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Peter Wolf Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France
Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria

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Alexandre Dormoy Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Luigi Maione Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Sylvie Salenave Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Jacques Young Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Peter Kamenický Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Philippe Chanson Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d’Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l’Hypophyse, Le Kremlin-Bicêtre, France

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Introduction Acromegaly results in a clinical syndrome following increased serum concentrations of growth hormone (GH) and insulin-like growth factor-1 (IGF-1). If not adequately treated, GH excess is associated with increased morbidity and

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Krzysztof C Lewandowski Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland
Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland

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Justyna Płusajska Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland

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Wojciech Horzelski Faculty of Mathematics and Computer Science, University of Lodz, Lodz, Poland

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Ewa Bieniek Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland

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Andrzej Lewiński Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland
Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland

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out. Though it is widely accepted that PCOS is characterised by insulin resistance ( 4 ), there is no consensus, either regarding the best method of assessment of insulin resistance (IR) in PCOS, nor in terms of the utility of such assessment for

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Róża Aleksandrowicz Department of Prophylaxis of Metabolic Diseases, Bialystok, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland

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Marek Strączkowski Department of Prophylaxis of Metabolic Diseases, Bialystok, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland

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secretion of many peptides ( 1 ). Skeletal muscle is the main metabolic tissue that uptakes about 85% of glucose in response to insulin stimulation via the glucose transporter type 4 (GLUT4). Therefore, disorders associated with lower sensitivity of skeletal

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Alberto Battezzati International Center for the Assessment of Nutritional Status, DeFENS, University of Milan, Milan, Italy

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Andrea Foppiani International Center for the Assessment of Nutritional Status, DeFENS, University of Milan, Milan, Italy

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Gianfranco Alicandro Cystic Fibrosis Center, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda, Ospedale Maggiore Policlinico, University of Milan, Milan, Italy

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Arianna Bisogno Cystic Fibrosis Center, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda, Ospedale Maggiore Policlinico, University of Milan, Milan, Italy

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Arianna Biffi Cystic Fibrosis Center, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda, Ospedale Maggiore Policlinico, University of Milan, Milan, Italy

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Giorgio Bedogni Department of Medical and Surgical Sciences, Alma Mater Studiorum University of Bologna, Bologna, Italy
Internal Medicine, S. Maria delle Croci Hospital, AUSL Romagna, Ravenna, Italy

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Simona Bertoli International Center for the Assessment of Nutritional Status, DeFENS, University of Milan, Milan, Italy
Istituto Auxologico Italiano, IRCCS, Obesity Unit - Laboratory of Nutrition and Obesity Research, Department of Endocrine and Metabolic Diseases, Milan, Italy

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Giulia De Carlo International Center for the Assessment of Nutritional Status, DeFENS, University of Milan, Milan, Italy

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Erica Nazzari Cystic Fibrosis Center, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda, Ospedale Maggiore Policlinico, University of Milan, Milan, Italy

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Carla Colombo Cystic Fibrosis Center, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda, Ospedale Maggiore Policlinico, University of Milan, Milan, Italy

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Introduction Insulin secretory defects in cystic fibrosis (CF) were initially shown in small-sized studies that employed various sophisticated techniques such as the hyperglycemic clamp ( 1 , 2 , 3 ) and intravenous glucose tolerance test

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Monika Karczewska-Kupczewska Department of Internal Medicine and Metabolic Diseases, Medical University of Białystok, Białystok, Poland

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Agnieszka Nikołajuk Department of Prophylaxis of Metabolic Diseases, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland

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Magdalena Stefanowicz Department of Metabolic Diseases, Medical University of Białystok, Białystok, Poland

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Natalia Matulewicz Department of Metabolic Diseases, Medical University of Białystok, Białystok, Poland

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Irina Kowalska Department of Internal Medicine and Metabolic Diseases, Medical University of Białystok, Białystok, Poland

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Marek Strączkowski Department of Prophylaxis of Metabolic Diseases, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland

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observed in different populations ( 8 , 11 , 13 ). Systemic chemerin levels were also found to be associated with markers of fatty liver disease ( 12 ). The main pathophysiological factor of obesity-related metabolic complications is insulin resistance

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Jan W Eriksson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Reem A Emad Department of Pharmacy, Uppsala University, Uppsala, Sweden

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Martin H Lundqvist Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Niclas Abrahamsson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Maria C Kjellsson Department of Pharmacy, Uppsala University, Uppsala, Sweden

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Introduction Development of type 2 diabetes has been perceived as a process that involves progressive insulin resistance in muscles, adipose tissue, and liver and a gradual failure of pancreatic beta cells to secrete sufficient amounts of

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Rama Lakshman Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK

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Charlotte Boughton Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK
Cambridge University Hospitals NHS Foundation Trust, Wolfson Diabetes and Endocrine Clinic, Cambridge, UK

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Roman Hovorka Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK

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Introduction Over nine million people worldwide live with type 1 diabetes (T1D) ( 1 ). In this condition, immune-mediated destruction of pancreatic beta-cells leads to insulin deficiency and resultant hyperglycaemia. The management of T1D

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M Boering Isala, Diabetes Centre, Zwolle, The Netherlands

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P R van Dijk Isala, Diabetes Centre, Zwolle, The Netherlands
Isala, Department of Internal Medicine, Zwolle, The Netherlands

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S J J Logtenberg Diakonessenhuis, Department of Internal Medicine, Utrecht, The Netherlands
Langerhans Medical Research group, Zwolle, The Netherlands

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K H Groenier Isala, Diabetes Centre, Zwolle, The Netherlands
Department of General Practice, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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B H R Wolffenbuttel Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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R O B Gans Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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N Kleefstra Isala, Diabetes Centre, Zwolle, The Netherlands
Langerhans Medical Research group, Zwolle, The Netherlands
Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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H J G Bilo Isala, Diabetes Centre, Zwolle, The Netherlands
Isala, Department of Internal Medicine, Zwolle, The Netherlands
Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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Introduction Among type 1 diabetes mellitus (T1DM) patients, subcutaneous (SC) insulin administration is associated with low portal insulin concentrations and a consequent hepatic underinsulinization ( 1 ). Hepatic underinsulinization has been

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Jakob Høgild Langdahl Department of Clinical Genetics, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
Department of Endocrinology, Hospital of Southwest Jutland, Esbjerg, Denmark

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Anja Lisbeth Frederiksen Department of Clinical Genetics, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark

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John Vissing Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, Copenhagen, Denmark

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Morten Frost Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
Steno Diabetes Center Odense, Odense University Hospital, Odense, Denmark

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Knud Bonnet Yderstræde Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
Steno Diabetes Center Odense, Odense University Hospital, Odense, Denmark

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Per Heden Andersen Department of Endocrinology, Hospital of Southwest Jutland, Esbjerg, Denmark

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muscle is inversely correlated to age of diabetes debut ( 14 ). It is debated whether the impaired glucose metabolism in m.3243A>G carriers is characterized by insulin resistance, insulin secretion defect or a combination. The nuclear gene encoded

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Esben Thyssen Vestergaard Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Morten B Krag Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Morten M Poulsen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Steen B Pedersen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Niels Moller Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Jens Otto Lunde Jorgensen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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Niels Jessen Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark

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GHS-R is also located in peripheral tissues indicates that ghrelin also exerts direct peripheral effects (5, 6) . It has recently been reported that exogenous ghrelin causes insulin resistance (7, 8, 9, 10, 11) and induces lipolysis (7, 9, 10, 11

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