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Bethany R L Aykroyd Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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Simon J Tunster Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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Amanda N Sferruzzi-Perri Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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The placenta regulates materno-fetal nutrient transfer and secretes hormones that enable maternal physiological support of the pregnancy. In mice, these functions are performed by the labyrinth (Lz) and junctional (Jz) zones, respectively. Insulin-like growth factor 2 (Igf2) is an imprinted gene expressed by the conceptus that is important for promoting fetal growth and placenta formation. However, the specific role of Igf2 in the Jz in regulating placental endocrine function and fetal development is unknown. This study used a novel model to investigate the effect of conditional loss of Igf2 in the Jz (Jz-Igf2UE) on placental endocrine cell formation and the expression of hormones and IGF signaling components in placentas from female and male fetuses. Jz-Igf2UE altered gross placental structure and expression of key endocrine and signaling genes in a sexually dimorphic manner. The volumes of spongiotrophoblast and glycogen trophoblast in the Jz were decreased in placentas from female but not male fetuses. Expression of insulin receptor was increased and expression of the MAPK pathway genes (Mek1, P38α) decreased in the placental Jz of female but not male fetuses. In contrast, expression of the type-1 and -2 IGF receptors and the MAPK pathway genes (H-ras, N-ras, K-ras) was decreased in the placental Jz from male but not female fetuses. Expression of the steroidogenic gene, Cyp17a1, was increased and placental lactogen-2 was decreased in the placenta of both sexes. In summary, we report that Jz-Igf2UE alters the cellular composition, IGF signaling components and hormone expression of the placental Jz in a manner largely dependent on fetal sex.

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Simin Younesi School of Health and Biomedical Sciences RMIT University, Melbourne, Victoria, Australia

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Alita Soch School of Health and Biomedical Sciences RMIT University, Melbourne, Victoria, Australia
The Florey Institute of Neuroscience and Mental Health, Microscopy Facility, Melbourne, Victoria, Australia

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Luba Sominsky School of Health and Biomedical Sciences RMIT University, Melbourne, Victoria, Australia
Barwon Health Laboratory, Barwon Health, University Hospital, Geelong, Victoria, Australia
Institute for Physical and Mental Health and Clinical Transformation, School of Medicine, Deakin University, Geelong, Victoria, Australia

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Sarah J Spencer School of Health and Biomedical Sciences RMIT University, Melbourne, Victoria, Australia
ARC Centre of Excellence for Nanoscale Biophotonics, RMIT University, Melbourne, Victoria, Australia

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neonatal nutrition causes perturbations in hypothalamic neural circuits controlling reproductive function . Journal of Neuroscience 32 11486 – 11494 . ( https://doi.org/10.1523/JNEUROSCI.6074-11.2012 ) 10.1523/JNEUROSCI.6074-11.2012 Chan KA Jazwiec

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Hui Yu Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA

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Zoe Thompson Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA

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Sylee Kiran Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA
School of Literature, Science, and Arts, University of Michigan, Ann Arbor, Michigan, USA

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Graham L Jones Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA
Neuroscience Graduate Program, University of Michigan, Ann Arbor, Michigan, USA

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Lakshmi Mundada Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA

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Surbhi Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA

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Marcelo Rubinstein Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA
Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos, Buenos Aires, Argentina

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Malcolm J Low Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA

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2018a Leptin and brain-adipose crosstalks . Nature Reviews: Neuroscience 19 153 – 165 . ( https://doi.org/10.1038/nrn.2018.7 ) Caron A Dungan Lemko HM Castorena CM Fujikawa T Lee S Lord CC Ahmed N Lee CE Holland WL Liu C

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K L Davies Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK

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J Miles Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK

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E J Camm Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK
The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Australia

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D J Smith Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK

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P Barker MRC Metabolic Diseases Unit, Mouse Biochemistry Laboratory, Cambridge Biomedical Campus, Cambridge, UK

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K Taylor Endocrine Laboratory, Blood Sciences, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, UK

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A J Forhead Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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A L Fowden Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, UK

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hypothalamic-pituitary-adrenal axis: development, programming actions of hormones and maternal-fetal interactions . Frontiers in Behavioral Neuroscience 14 601939 . ( https://doi.org/10.3389/fnbeh.2020.601939 ) Sloboda DM Moss TJM Gurrin LC Challis

