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David M Golding School of Biosciences, Cardiff University, Cardiff, UK

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Daniel J Rees Institute of Life Sciences, College of Medicine, Swansea University, Swansea, UK

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Jennifer R Davies Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Dinko Relkovic Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Hannah V Furby Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Irina A Guschina School of Biosciences, Cardiff University, Cardiff, UK

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Anna L Hopkins School of Biosciences, Cardiff University, Cardiff, UK

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Jeffrey S Davies Institute of Life Sciences, College of Medicine, Swansea University, Swansea, UK

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James L Resnick Center for Mammalian Genetics, University of Florida, College of Medicine, Gainesville, Florida, USA

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Anthony R Isles Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Research Institute, Schools of Medicine & Psychology, Cardiff University, Cardiff, UK

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Timothy Wells School of Biosciences, Cardiff University, Cardiff, UK

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Introduction Prader–Willi syndrome (PWS) is caused by a lack of paternal gene expression from the 15q11–q13 imprinting cluster and results from large chromosomal deletions, chromosome 15 maternal uniparental disomy or imprinting-centre (IC

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0367
Volume/Issue:
Volume 232: Issue 1
Open access
Qinghua Wang State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China
Laboratory Animal Center, Nantong University, Nantong, Jiangsu, China

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Jing Tang State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China

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Shujun Jiang State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China
School of Traditional Chinese Medicine, China Pharmaceutical University, Nanjing, Jiangsu, China

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Zan Huang State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China
Laboratory of Gastrointestinal Microbiology, Jiangsu Key Laboratory of Gastrointestinal Nutrition and Animal Health, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, Jiangsu, China

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Anying Song State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China

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Siyuan Hou State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China

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Xiang Gao State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu, China

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Hai-Bin Ruan Department of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA

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2017 ). MAGEL2 and NECDIN are two of the five genes inactivated in Prader–Willi syndrome (PWS), a genetic condition that causes hyperphagia and severe obesity in affected children. Mice lacking the Magel2 gene phenocopy human PWS, being overweight

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DOI:
https://doi.org/10.1530/JOE-18-0349
Volume/Issue:
Volume 239: Issue 2
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A J Conley
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R M Bernstein Department of Population Health and Reproduction, Department of Anthropology, VM-PHR, School of Veterinary Medicine, University of California, Davis, Davis, California 95616, USA

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A D Nguyen
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hypogonadotropic hypogonadism, gonadotropins are elevated in boys with hypogonadism due to Prader–Willi syndrome ( Siemensma et al . 2011 ), and hypogonadism is associated with elevated DHEAS in these subjects ( Unanue et al . 2007 ). Similarly, gonadotropins are

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DOI:
https://doi.org/10.1530/JOE-11-0467
Volume/Issue:
Volume 214: Issue 2
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Katie Wynne Endocrine Unit, Imperial College Faculty of Medicine, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK

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Sarah Stanley Endocrine Unit, Imperial College Faculty of Medicine, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK

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Barbara McGowan Endocrine Unit, Imperial College Faculty of Medicine, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK

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Steve Bloom Endocrine Unit, Imperial College Faculty of Medicine, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK

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% ( Wren et al. 2001b ), and rising pre-prandial levels correlate with hunger scores in humans initiating meals spontaneously ( Cummings et al. 2004 ). The severe hyperphagia seen in Prader–Willi syndrome is associated with elevated ghrelin levels

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DOI:
https://doi.org/10.1677/joe.1.05866
Volume/Issue:
Volume 184: Issue 2
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Lucia Gajdosechova Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Katarina Krskova Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Ana Belen Segarra Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Andrea Spolcova Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Maciej Suski Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Rafal Olszanecki Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Stefan Zorad Institute of Experimental Endocrinology, Unit of Physiology, Institute of Organic Chemistry and Biochemistry, Chair of Pharmacology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia

