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Patricia Iozzo Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy

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Maria Angela Guzzardi Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy

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-specific insulin receptor density few days post-natally, followed by deficiency in insulin receptors and insulin-dependent glucose transporters (GLUT4) in the cortex and hypothalamus ( 70 ). Also the combination of high fat dieting and AD type pathology in mice is

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-19-0348
Volume/Issue:
Volume 8: Issue 11
Open access
Michaela Keuper Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

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. Journal of Clinical Endocrinology and Metabolism 2003 88 . ( https://doi.org/10.1210/jc.2002-021687 ) 128 Hotamisligil GS Murray DL Choy LN Spiegelman BM . Tumor necrosis factor alpha inhibits signaling from the insulin receptor . PNAS

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-19-0016
Volume/Issue:
Volume 8: Issue 6
Open access
Thomas Reinehr Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Alexandra Kulle Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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Juliane Rothermel Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Caroline Knop-Schmenn Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Nina Lass Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Christina Bosse Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Paul-Martin Holterhus Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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expression can be enhanced via an insulin-receptor substrate (IRS) 1- and 2-dependent pathway in different tissue types ( 27 ). Therefore, the elevated insulin concentrations in obesity could activate this enzymatic step, thus contributing to the observed

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0051
Volume/Issue:
Volume 6: Issue 4
Open access
Flavia Letícia Martins Peçanha Instituto de Bioquímica Médica Leopoldo de Meis, Laboratório de Adaptações Metabólicas, Programa de Bioquímica e Biofísica Celular, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Rio de Janeiro, Brazil

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Reinaldo Sousa dos Santos Instituto de Bioquímica Médica Leopoldo de Meis, Laboratório de Adaptações Metabólicas, Programa de Bioquímica e Biofísica Celular, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Rio de Janeiro, Brazil

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Wagner Seixas da-Silva Instituto de Bioquímica Médica Leopoldo de Meis, Laboratório de Adaptações Metabólicas, Programa de Bioquímica e Biofísica Celular, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Rio de Janeiro, Brazil

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,5,3′ Triiodo-L-thyronine stimulates 2-deoxy-D-glucose transport into L6 muscle cells through the phosphorylation of insulin receptor beta and the activation of PI-3k . Thyroid 2006 16 521 – 529 . ( doi:10.1089/thy.2006.16.521 ) 6 Lin Y Sun Z

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0059
Volume/Issue:
Volume 6: Issue 5
Open access
P G Murray Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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D Hanson Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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T Coulson Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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A Stevens Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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A Whatmore Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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R L Poole Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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D J Mackay Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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G C M Black Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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P E Clayton Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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Nakajima H Nakajima HO Field LJ . The CUL7 E3 ubiquitin ligase targets insulin receptor substrate 1 for ubiquitin-dependent degradation . Molecular Cell 2008 30 403 – 414 . ( doi:10.1016/j.molcel.2008.03.009 ). 10 Andrews P He YJ Xiong

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-13-0065
Volume/Issue:
Volume 2: Issue 4
Open access
Davoud Jafari-Gharabaghlou Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Mostafa Vaghari-Tabari Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Hajar Oghbaei Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran

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Laura Lotz Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany

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Reza Zarezadeh Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Yeganeh Rastgar Rezaei Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran

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Mahnaz Ranjkesh Medical Radiation Science Research Group (MRSRG), Tabriz University of Medical Sciences, Tabriz, Iran

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Mohammad Nouri Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Reproductive Biology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran

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Amir Fattahi Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany
Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

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Saba Nikanfar Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Ralf Dittrich Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany

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bind and activate the Toll-like receptor 4 ( 95 ) and also due to its insulin-mimetic activity, can bind the insulin receptor and cause insulin resistance and consequently regulate glucose levels ( 96 ). Based on the immunohistochemical findings

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-21-0288
Volume/Issue:
Volume 10: Issue 11
Open access
Jun-Xin Yan The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China

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Bin-Jing Pan The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China

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Ping-Ping Zhao The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China

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Li-Ting Wang The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China

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Jing-Fang Liu The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China

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Song-Bo Fu The First Clinical Medical College, Lanzhou University, Lanzhou, Gansu, China
Department of Endocrinology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China

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, this results in an accumulation of free fatty acids (FFAs) inside the liver (FFA), which aggravates insulin resistance by inhibiting insulin receptor signaling pathway. Finally, genetic and epidemiological factors, including diet, lifestyle

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0367
Volume/Issue:
Volume 10: Issue 12
Open access
Sakina H Bharmal School of Medicine, University of Auckland, Auckland, New Zealand

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Wandia Kimita School of Medicine, University of Auckland, Auckland, New Zealand

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Juyeon Ko School of Medicine, University of Auckland, Auckland, New Zealand

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Maxim S Petrov School of Medicine, University of Auckland, Auckland, New Zealand

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possible mechanisms of hyperinsulinaemia (i.e. downregulation of insulin receptors, differences in β -cell size and mass, altered hypothalamic and parasympathetic signalling pathways) warrant investigations in purposely designed mechanistic studies ( 31

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0229
Volume/Issue:
Volume 10: Issue 7
Open access
Chao Xu Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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Xiang-Fei Li Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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Hong-Yan Tian Department of Ocean Technology, College of Marine and Biology Engineering, Yancheng Institute of Technology, Yancheng, Province Jiangsu, China

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Hua-Juan Shi Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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Ding-Dong Zhang Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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Kenneth Prudence Abasubong Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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Wen-Bin Liu Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China

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the poor utilization of dietary carbohydrates by fish, including a relatively low number of insulin receptors, a poor capacity for hepatic lipogenesis from glucose, a higher potency of amino acids as insulin secretagogues than glucose and an imbalance

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0517
Volume/Issue:
Volume 8: Issue 3
Open access
Felix Reschke Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Torben Biester Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Thekla von dem Berge Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Dagmar Jamiolkowski Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Laura Hasse Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Francesca Dassie Padua University Hospital, Clinica Medica 3, Department of Medicine (DIMED), Padova, Veneto, Italy

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Pietro Maffei Padua University Hospital, Clinica Medica 3, Department of Medicine (DIMED), Padova, Veneto, Italy

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Katharina Klee Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Olga Kordonouri Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Hagen Ott Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Thomas Danne Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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the axillary region and the head and neck areas ( Fig. 4 and 5 ). The cause is thought to be an elevated insulin level due to a defect or absence of the insulin receptor, leading to keratinocyte proliferation. Acanthosis nigricans occurs hereditarily

Article Type:
Review Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-22-0410
Volume/Issue:
Volume 12: Issue 7
Open access