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Marenao Tana Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
Tanaka Medical Clinic, Yoichi, Japan

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Tomohito Gohda Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan

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Nozomu Kamei Department of Endocrinology and Metabolism, Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital, Hiroshima, Japan
Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan

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Maki Murakoshi Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan

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Tatsuya Sato Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine, Sapporo, Japan

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Mitsunobu Kubota Department of Endocrinology and Diabetology, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan

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Michiyoshi Sanuki Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan

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Erika Ishiwata Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan

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Keisuke Endo Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan

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Yusuke Suzuki Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan

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Masato Furuhashi Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan

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biomarker of glomerular damage ( 17 , 42 ). It has also been reported that exposure of kidney organ culture to TNFR1 or TNFR2 increases apoptosis mainly in tubules ( 43 ) and that individual knockout mouse models of TNFR1 or TNFR2 have a delay in the

Article Type:
Research Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-24-0343
Volume/Issue:
Volume 13: Issue 11
Open access
Jairo Arturo Pinzón-Cortés Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia
School of Medicine, Universidad de los Andes, Bogotá, Colombia

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Angelina Perna-Chaux Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia

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Nicolás Steven Rojas-Villamizar Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia

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Angélica Díaz-Basabe Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia

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Diana Carolina Polanía-Villanueva Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia

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María Fernanda Jácome Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia

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Carlos Olimpo Mendivil School of Medicine, Universidad de los Andes, Bogotá, Colombia
Endocrinology Section, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, Colombia

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Helena Groot Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia
School of Medicine, Universidad de los Andes, Bogotá, Colombia

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Valeriano López-Segura Biological Sciences Department, Laboratory of Human Genetics, Universidad de los Andes, Bogotá, Colombia
School of Medicine, Universidad de los Andes, Bogotá, Colombia

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methylation, which may induce changes in the gene expression that favor the development of many features of the diabetes phenotype and of end-organ complications ( 14 , 15 ). In a rat model of type 1 diabetes mellitus (T1DM), Williams and coworkers ( 16

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0199
Volume/Issue:
Volume 6: Issue 8
Open access
Min Li Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

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Ying Chen Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

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Jingjing Jiang Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

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Yan Lu Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

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Zhiyi Song Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Shengjie Zhang CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China

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Chao Sun CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China

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Hao Ying CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China

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Xiaofang Fan Department of Endocrinology and Metabolism, Minhang Branch, Zhongshan Hospital, Central Hospital of Minhang District, Shanghai Minhang Hospital, Fudan University, Shanghai, China

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Yuping Song Department of Endocrinology and Metabolism, Minhang Branch, Zhongshan Hospital, Central Hospital of Minhang District, Shanghai Minhang Hospital, Fudan University, Shanghai, China

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Jialin Yang Department of Endocrinology and Metabolism, Minhang Branch, Zhongshan Hospital, Central Hospital of Minhang District, Shanghai Minhang Hospital, Fudan University, Shanghai, China

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Lin Zhao Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

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insulin, free T 3 , free T 4 and TSH concentrations were measured by using electrochemiluminescence assays (Modular E170, Roche). The homeostasis model assessment of insulin resistance index (HOMA_IR) was calculated as fasting insulin (μIU/ml) × fasting

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-19-0175
Volume/Issue:
Volume 8: Issue 6
Open access
Jan-Bernd Stukenborg NORDFERTIL Research Lab Stockholm, Pediatric Endocrinology Unit, Department of Women’s and Children’s Health, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Kirsi Jahnukainen NORDFERTIL Research Lab Stockholm, Pediatric Endocrinology Unit, Department of Women’s and Children’s Health, Karolinska Institutet and University Hospital, Stockholm, Sweden
Division of Haematology-Oncology and Stem Cell Transplantation, Children’s Hospital, University of Helsinki, Helsinki University Central Hospital, Helsinki, Finland

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Marsida Hutka MRC Centre for Reproductive Health, The Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, UK

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Rod T Mitchell MRC Centre for Reproductive Health, The Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, UK
Edinburgh Royal Hospital for Sick Children, Edinburgh, UK

