DOCSLIB.ORG

The Fascinating and Complex Role of the Placenta in Pregnancy and Fetal Well-Being CEU Gwen Latendresse, CNM, Phd, Sandra Founds, CNM, Phd, FNP-BC

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Fascinating and Complex Role of the Placenta in Pregnancy and Fetal Well-Being CEU Gwen Latendresse, CNM, Phd, Sandra Founds, CNM, Phd, FNP-BC Journal of Midwifery & Women’s Health www.jmwh.org Original Review The Fascinating and Complex Role of the Placenta in Pregnancy and Fetal Well-being CEU Gwen Latendresse, CNM, PhD, Sandra Founds, CNM, PhD, FNP-BC Existing evidence implicates the placenta as the origin of some common pregnancy complications. Moreover, some maternal conditions, such as inadequate nutrition, diabetes, and obesity, are known to adversely affect placental function, with subsequent negative impact on the fetus and newborn. The placenta may also contribute to fetal programming with health consequences into adulthood, such as cardiovascular, metabolic, and mental health disorders. There is evidence that altered placental development, specifically impaired trophoblast invasion and spiral artery remodeling in the first trimester, is the origin of preeclampsia. Prenatal care providers who understand the relationships between placental health and maternal-newborn health can better inform and guide women to optimize health early in pregnancy and prior to conception. This article reviews the current understanding of placental function; placental contributions to normal fetal brain development and timing of birth; and impact of maternal nutrition, obesity, and diabetes on the placenta. J Midwifery Womens Health 2015;60:360–370 c 2015 by the American College of Nurse-Midwives. Keywords: fetal origins of adult disease, placenta, pregnancy INTRODUCTION pregnancy complications, such as preeclampsia and preterm The placenta is an amazing organ. Not only does it play birth. Implications for clinical practice are also addressed. avitalroleinthedeliveryofnutrientsandoxygentothe growing fetus, but also it contributes significantly to the hor- monal milieu of both mother and fetus during pregnancy. The PLACENTAL DEVELOPMENT word placenta originates from the Greek word plakoenta, meaning flat, slab-like object. The placenta is variously re- A brief review and overview of placental development dur- garded and dispatched based on cultural, societal, personal, ing pregnancy may assist the reader to better understand or institutional foundations; that is, some are planted un- how the placenta contributes to perinatal outcomes, such as der a tree, some are eaten, some are incinerated, and some preeclampsia and preterm birth (PTB), and how maternal receive ceremonial treatment and burial.1 Readers are re- conditions, such as diabetes and obesity, can negatively im- ferred to the companion article in this issue of the Journal pact placental function. of Midwifery & Women’s Health to learn more about the The fertilized ovum develops into the blastocyst by the contemporary Western trend in the practice of consuming fifth day postconception. The multistructured blastocyst con- one’splacenta(seeTable1).2,3 However, how much do we re- sists of the embryonic inner cell mass; a fluid-filled cavity; ally know about what the placenta does? and the surrounding trophectoderm, which becomes the pla- Prenatal and intrapartum care providers obtain essential centa. The trophectoderm bilayer is comprised of 2 types of knowledge and skills pertinent to the identification and ap- trophoblasts: the cytotrophoblast stem cells, some of which propriate management of placental abnormalities, such as pla- develop into the outermost layer of syncytiotrophoblasts. The centa previa and abruption. Midwives and other intrapartum blastocyst implants within the maternal decidua, and at 10 to care providers also inspect the placenta after the birth to 12 days postconception is encased in a mantle of syncytiotro- 4 ensure that it is intact and appears normal. However, in recent phoblasts (Figure 1). Lacunaearefluid-filledpocketsamong years the depth of knowledge regarding placental function has the syncytiotrophoblasts. These grow and eventually merge to expanded profoundly. Maternity care providers can benefit form the intervillous spaces that later fill with maternal blood. by increasing their awareness of new insights into placental The syncytiotrophoblast layer remains in direct contact with function and contributions to maternal and fetal outcomes. maternal blood throughout pregnancy. Syncytiotrophoblasts 4 This article 1) reviews current understanding of placental produce hormones as well as deliver nutrients to the fetus. development and function, including placental contributions At 12 days postconception, the cytotrophoblasts pro- to normal fetal brain development and stress response system; liferate and penetrate into the lacunar spaces (Figure 1). 