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David R Grattan Centre for Neuroendocrinology and Department of Anatomy, Maurice Wilkins Centre for Molecular Biodiscovery, University of Otago, PO Box 913, Dunedin 9054, New Zealand
Centre for Neuroendocrinology and Department of Anatomy, Maurice Wilkins Centre for Molecular Biodiscovery, University of Otago, PO Box 913, Dunedin 9054, New Zealand

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Introduction When Geoffrey Harris wrote his influential monograph on ‘Neural Control of the Pituitary Gland’, it was already apparent that prolactin, or ‘lactogenic hormone’ as he referred to it, might be controlled differently to the other

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Emma Castrique Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, Division of Molecular Neuroendocrinology, Department of Cellular and Molecular Medicine, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Marta Fernandez-Fuente Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, Division of Molecular Neuroendocrinology, Department of Cellular and Molecular Medicine, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Paul Le Tissier Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, Division of Molecular Neuroendocrinology, Department of Cellular and Molecular Medicine, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Andy Herman Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, Division of Molecular Neuroendocrinology, Department of Cellular and Molecular Medicine, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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Andy Levy Henry Wellcome Labs for Integrative Neuroscience and Endocrinology, Division of Molecular Neuroendocrinology, Department of Cellular and Molecular Medicine, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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the physical expansion of the pituitary during pregnancy and lactation ( Gonzalez et al . 1988 , Elster et al . 1991 , Dinc et al . 1998 , Chanson et al . 2001 ). Several morphometric studies have identified the prolactin (PRL) cell population

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Dominik Simon Botermann Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Nadine Brandes Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Anke Frommhold Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Ina Heß Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Alexander Wolff Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Arne Zibat Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Heidi Hahn Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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Rolf Buslei Institute of Pathology, Sozialstiftung Bamberg, Klinikum am Bruderwald, Bamberg, Germany

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Anja Uhmann Institute of Human Genetics, Molecular Developmental Genetics and Tumor Genetics Group, University Medical Center, Göttingen, Germany

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/adrenocorticotropic hormone- (Acth), somatotrophs/growth hormone- (Gh), prolactin- (Prl), thyroid-stimulating hormone-, luteinizing hormone-, follicle-stimulating hormone-secreting cells), the anterior lobe (AL) of the pituitary consists of Sox2 + (stem) cells and a meshwork

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Thomas G Hill Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, Churchill Hospital, University of Oxford, Oxford, UK

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Lorna I F Smith Diabetes Research Group, School of Cardiovascular and Metabolic Medicine and Sciences, King’s College London, London, UK

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Inmaculada Ruz-Maldonado Department of Internal Medicine (Endocrinology), Yale University, New Haven, Connecticut, USA

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Peter M Jones Diabetes Research Group, School of Cardiovascular and Metabolic Medicine and Sciences, King’s College London, London, UK

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James E Bowe Diabetes Research Group, School of Cardiovascular and Metabolic Medicine and Sciences, King’s College London, London, UK

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-cell adaptive changes during gestation are not fully understood. It is well established that the lactogenic hormones, prolactin (Prl) and placental lactogen (PL), play an important role in driving β-cell proliferation and increasing glucose-stimulated insulin

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Shona Wood Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK

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Andrew Loudon Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK

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-out of the seasonal response is seen in the expression of a seasonal pituitary prolactin rhythm, which is activated by long photoperiods, driving moult cycles in birds and mammals ( Fig. 1 ). In small short-lived mammals such as Siberian hamsters, LD

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L A Nolan Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK

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

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suckling does not take place, lactotroph mass returns to almost normal within 1–3 weeks, but remains slightly higher after pregnancy than in nulliparous rats, implying that pregnancy-induced changes in the size of the prolactin immunopositive population are

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Nadia Schoenmakers University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Kyriaki S Alatzoglou University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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V Krishna Chatterjee University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Mehul T Dattani University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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αGSU will only be detected in thyrotropes and gonadotropes ( Ericson et al . 1998 , Himes & Raetzman 2009 , Kelberman et al . 2009 ). The expression of GH and Prolactin ( Prl ) by E15.5 is the hallmark of the differentiation of somatotrope and

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Koichiro Taguchi Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Kazuo Kajita Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Yoshihiko Kitada Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Masayuki Fuwa Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Motochika Asano Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Takahide Ikeda Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Toshiko Kajita Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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Tatsuo Ishizuka Department of General Internal Medicine and Rheumatology, Gifu Municipal Hospital, Gifu, Japan

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Itaru Kojima Laboratory of Cell Physiology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan

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Hiroyuki Morita Department of General Internal Medicine, Gifu University Graduate School of Medicine, Gifu, Japan

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, expression levels of members of the prolactin family, prolactin family 2, subfamily c, member 3 ( Prl2c3: Plf ) and prolactin family 2, subfamily c, member 5 ( Prl2c5 ) were elevated only in SPA. On the other hand, microarray revealed that numerous adipocyte

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Sian J S Simpson Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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Lorna I F Smith Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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Peter M Jones Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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James E Bowe Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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organ, secreting numerous hormonal signals, which influence maternal and foetal physiology ( Jansson 2016 ). The lactogenic hormones, prolactin and placental lactogen, are important pregnancy-associated signals, well-established to act via β

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F Wahab Stem Cell Biology Unit, Laboratory of Reproductive Neuroendocrinology, Leibniz Institute for Primate Research, German Primate Center, Kellnerweg 4, D-37077 Göttingen, Germany

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M Shahab Stem Cell Biology Unit, Laboratory of Reproductive Neuroendocrinology, Leibniz Institute for Primate Research, German Primate Center, Kellnerweg 4, D-37077 Göttingen, Germany

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R Behr Stem Cell Biology Unit, Laboratory of Reproductive Neuroendocrinology, Leibniz Institute for Primate Research, German Primate Center, Kellnerweg 4, D-37077 Göttingen, Germany

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very recent study demonstrated an important role of prolactin in the lactation-induced suppression of KP release and reproduction ( Brown et al . 2014 ). Figure 3 A possible mechanism of lactation-induced suppression of the reproductive axis. Metabolic

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