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affected by cancer and its treatment. We will describe the experimental models that can be used to assess somatic cell function and discuss studies that have attempted to preserve fertility in males, which may involve manipulation of the somatic cells in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-17-0382
Volume/Issue:
Volume 7: Issue 2
Open access
Lei Lei Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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Yi-Hua Bai Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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Hong-Ying Jiang Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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Ting He Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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Meng Li Department of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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Jia-Ping Wang Department of Radiology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China

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.1080/15548627.2015.1042195 ) 20 Patra KC Wang Q Bhaskar PT Miller L Wang Z Wheaton W Chandel N Laakso M Muller WJ Allen EL Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0328
Volume/Issue:
Volume 10: Issue 10
Open access
Brenda Anguiano Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Querétaro, México

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Carlos Montes de Oca Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Querétaro, México

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Evangelina Delgado-González Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Querétaro, México

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Carmen Aceves Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Querétaro, México

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physiological supply of T3 reduced prostate tumor weight and epithelial PCNA levels in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model. These effects could be directly related to both an increase in T3 and a reduction in T4 levels as a result

Article Type:
Review Article
Collections:
Thyroid
DOI:
https://doi.org/10.1530/EC-21-0581
Volume/Issue:
Volume 11: Issue 2
Open access
Xue-Lian Zhang Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Xinyi Zhao Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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Yong Wu Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wen-qing Huang Department of Transfusion Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China

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Jun-jiang Chen Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Peijie Hu Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wei Liu Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Yi-Wen Chen Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Jin Hao Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Rong-Rong Xie Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Hsiao Chang Chan Epithelial Cell Biology Research Center, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China

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Ye Chun Ruan Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Hui Chen Cell-Gene Therapy Translational Medicine Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China

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Jinghui Guo Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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diabetes, the depressor arm has been found to exert a protective role ( 5 ). Ang(1–7) prevents systolic hypertension and attenuates kidney fibrosis in the type 1 diabetes mouse model ( 6 ). Long-term administration of Ang(1–7) prevents heart and lung

Article Type:
Research Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-21-0357
Volume/Issue:
Volume 11: Issue 1
Open access
A Daniel Bird Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia

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Spencer Greatorex Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia

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David Reser Department of Physiology, Monash University, Melbourne, Victoria, Australia

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Gareth G Lavery Institute of Metabolism and Systems Research, 2nd Floor IBR Tower, University of Birmingham, Birmingham, UK
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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Timothy J Cole Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia

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common laboratory rodent models makes characterisation of these new genes much more difficult and loss-of-functional analysis almost impossible. We have therefore extended our understanding of HSD11B1L expression, and tissue and cell localisation by

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0119
Volume/Issue:
Volume 6: Issue 7
Open access
Susana Pastor Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain
Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Abdelmounaim Akdi Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Eddy R González Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Juan Castell Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Josefina Biarnés Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Ricard Marcos Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain
Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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Antonia Velázquez Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain
Grup de Mutagènesi, CIBER Epidemiología y Salud Pública, Servei de Medicina Nuclear, Unidad de Endocrinología, Departament de Genètica i de Microbiologia, Facultat de Biociències, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Barcelona, Spain

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together with a study using mouse models with deleted Thra and Thrb genes support the tumour suppressor functions of the TR genes (20) . Three studies have reported the association of genetic variants in the THRA gene with thyroid cancer risk, but

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-12-0017
Volume/Issue:
Volume 1: Issue 2
Open access
Taísa A R Vicente
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Ívina E S Rocha
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Roberto Salvatori Division of Endocrinology, Division of Endocrinology, National Research Council, Federal University of Sergipe, Aracaju, Sergipe 49060-100, Brazil

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Carla R P Oliveira
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Rossana M C Pereira
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Anita H O Souza
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Viviane C Campos
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Elenilde G Santos
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Rachel D C Araújo Diniz
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Eugênia H O Valença
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Carlos C Epitácio-Pereira
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Mario C P Oliveira
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Andrea Mari Division of Endocrinology, Division of Endocrinology, National Research Council, Federal University of Sergipe, Aracaju, Sergipe 49060-100, Brazil

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Manuel H Aguiar-Oliveira
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metabolism and growth: studies of a novel mouse model combining lactogen resistance and growth hormone deficiency . Endocrinology 2005 146 103 – 112 . ( doi:10.1210/en.2004-0744 ). * (These authors contributed equally to this work)

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-13-0014
Volume/Issue:
Volume 2: Issue 2
Open access