2) describes the impact of nutrition, maternal obesity, and Approximately 2 days later, these cells grow laterally to form diabetes on placental function; and 3) explores existing ev- the cytotrophoblastic shell. These first developmental events Ͻ idence regarding the relationships between the placenta and occur in relatively hypoxic conditions ( 15 mm Hg pO2)that favor cell proliferation (multiplication of cells).5 Appropriate oxygen tension is critical to normal processes to establish a Address correspondence to Gwen Latendresse, CNM, PhD, University of healthy placenta and pregnancy. Cytotrophoblasts leaving Utah College of Nursing, 10 South 2000 East, Salt Lake City, UT 84112. the shell differentiate into extravillous trophoblasts (EVTs). E-mail: [email protected] Proliferative EVTs in cell columns anchor the placenta to 360 1526-9523/09/$36.00 doi:10.1111/jmwh.12344 c 2015 by the American College of Nurse-Midwives ✦ The placenta is a major source of steroid and peptide hormones, such as corticotropin-releasing hormone, which orches- trate the timing of birth, and serotonin, which is essential for fetal neurodevelopment. ✦ The origins of preeclampsia can be traced to inadequate trophoblast invasion and spiral artery remodeling in the placenta during the first trimester of pregnancy. ✦ The placenta may contribute to fetal programming for adult cardiovascular, metabolic, and mental health disorders by failing to protect the fetus from glucocorticoid overexposure. the maternal decidua. Endovascular EVTs form plugs in the to the hormonal environment for both mother and the de- maternal spiral arteries, maintaining the relatively hypoxic en- veloping fetus throughout pregnancy.5 This hormonal envi- vironment early in pregnancy. Deeper layers of decidua and ronment contributes to fetal brain development, continuance maternal blood vessels increase the oxygen tension, which of the pregnancy, labor initiation, and maturation of the fetal stimulates invasiveness of the EVTs migrating into maternal stress response via the hypothalamic-pituitary-adrenal (HPA) tissue.6 Interstitial EVTs invade the decidua and inner one- axis.5,15,18–20 third of the maternal myometrium to remodel 100 to 150 spi- ral arteries. The EVT plugs dissipate at 10 to 12 weeks’ ges- Role of Placental Hormones in Fetal Development tation, establishing early uteroplacental circulation and in- and Fetal Programming creased oxygenation. Remodeling continues in the myome- trial portion of maternal vessels until 20 to 22 weeks’ gestation Recent evidence indicates that placental production of to create low-resistance, high-flow funnels providing mater- some substances, such as serotonin, directly or indirectly nal blood to the intervillous spaces (Figure 2).4,7 contributes to fetal neurodevelopment or neuroprotection. The placenta is a vascular organ (Figure 3),8 which is ap- For example, the placenta synthesizes serotonin from its parent to clinicians upon delivery and inspection. The pla- precursor, tryptophan, which is obtained from maternal 21 cental vasculature begins to develop at 5 weeks’ gestation. dietary sources. Normal fetal brain development requires Bloodvesselsformfromvillousmesenchymalcellsunderthe serotonin, a neurotransmitter crucial for fetal forebrain 22 influence of growth factors, such as fibroblast growth fac- neurogenesis and interconnection between neurons. This tor and vascular endothelial growth factor (see Table 2).5,7,9 process begins early in gestation, with increasing concentra- Angiogenesis, the branching outgrowths of vessels, contin- tions of serotonin and serotonin receptors within the fetal ues throughout pregnancy, later forming capillary sprouts and brain. The fetal brain also selectively accumulates placentally loops that become the mature terminal placental villi.10,11 At derived serotonin over time. Data implicate sensitivity of the maternal–fetal interface, trophoblasts remodel maternal the fetal brain to placental serotonin. Disruptions in the spiral arteries. Meanwhile, vasculogenesis and angiogenesis fetal serotonin system are observed in association with an occur within the fetoplacental tissues. increased risk of serotonin-associated mental illness and behavioral abnormalities in offspring. The consequences of PLACENTAL FUNCTION disruption may extend into adulthood.21–23 The placenta plays several essential roles during pregnancy, Another example is the placental production of enzymes such as delivering nutrients to the growing fetus, exchang- that are often precursors to fetal neuroactive steroids syn- 24 ing oxygen and carbon dioxide, and serving as gatekeeper be- thesized in the placenta and the fetal brain. For example, tween the mother and fetus.12 The placenta is both a passive allopregnanolone is a neuroactive steroid known to provide filter and an active participant in these exchanges.13 neuroprotection to the fetus, but it requires placentally pro- Thegatekeeperroleincludesprotectionofthefetus duced 5-alpha reductase for
Load more

Recommended publications
  • Strategies to Increase ß-Cell Mass Expansion
    This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents .................................................................................................