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Tatiane Aparecida Ribeiro Department of Biochemistry and Biomedical Science, McMaster University, Hamilton Ontario, Canada
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Audrei Pavanello Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Laize Peron Tófolo Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Júlio Cezar de Oliveira Institute of Health Sciences, Federal University of Mato Grosso, Sinop, Mato Grosso, Brazil

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Ana Maria Praxedes de Moraes Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Claudinéia Conationi da Silva Franco Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Kelly Valério Prates Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Isabela Peixoto Martins Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Kesia Palma-Rigo Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Rosana Torrezan Department of Physiologic Science, State University of Maringá – Maringá, Parana, Brazil

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Erica Yeo Department of Biochemistry and Biomedical Science, McMaster University, Hamilton Ontario, Canada

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Rodrigo Mello Gomes Laboratory of Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil

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Flávio Andrade Francisco Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Paulo Cezar de Freitas Mathias Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Ananda Malta Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil

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Miranda RA Palma-Rigo K , 2018 Treatment with soy isoflavones during early adulthood improves metabolism in early postnatally overfed rats . Nutritional Neuroscience 21 25 – 32 . ( https://doi.org/10.1080/1028415X.2016.1213007 ) Talaei M

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Ann R Finch Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Kathleen R Sedgley Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Christopher J Caunt Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Craig A McArdle Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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In heterologous expression systems, human GnRH receptors (hGnRHRs) are poorly expressed at the cell surface and this may reflect inefficient exit from the endoplasmic reticulum. Here, we have defined the proportion of GnRHRs at the cell surface using a novel assay based on adenoviral transduction with epitope-tagged GnRHRs followed by staining and semi-automated imaging. We find that in MCF7 (breast cancer) cells, the proportional cell surface expression (PCSE) of hGnRHRs is remarkably low (<1%), when compared with Xenopus laevis (X) GnRHRs (∼40%). This distinction is retained at comparable whole cell expression levels, and the hGnRHR PCSE is increased by addition of the XGnRHR C-tail (h.XGnRHR) or by a membrane-permeant pharmacological chaperone (IN3). The IN3 effect is concentration- and time-dependent and IN3 also enhances the hGnRHR-mediated (but not h.XGnRHR- or mouse GnRHR-mediated) stimulation of [3H]inositol phosphate accumulation and the hGnRHR-mediated reduction in cell number. We also find that the PCSE for hGnRHRs and h.XGnRHRs is low and is greatly increased by IN3 in two hormone-dependent cancer lines, but is higher and less sensitive to IN3 in a gonadotrope line. Finally, we show that the effect of IN3 on hGnRHR PCSE is not mimicked or blocked by two peptide antagonists although they do increase the PCSE for h.XGnRHRs, revealing that an antagonist-occupied cell surface GnRHR conformation can differ from that of the unoccupied receptor. The low PCSE of hGnRHRs and this novel peptide antagonist effect may be important for understanding GnRHR function in extrapituitary sites.

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K L Franko Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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D A Giussani Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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A J Forhead Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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A L Fowden Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

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Fetal glucocorticoids have an important role in the pre-partum maturation of physiological systems essential for neonatal survival such as glucogenesis. Consequently, in clinical practice, synthetic glucocorticoids, like dexamethasone, are given routinely to pregnant women threatened with pre-term delivery to improve the viability of their infants. However, little is known about the effects of maternal dexamethasone treatment on the glucogenic capacity of either the fetus or mother. This study investigated the effects of dexamethasone treatment using a clinically relevant dose and regime on glycogen deposition and the activities of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver and kidney of pregnant ewes and their fetuses, and of non-pregnant ewes. Dexamethasone administration increased the glycogen content of both the fetal and adult liver within 36 h of beginning treatment. It also increased G6Pase activity in the liver and kidney of the fetuses but not of their mothers or the non-pregnant ewes. Neither hepatic nor renal PEPCK activity was affected by dexamethasone in any group of animals. These changes in glycogen content and G6Pase activity were accompanied by rises in the plasma glucose and insulin concentrations and by a fall in the plasma cortisol level in the fetus and both groups of adult animals. In addition, dexamethasone treatment raised fetal plasma tri-iodothyronine (T3) concentrations and reduced maternal levels of plasma T3 and thyroxine, but had no effect on thyroid hormone concentrations in the non-pregnant ewes. These findings show that maternal dexamethasone treatment increases the glucogenic capacity of both the mother and fetus and has major implications for glucose availability both before and after birth.