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Research 33 625 – 633 . ( doi:10.1590/S0100-879X2000000600003 ) Hoybye C Barkeling B Espelund U Petersson M Thoren M 2003 Peptides associated with hyperphagia in adults with Prader–Willi syndrome before and during GH treatment . Growth

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https://doi.org/10.1530/JOE-13-0417
Volume/Issue:
Volume 220: Issue 3
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K Scrimgeour
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M J Gresham
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L R Giles Faculty of Veterinary Science, Department of Primary Industries, University of Sydney, Camden, New South Wales 2570, Australia

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P C Thomson
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P C Wynn
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R E Newman
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sensitivity in children with Prader–Willi syndrome . Journal of Clinical Endocrinology and Metabolism 91 1876 – 1881 . Pauly JE Scheving LE 1967 Circadian rhythms in blood glucose and the effect of different lighting schedules, hypophysectomy, adrenal

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DOI:
https://doi.org/10.1677/JOE-07-0627
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Volume 198: Issue 1
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Jie Xu Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA

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Shaonin Ji Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA

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Derwei Y Venable Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA

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John L Franklin Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA

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Joseph L Messina Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA

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1997 , Cuneo et al. 1998 ). Abdominal adiposity is prevalent in human diseases of impaired GH function, including Laron syndrome, a GH-resistant syndrome due to mutation of the GH receptor (GHR), and Prader-Willi syndrome in which there is diminished

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DOI:
https://doi.org/10.1677/joe.1.05977
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Volume 184: Issue 3
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Han Yan
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Matthew Mitschelen
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Georgina V Bixler Reynolds Oklahoma Center on Aging, Genome Sciences Facility, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, 975 NE 10th ST BRC 1305, Oklahoma City, Oklahoma 73104, USA

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Robert M Brucklacher Reynolds Oklahoma Center on Aging, Genome Sciences Facility, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, 975 NE 10th ST BRC 1305, Oklahoma City, Oklahoma 73104, USA

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Julie A Farley
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Song Han
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Willard M Freeman Reynolds Oklahoma Center on Aging, Genome Sciences Facility, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, 975 NE 10th ST BRC 1305, Oklahoma City, Oklahoma 73104, USA

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William E Sonntag
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. Histochemistry. Histochimie 37 161 – 168 . doi:10.1007/BF00305587 . Myers SE Whitman BY Carrel AL Moerchen V Bekx MT Allen DB 2007 Two years of growth hormone therapy in young children with Prader–Willi syndrome: physical and

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DOI:
https://doi.org/10.1530/JOE-11-0200
Volume/Issue:
Volume 211: Issue 1
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Mone Zaidi The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Maria I New The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Harry C Blair The Pittsburgh VA Medical Center and Departments of Pathology and of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

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Alberta Zallone Department of Histology, University of Bari, Bari, Italy

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Ramkumarie Baliram The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Terry F Davies The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Christopher Cardozo The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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James Iqbal The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Li Sun The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Clifford J Rosen Maine Medical Center Research Institute, Scarborough, Maine, USA

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Tony Yuen The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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secretion from the pituitary ( Kublaoui et al . 2008 , Zhang & Cai 2011 ). Fourth, patients affected by SIM1 gene mutation and by Prader–Willi syndrome, in whom hyperphagia and obesity are characteristic clinical features, displayed reduced numbers and

Article Type:
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DOI:
https://doi.org/10.1530/JOE-17-0680
Volume/Issue:
Volume 237: Issue 3
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P G Murray Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK

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C E Higham Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK

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P E Clayton Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK

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following conditions (with variation in licences between countries): chronic renal insufficiency (FDA approved in 1993), adult GHD (FDA approved in 1996), Turner syndrome (FDA approved in 1996), Prader–Willi syndrome (FDA approved in 2000), children born

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Review Article
DOI:
https://doi.org/10.1530/JOE-15-0120
Volume/Issue:
Volume 226: Issue 2
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