    [Show full text]
  • Placental Growth Hormone-Related Proteins and Prolactin-Related Proteins
    Placental Growth Hormone-Related Proteins and Prolactin-Related Proteins The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Haig, D. 2008. Placental growth hormone-related proteins and prolactin-related proteins. Placenta 29: 36-41. Published Version doi:10.1016/j.placenta.2007.09.010 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11148777 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Placental growth hormone-related proteins and prolactin-related proteins. David Haig Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford Street, Cambridge MA 02138. e-mail: [email protected] phone: 617-496-5125 fax: 617-495-5667 Keywords: GH, PRL, placenta, endometrial glands, placental lactogen The placentas of ruminants and muroid rodents express prolactin (PRL)-related genes whereas the placentas of anthropoid primates express growth hormone (GH)-related genes. The evolution of placental expression is associated with acclerated evolution of the corresponding pituitary hormone and destabilization of conserved endocrine systems. In particular, placental hormones often evolve novel interactions with new receptors. The adaptive functions of some placental hormones may be revealed only under conditions of physiological stress. Introduction Placental hormones are produced by offspring, but act on receptors of mothers. As such, placental hormones and maternal receptors are prime candidates for the expression of parent-offspring conflict [1,2].
    [Show full text]
  • Pathophysiology of Gestational Diabetes Mellitus: the Past, the Present and the Future
    6 Pathophysiology of Gestational Diabetes Mellitus: The Past, the Present and the Future Mohammed Chyad Al-Noaemi1 and Mohammed Helmy Faris Shalayel2 1Al-Yarmouk College, Khartoum, 2National College for Medical and Technical Studies, Khartoum, Sudan 1. Introduction It is just to remember that “Pathophysiology” refers to the study of alterations in normal body function (physiology and biochemistry) which result in disease. E.g. changes in the normal thyroid hormone level causes either hyper or hypothyroidism. Changes in insulin level as a decrease in its blood level or a decrease in its action will cause hyperglycemia and finally diabetes mellitus. Scientists agreed that gestational diabetes mellitus (GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy. From our experience most women with GDM in the developing countries are not aware of the symptoms (i.e., the disease will be symptomless). While some of the women will have few symptoms and their GDM is most commonly diagnosed by routine blood examinations during pregnancy which detect inappropriate high level of glucose in their blood samples. GDM should be confirmed by doing fasting blood glucose and oral glucose tolerance test (OGTT), according to the WHO diagnostic criteria for diabetes. A decrease in insulin sensitivity (i.e. an increase in insulin resistance) is normally seen during pregnancy to spare the glucose for the fetus. This is attributed to the effects of placental hormones. In a few women the physiological changes during pregnancy result in impaired glucose tolerance which might develop diabetes mellitus (GDM). The prevalence of GDM ranges from 1% to 14% of all pregnancies depending on the population studied and the diagnostic tests used.