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Galit Levi Dunietz Department of Neurology, Division of Sleep Medicine, University of Michigan, Ann Arbor, Michigan, USA

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Lucas J Tittle Department of Psychology, University of Michigan, Ann Arbor, Michigan, USA

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Sunni L Mumford Department of Biostatistics, Epidemiology and Informatics and Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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Louise M O’Brien Department of Neurology, Division of Sleep Medicine, University of Michigan, Ann Arbor, Michigan, USA
Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan, USA

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Ana Baylin Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA

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Enrique F Schisterman Department of Biostatistics, Epidemiology and Informatics and Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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Ronald D Chervin Department of Neurology, Division of Sleep Medicine, University of Michigan, Ann Arbor, Michigan, USA

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Larry J Young Center for Translational Social Neuroscience, Emory National Primate Research Center, Emory University, Atlanta, Georgia, USA
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA

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Bosch OJ Miklos S Torner L Wales L Waldherr M & Neumann ID 2008 Oxytocin reduces anxiety via ERK1/2 activation: local effect within the rat hypothalamic paraventricular nucleus . European Journal of Neuroscience 27 1947 – 1956 . ( https

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Isis Gabrielli Barbieri de Oliveira Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Marcos Divino Ferreira Junior Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Paulo Ricardo Lopes Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Dhiogenes Balsanufo Taveira Campos Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Marcos Luiz Ferreira-Neto Departament of Physiology, Institute of Biomedical Science, Laboratory of Electrophysiology and Cardiovascular Physiology, Federal University of Uberlândia, Uberlândia, Minas Gerais, Brazil

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Eduardo Henrique Rosa Santos Departament of Physiology, Institute of Biomedical Science, Laboratory of Electrophysiology and Cardiovascular Physiology, Federal University of Uberlândia, Uberlândia, Minas Gerais, Brazil

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Paulo Cezar de Freitas Mathias Department of Biotechnology, Genetics and Cell Biology, Laboratory of Secretion Cell Biology, State University of Maringá, Maringá, Paraná, Brazil

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Flávio Andrade Francisco Department of Biotechnology, Genetics and Cell Biology, Laboratory of Secretion Cell Biology, State University of Maringá, Maringá, Paraná, Brazil

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Bruna Del Vechio Koike Medical Department, Federal University of San Francisco Valley, Petrolina, Pernambuco, Brazil

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Carlos Henrique de Castro Department of Physiological Science, Integrative Laboratory of Cardiovascular and Neurological Pathophysiology, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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André Henrique Freiria-Oliveira Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Gustavo Rodrigues Pedrino Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Rodrigo Mello Gomes Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Daniel Alves Rosa Center of Neuroscience and Cardiovascular Research, Biological Science Institute, Federal University of Goiás, Goiânia, Goiás, Brazil

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Scheer FAJL Perusquía M Centurion D Buijs RM 2014 The suprachiasmatic nucleus is part of a neural feedback circuit adapting blood pressure response . Neuroscience 266 197 – 207 . ( https://doi.org/10.1016/j.neuroscience.2014.02.018 ) 24583038 10

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Hannah M Eggink Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands

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Lauren L Tambyrajah Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Rosa van den Berg Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Isabel M Mol Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Jose K van den Heuvel Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Martijn Koehorst Department of Pediatrics and Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands

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Albert K Groen Department of Pediatrics and Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
Department of Vascular Medicine, Amsterdam Diabetes Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Anita Boelen Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Andries Kalsbeek Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands

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Johannes A Romijn Department of Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Patrick C N Rensen Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Sander Kooijman Division of Endocrinology, Department of Medicine, Leiden University Medical Centre, Leiden, The Netherlands
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands

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Maarten R Soeters Department of Endocrinology and Metabolism, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

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Kalsbeek A Soeters MR Eggink HM 2017 Bile acid signaling pathways from the enterohepatic circulation to the central nervous system . Frontiers in Neuroscience 11 617 . 10.3389/fnins.2017.00617 29163019 Naqvi SH Nicholas HJ 1970 Conversion

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