptor, in liver and steroidogenic tissues of the rat. Lang, I. Immunohistochemical evidence for the heterogeneity of maternal and fetal vascular endothelial cells in human full-term placenta.

Cell Tissue Res. Heterogeneity of microvascular endothelial cells isolated from human term placenta and macrovascular umbilical vein endothelial cells. Cell Biol. Human fetal placental endothelial cells have a mature arterial and a juvenile venous phenotype with adipogenic and osteogenic differentiation potential. Differentiation 76, — Larkin, J. The influence of ligand-activated LXR on primary human trophoblasts.

Lassance, L. Obesity-induced down-regulation of the mitochondrial translocator protein TSPO impairs placental steroid production. Lasuncion, M. Mechanism of the HDL2 stimulation of progesterone secretion in cultured placental trophoblast. Leduc, L. Oxidized low-density lipoproteins in cord blood from neonates with intra-uterine growth restriction. Leeder, J. Variability of CYP3A7 expression in human fetal liver. Levitan, I. Oxidized LDL: diversity, patterns of recognition, and pathophysiology.

Redox Signal. Levkovitz, R. In vitro simulation of placental transport: part I. Biological model of the placental barrier. In vitro simulation of placental transport: part II. Glucose transfer across the placental barrier model. Li, Y. Expression of 3beta-hydroxysteroid dehydrogenase type 1, P aromatase, and 17beta-hydroxysteroid dehydrogenase types 1, 2, 5 and 7 mRNAs in human early and mid-gestation placentas.

Placenta 26, — Lin, D. Placental transfer of cholesterol into the human fetus. Lindegaard, M. Endothelial and lipoprotein lipases in human and mouse placenta. Linton, M. SR-BI: a multifunctional receptor in cholesterol homeostasis and atherosclerosis. Liu, L. Expression and clinical significance of ATP-binding cassette transporter 1 in serum and placental tissue in Chinese patients with preeclampsia.

Liu, S. Pharmacology 97, — Lou, H. Assisted reproductive technologies impair the expression and methylation of insulin-induced gene 1 and sterol regulatory element-binding factor 1 in the fetus and placenta. Luo, J. Routes and mechanisms of post-endosomal cholesterol trafficking: a story that never ends.

Traffic 18, — Madsen, E. Human placenta secretes apolipoprotein Bcontaining lipoproteins. Maezawa, K. Majzoub, J. Placental corticotropin-releasing hormone: function and regulation. Makedou, K. Oxidized low-density lipoprotein and adiponectin levels in pregnancy. Malassine, A. A comparison of placental development and endocrine functions between the human and mouse model.

Update 9, — Maliqueo, M.

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Additionally, cholesterol is also a precursor for placental progesterone and estrogen synthesis. Placental estrogen synthesis requires delivery of sulfate-conjugated precursor molecules from fetal and maternal serum. Maternal-fetal glucocorticoid transport has to be tightly regulated in order to ensure healthy fetal growth and development. This article also summarizes the impact of diverse compounds and diseases on the expression level and activity of the involved transporters, receptors, and metabolizing enzymes and concludes that the regulatory mechanisms changing the physiological to a pathophysiological state are barely explored.

The structure and the cellular composition of the human placental barrier are introduced. While steroid production, metabolism and transport in the placental syncytiotrophoblast have been explored for decades, few information is available for the role of placental-fetal endothelial cells in these processes. With regard to placental structure and function, significant differences exist between species. The pituitary and the adrenal cortex.

Elsevier; Accessed Oct. Grennan D, et al. Steroid side effects. Saag KG, et al. Major side effects of systemic glucocorticoids. Major side effects of inhaled glucocorticoids. Roberts WN, et al. Joint aspiration or injection in adults: Complications. Nieman LK.

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Giant cell arteritis Glomerulonephritis Hip labral tear How do I reduce fatigue from rheumatoid arthritis? How to treat baby eczema Hyperinflated lungs: What does it mean? Hypopituitarism I have atopic dermatitis. How can I sleep better? Interstitial lung disease Is depression a factor in rheumatoid arthritis? Is there a multiple sclerosis diet? Juvenile idiopathic arthritis Knee bursitis Knee pain LABAs for asthma Living better with atopic dermatitis eczema Living better with rheumatoid arthritis Long-term safety of natalizumab for treating multiple sclerosis Managing anxiety in MS: What works?

Mayo Clinic Minute: Prevent migraines with magnetic stimulation Mayo Clinic Minute Weathering migraines Mayo Clinic Minute: What parents need to know about pink eye Medication overuse headaches Migraine Migraine medications and antidepressants Migraine treatment: Can antidepressants help?

Migraines and Vertigo Migraines: Are they triggered by weather changes? Alleviating migraine pain Mindfulness practice: Can it reduce symptoms of MS? Mixed connective tissue disease Mononucleosis Mononucleosis: Can it recur? Mononucleosis and Epstein-Barr: What's the connection? MSM for arthritis pain: Is it safe? Myasthenia gravis Nasal Cleaning Nasal spray addiction: Is it real? Ocular migraine: When to seek help Oil of oregano: Can it treat sinusitis?

Oral lichen planus Osteoporosis and long-term prednisone: What is the risk? Ozone air purifiers Palindromic rheumatism: Precursor to rheumatoid arthritis? Paraneoplastic syndromes of the nervous system Personalized therapy for multiple sclerosis MS Pink eye conjunctivitis Pink eye: How long is it contagious? Pink eye treatment: What if I wear contact lenses? Plantar fasciitis Pneumonitis Polymyalgia rheumatica Polymyositis Polymyositis: Can it affect my lungs?

Prednisone withdrawal: Why taper down slowly? Preeclampsia Preterm labor Protect your joints while housecleaning Pseudoclaudication: Is it related to claudication? Ramsay Hunt syndrome Reactive airway disease: Is it asthma? Rheumatoid arthritis and exercise Rheumatoid arthritis: Vaccines Rheumatoid arthritis diet Rheumatoid arthritis: Can it affect the eyes?