    [Show full text]
  • Fetal Growth Signals
    Arch Dis Child: first published as 10.1136/adc.64.1_Spec_No.53 on 1 January 1989. Downloaded from Archives of Disease in Childhood, 1989, 64, 53-57 Current topic Fetal growth signals R D G MILNER AND D J HILL Department of Paediatrics, Children's Hospital, Sheffield Human fetal growth is not uniform. Tissue patterns growth factor fi like peptide is found in the vegetal and organ primordia are established during embryo- pole ectoderm of the early Xenopus embryo and is genesis, then from the end of the first trimester and transcribed by a maternally derived gene designated throughout the second the fetus undergoes massive Vgl. An ectodermal cell line, XTC, from the meta- hyperplasia. In the third trimester further organ morphosing tadpole releases a transforming growth modelling and functional maturation occur in pre- factor I8 like peptide in vitro.5 In the 11-18 day fetal paration for extrauterine life. Each aspect ofdevelop- mouse transforming growth factor 3 can be detected ment requires orchestrated intercellular signalling at in bone and connective tissue, particularly that two levels. The release of peptide growth factors derived from neural crest such as palate, larynx, and the modulation of an extracellular matrix are facial mesenchyme, and teeth.6 Staining was most paracrine actions that occur within cell populations intense at sites of tissue morphogenesis affecting and between adjacent germ layers. In contrast, mesodermal and epithelial interaction such as hair endocrine hormones may stimulate growth non- follicles, teeth, and secondary palate. copyright. specifically or promote specific maturational events. Recently both fibroblast growth factor and trans- The interactions between paracrinology, endocrino- forming growth factor i have been shown to exert logy, and environmental constraints to growth remarkable effects on embryonal morphology.
    [Show full text]
  • The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones
    Placenlal Function and Fetal Nutrition, edited by Frederick C. Battaglia, Nestle Nutrition Workshop Series. Vol. 39. Nestec Ltd.. Vevey/Lippincott-Raven Publishers. Philadelphia. © 1997. The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones Lise Cedard U. 361 INSERM, Maternite Baudelocque, 121 Boulevard de Port-Royal Paris, France The placenta is classically considered to be a source of hormones that play an important role in the establishment and maintenance of pregnancy. Because of its hemochorial structure, the human placenta produces hormones and easily secretes them into the maternal circulation. They include steroid hormones, such as estrogens and progesterone, and protein hormones, the most important of which are the chori- onic gonadotrophins (hCG), discovered in 1927. During the period from 1960 to 1980, the concept of a fetoplacental unit (1) with a complementary role for the fetus in steroid production offered a new approach to steroid metabolism, and since then new proteins and neuropeptides have been discovered (2,3). However, the lack of innervation of placental tissue highlights the importance of understanding neuroen- docrine regulation of placental physiology. Sophisticated culture methods enabling the study of biologic phenomena occurring during transformation of cytotrophoblast cells into a syncytiotrophoblast (4) have been combined with electron microscopy and histochemistry. Possibilities offered by molecular biology, including in situ hybridization and molecular cloning studies,
    [Show full text]
  • Regulation of Glucokinase As Lslets Adapt to Pregnancy
    Matschinsky FM, Magnuson MA (eds): Glucokinase and Glycemic Disease: From Basics to Novel Therapeutics. Front Diabetes. Basel, Karger, 2004, vol 16, pp 222-239 Regulationof Glucokinaseas lsletsAdapt to Pregnancy RobertL. Sorenson,Anthony J. Weinhaus,T. Clark Brelje Department of Genetics Cell Biology and Development, University of Minnesota Medical School, Minneapolis,Minn., USA Pregnancyis an occasionin the life history of the B-cell where there is an increasedneed for insulinthat'occurs over a relativelyshort period of time. This amountsto daysin rodentsand monthsin humans.The needfor enhanced islet function emergesas a consequenceof an increasein peripheralinsulin resistanceat the sametime as the placenta,a major targetorgan for insulin, develops.To accommodatethis increasein insulin demand,the islet must undergochanges that lead to increasedinsulin secretionunder normal glucose conditions. The primary short-termregulation of insulin secretionis achievedby ele- vating the glucoseconcentration. However, if this were the primary adaptive mechanismsduring pregnancy,there would be a need for persistenthyper- glycemia- a conditiondeleterious to the developingembryo, fetus and mother. Thus, in the face of this increaseddemand for insulin, islets must undergo structuraland functional changes.The outcomeof this long term upregulation of isletsmust be enhancedinsulin secretion at normalglucose levels. Failure of this long-termadaptive process can lead to gestationaldiabetes. Evidence for functional changes in islets during pregnancy first appearedin the 1960sshortly after the developmentof a sensitiveradioimm- unoassayfor insulin. Spellacyand coworkers[1 3] reportedthat there was a progressiveincrease in both fasting and glucose-stimulatedinsulin secretion throughoutthe courseof pregnancy.These and subsequentstudies led to the charucterizationof pregnancyas a condition of elevatedserum insulin levels, slightly lower blood glucose levels and peripheralinsulin resistance(see reviews[4, 5]).
    [Show full text]
  • Hormonal Regulation of Fetal Growth
    Inrntuterine Growth Reianlaliim, edited by Jacques Senterre. Nestle Nutrition Workshop Scries, Vol. 18. Nestec Ltd.. Vevey/Raven Press. Ltd., New York © 1989. Hormonal Regulation of Fetal Growth Jean Girard Centre de Recherche sur la Nutrition (CNRS), 92190 Meudon-Bellevue, France The regulation of fetal growth is complex and still very poorly understood. It in- volves genetic factors, maternal nutrition and cardiovascular adaptations, placental growth and function, and to a lesser extent fetal factors, including fetal hormones. The influence of genetic, maternal, and placental factors on fetal growth has been reviewed recently (1) and will not be discussed. The purpose of this chapter is to analyze the specific role of endocrine factors in the determination of fetal growth, assuming that the nutritional supply to the placenta and to the fetus remains un- altered. The major endocrine factors involved in postnatal growth are: (a) growth hor- mone (GH) via the secretion of somatomedin; (b) thyroid hormones; (c) cortisol; and (d) sex steroids at puberty (2,3). Insulin is considered to have a merely permis- sive role in postnatal growth (2,3). In recent years, a body of evidence has accumu- lated to indicate that the fetus may be less dependent on pituitary and thyroid hormones for growth than the older organism, and more dependent on insulin and tissue growth factors. Studies on the endocrine regulation of fetal growth have in- volved several major approaches: ablation of fetal endocrine glands; examination of newborns with congenital endocrine deficiencies; treatment of fetuses with hor- mones; measurement of plasma hormone concentrations and tissue receptor levels during normal or abnormal growth; and in vitro studies of hormone effects on fetal tissues.
    [Show full text]
  • Hormonal Physiology of Childbearing: Evidence and Implications for Women, Babies, and Maternity Care
    Hormonal Physiology of Childbearing: Evidence and Implications for Women, Babies, and Maternity Care Sarah J. Buckley January 2015 Childbirth Connection A Program of the National Partnership for Women & Families About the National Partnership for Women & Families At the National Partnership for Women & Families, we believe that actions speak louder than words, and for four decades we have fought for every major policy advance that has helped women and families. Today, we promote reproductive and maternal-newborn health and rights, access to quality, affordable health care, fairness in the workplace, and policies that help women and men meet the dual demands of work and family. Our goal is to create a society that is free, fair and just, where nobody has to experi- ence discrimination, all workplaces are family friendly and no family is without quality, affordable health care and real economic security. Founded in 1971 as the Women’s Legal Defense Fund, the National Partnership for Women & Families is a nonprofit, nonpartisan 501(c)3 organization located in Washington, D.C. About Childbirth Connection Programs Founded in 1918 as Maternity Center Association, Childbirth Connection became a core program of the National Partnership for Women & Families in 2014. Throughout its history, Childbirth Connection pioneered strategies to promote safe, effective evidence-based maternity care, improve maternity care policy and quality, and help women navigate the complex health care system and make informed deci- sions about their care. Childbirth Connection Programs serve as a voice for the needs and interests of childbearing women and families, and work to improve the quality and value of maternity care through consumer engagement and health system transformation.
    [Show full text]
  • Disertasi Pengaruh Human Placental Lactogen, Leptin
    i DISERTASI PENGARUH HUMAN PLACENTAL LACTOGEN, LEPTIN, ASUPAN KALORI DAN IMT PRA-HAMIL TERHADAP PENINGKATAN MASSA LEMAK IBU DALAM KEHAMILAN Studi Terhadap Adaptasi Hemostasis Energi Dalam Kehamilan Sebagai Faktor Risiko Obesitas Pada Perempuan Dan Peranan Human Placental Lactogen Dalam Kesinambungan Suplai Nutrisi Maternal-Fetal THE INFLUENCE OF HUMAN PLACENTAL LACTOGEN, LEPTIN, CALORIE INTAKES AND PRE-PREGNANCY BMI ON BODY FAT MASS GAIN IN PREGNANT WOMEN A Study On Adaptation Of Maternal Energy Hemostasis During Pregnancy As The Risk Factor Of Obesity In Women And The Role Of Human Placental Lactogen In Continuity Of Fetal Nutrition. YUANITA ASRI LANGI P0200313022 SEKOLAH PASCASARJANA PROGRAM S3 ILMU KEDOKTERAN UNIVERSITAS HASANUDDIN MAKASSAR 2017 ii PENGARUH HUMAN PLACENTAL LACTOGEN, LEPTIN, ASUPAN KALORI DAN IMT PRA-HAMIL TERHADAP PENINGKATAN MASSA LEMAK IBU DALAM KEHAMILAN Studi Terhadap Adaptasi Hemostasis Energi Dalam Kehamilan Sebagai Faktor Risiko Obesitas Pada Perempuan Dan Peranan Human Placental Lactogen Dalam Kesinambungan Suplai Nutrisi Maternal-Fetal Disertasi Sebagai Salah Satu Syarat Untuk Mencapai Gelar Doktor Program Studi Ilmu Kedokteran Disusun dan diajukan oleh YUANITA ASRI LANGI P0200313022 Kepada SEKOLAH PASCASARJANA PROGRAM S3 ILMU KEDOKTERAN UNIVERSITAS HASANUDDIN MAKASSAR 2017 iii iv PERNYATAAN KEASLIAN DISERTASI Yang bertanda tangan di bawah ini : Nama : YUANITA ASRI LANGI Nomor Mahasiswa : P0200313022 Program Studi : Ilmu Kedokteran Menyatakan dengan sebenarnya bahwa disertasi yang saya tulis ini benar- benar
    [Show full text]
  • A Hormone Which Induces Insulin Resistance Is Increased in Normal Pregnancy
    Article in press - uncorrected proof J. Perinat. Med. 35 (2007) 513–521 • Copyright ᮊ by Walter de Gruyter • Berlin • New York. DOI 10.1515/JPM.2007.122 Resistin: a hormone which induces insulin resistance is increased in normal pregnancy Jyh Kae Nien1, Shali Mazaki-Tovi1,2, Roberto for resistin concentration were determined for five pre- Romero1,3,*, Juan Pedro Kusanovic1, Offer specified windows of gestational age. Plasma resistin Erez1, Francesca Gotsch1, Beth L. Pineles1, concentration was determined by immunoassay. Non- Lara A. Friel1,2, Jimmy Espinoza1,2, Luis parametric statistics were used for analysis. Goncalves1, Joaquin Santolaya1, Ricardo Results: The median maternal plasma concentration of Gomez4, Joon-Seok Hong1, Samuel Edwin1, resistin between 11 to 14 weeks of gestation in women Eleazar Soto1, Karina Richani1, Moshe Mazor5 of normal weight was significantly higher than non-preg- and Sonia S. Hassan1,2 nant women; the plasma concentration of resistin increased with gestational age. 1 Perinatology Research Branch, Intramural Division, Conclusions: Normal pregnant women have a higher NICHD/NIH/DHHS, Hutzel Women’s Hospital, median plasma concentration of resistin than non-preg- Bethesda, MD, and Detroit, MI, USA nant women and the concentration of this adipokine 2 Department of Obstetrics and Gynecology, Wayne increases with advancing gestation. Alterations in the State University/Hutzel Women’s Hospital, Detroit, maternal plasma concentration of resistin during MI, USA pregnancy could contribute to metabolic changes of 3 Center for Molecular Medicine and Genetics, Wayne pregnancy. State University, Detroit, MI, USA Keywords: Adipokines; nomogram; obesity; pregnancy; 4 Center for Perinatal Diagnosis and Research (CEDIP), resistin. Hospital Sotero del Rio, P.
    [Show full text]
  • EARLY DEVELOPMENT of BODY-WEIGHT REGULATION SYSTEMS in the NONHUMAN PRIMATE: in UTERO EFFECTS of HIGH-FAT DIET by Bernadette
    EARLY DEVELOPMENT OF BODY-WEIGHT REGULATION SYSTEMS IN THE NONHUMAN PRIMATE: IN UTERO EFFECTS OF HIGH-FAT DIET by Bernadette Elizabeth Grayson A DISSERTATION Presented to the Neuroscience Graduate Program and the Oregon Health & Science University School of Medicine in partial fulfillment of the requirements of the degree of Doctor of Philosophy April 2009 School of Medicine Oregon Health & Science University ___________________________________ CERTIFICATE OF APPROVAL ___________________________________ This is to certify that the Ph.D. dissertation of Bernadette Elizabeth Grayson has been approved ______________________________________ Mentor/Advisor - Kevin Grove, PhD ______________________________________ Chairman - Daniel Marks, PhD ______________________________________ Member - Cynthia Bethea, PhD ______________________________________ Member - M. Susan Smith, PhD TABLE OF CONTENTS TABLE OF CONTENTS ........................................................................................ i LIST OF FIGURES ................................................................................................ iii LIST OF TABLES .................................................................................................. v LIST OF ABBREVIATIONS ................................................................................. vi ACKNOWLEDGEMENTS .................................................................................... ix PREFACE…… ......................................................................................................
    [Show full text]
  • Human Placental Lactogen Administration in the Pregnant Rat: Acceleration of Fetal Growth
    003 1-399818812406-0663$02.00/0 PEDIATRIC RESEARCH Vol. 24, No. 6, 1988 Copyright O 1988 International Pediatric Research Foundation, Inc. Printed in U.S.A. Human Placental Lactogen Administration in the Pregnant Rat: Acceleration of Fetal Growth JAMES W. COLLINS, JR., SANDRA L. FINLEY, DANIEL MERRICK, AND EDWARD S. OGATA Departments of Pediatrics, Obstetrics and Gynecology, Northwestern University Medical School and Prentice Women's Hospital of Northwestern Memorial Hospital and Children's Memorial Hospital, Chicago, Illinois 60611 ABSTRACT. To determine whether administration of hu- servations suggest that placental lactogen may also directly stim- man placental lactogen (hPL) to pregnant rats during late ulate fetal growth. Ovine placental lactogen stimulates glycoge- gestation might enhance fetal growth, we implanted os- nesis in hepatocytes of the fetal rat (4) and sheep (5) and motically driven minipumps to provide 75 pg h PL/24 h on aminoisobutyric acid uptake in diaphragmatic muscle of the fetal day 14 of the rat's 21.5-day gestation. This substantially rat (6). It also stimulates ornithine decarboxylase activity in fetal increased maternal and fetal plasma hPL concentrations. rat liver (7) and somatomedin secretion in fetal and adult tissue By day 18, hPL fetuses were significantly heavier and had (8-10). Handwerger (11) has suggested that these and other larger placentas than controls. From this point until term, observations indicate a critical role for placental lactogen in not their rate of growth (1.20 g/24 h) significantly exceeded only indirectly but also directly stimulating normal fetal growth that of controls (0.95 g/24 h).
    [Show full text]