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Yasminye D Pettway Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA

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Diane C Saunders Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA

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Marcela Brissova Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA

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-threatening hypoglycemia via the actions of glucagon on peripheral organs, thereby opposing the peripheral effects of β cell-derived insulin on glucose homeostasis. Additionally, multiple lines of evidence have implicated the α cell in disease, most notably diabetes. Early

Article Type:
Review Article
Collections:
100 years of glucagon: Anniversary collection
DOI:
https://doi.org/10.1530/JOE-22-0298
Volume/Issue:
Volume 258: Issue 1
Free access
João A B Pedroso Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Pedro O R de Mendonca Department of Anatomy, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil

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Marco A S Fortes Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Igor Tomaz Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Vitor L Pecorali Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Thais B Auricino Department of Anatomy, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil

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Ismael C Costa Department of Anatomy, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil

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Leandro B Lima Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Isadora C Furigo Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Debora N Bueno Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Angela M Ramos-Lobo Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Claudimara F P Lotfi Department of Anatomy, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil

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Jose Donato Jr Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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glucoregulatory responses required to reestablish glycemia under metabolic challenges like hypoglycemia or 2DG administration ( Flak et al . 2014 , Verberne et al . 2014 , Meek et al . 2016 ). Thus, we assessed whether SF1 Socs3 KO mice exhibit changes to the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0255
Volume/Issue:
Volume 235: Issue 3
Free access
Ivan Quesada CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) and Instituto de Bioingeniería, Universidad Miguel Hernández, Avenida de la Universidad s/n, 03202 Elche, Spain

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Eva Tudurí CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) and Instituto de Bioingeniería, Universidad Miguel Hernández, Avenida de la Universidad s/n, 03202 Elche, Spain

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Cristina Ripoll CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) and Instituto de Bioingeniería, Universidad Miguel Hernández, Avenida de la Universidad s/n, 03202 Elche, Spain

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Ángel Nadal CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) and Instituto de Bioingeniería, Universidad Miguel Hernández, Avenida de la Universidad s/n, 03202 Elche, Spain

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Brines ML Shulman GI 1994 Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia . Journal of Clinical Investigation 93 1677 – 1682 . Brelje TC Scharp DW Sorenson RL 1989 Three

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0290
Volume/Issue:
Volume 199: Issue 1
Free access
Saeed Alshahrani Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Mohammed Mashari Almutairi Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Shams Kursan Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Eduardo Dias-Junior Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Mohamed Mahmoud Almiahuob Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Lydia Aguilar-Bryan Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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Mauricio Di Fulvio Department of Pharmacology and Toxicology, Pacific Northwest Diabetes Research Institute, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, 216 HSB, Dayton, Ohio 45435, USA

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activating mutations in one of the two subunits forming this channel, i.e., the sulfonylurea receptor-1 gene (SUR1, ABCC8 ) or the inward rectifier K + channel (Kir 6.2 , KCNJ11 ), cause congenital hyperinsulinemic hypoglycemia ( Thomas et al . 1995 ) and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0327
Volume/Issue:
Volume 227: Issue 3
Open access
Zengmin Wang Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China
Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA

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Gail J Mick Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA

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Rongrong Xie Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA
Department of Endocrinology, Children’s Hospital of Soochow University, Suzhou, Jiangsu, PR China

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Xudong Wang Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA

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Xuemei Xie Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA

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Guimei Li Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China

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Kenneth L McCormick Division of Pediatric Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA

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not their 11-oxosteroid counterparts, inhibit glucose utilization and accelerate hepatic gluconeogenesis, both of which may avert hypoglycemia. Cortisol serves as a counter-regulatory hormone to insulin by stimulating the gene expression of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0006
Volume/Issue:
Volume 229: Issue 1
Free access
Michael Merkhassine Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA
VCA Colonial Animal Hospital, Ithaca, New York, USA

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Reilly W Coch Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA
Weill Cornell College of Medicine, New York, New York, USA

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Carol E Frederick Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA

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Lucinda L Bennett Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA

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Seth A Peng Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA
Fate Therapeutics, San Diego, California, USA

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Benjamin Morse Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA

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Bethany P Cummings Center for Alimentary and Metabolic Science, Department of Surgery, School of Medicine, University of California, Davis, Sacramento, California, USA
Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, Davis, California, USA

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John P Loftus Loftus Laboratory, Department of Clinical Sciences, Cornell University, College of Veterinary Medicine, Ithaca, New York, USA

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as an antidote for hypoglycemia caused by exogenous insulin administration ( Datte et al. 2016 , Harris et al. 2020 ). Elevated glucagon levels are seen in virtually all forms of diabetes mellitus (DM), α-cell hyperplasia, and, most dramatically

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-24-0051
Volume/Issue:
Volume 262: Issue 2
Open access
Hidetada Ogata Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Yusuke Seino Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Norio Harada Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Atsushi Iida Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Kazuyo Suzuki Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Takako Izumoto Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Kota Ishikawa Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Eita Uenishi Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Nobuaki Ozaki Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Yoshitaka Hayashi Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Takashi Miki Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Nobuya Inagaki Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Shin Tsunekawa Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Yoji Hamada Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Susumu Seino Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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Yutaka Oiso Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

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upper and lower intestine. Gain-of-function mutations of the K ATP channel cause neonatal diabetes and loss-of-function mutations of the K ATP channel cause persistent hyperinsulinemic hypoglycemia of infancy ( McTaggart et al . 2010 ). In patients

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0161
Volume/Issue:
Volume 222: Issue 2
Free access
Linda Ahlkvist Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Bilal Omar Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Anders Valeur Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Keld Fosgerau Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Bo Ahrén Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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mice ( Malmgren & Ahren 2015 ), however, only two times higher than that of the glucagon response to hypoglycemia ( Berglund et al . 2008 ). The elevation of plasma ZP-GA-1 resulted in a significant lowering of insulin secretion in response to glucose

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0371
Volume/Issue:
Volume 228: Issue 3
Free access
Xiumin Wang Department of Endocrinology, The Children’s Hospital of Zhejiang University School of Medicine, 57 Zhugan Xiang, Hangzhou 310003, China

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Li Liang Department of Endocrinology, The Children’s Hospital of Zhejiang University School of Medicine, 57 Zhugan Xiang, Hangzhou 310003, China

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Lizhong Du Department of Endocrinology, The Children’s Hospital of Zhejiang University School of Medicine, 57 Zhugan Xiang, Hangzhou 310003, China

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insulin concentrations after a meal. Most human and animal studies have shown that hyperglycemia and insulin (without hypoglycemia) decrease plasma ghrelin. In human neonates, a large amount of ghrelin is present in umbilical cord plasma samples ( Farquhar

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0057
Volume/Issue:
Volume 194: Issue 1
Free access
Marta Montolio Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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Montse Biarnés Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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Noèlia Téllez Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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Jessica Escoriza Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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Joan Soler Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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Eduard Montanya Institut d’Investigació Biomèdica de Bellvitge (IDIBELL); Endocrine Unit, Hospital Universitari de Bellvitge, Barcelona, Spain
Department of Clinical Sciences, University of Barcelona, Barcelona, Spain

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group of normoglycemic rats, not injected with STZ ( n = 3), that was transplanted with 500 islets to determine whether hypoglycemia could play a role in the higher IL-1β and iNOS mRNA expressions. In these strictly normoglycemic rats, IL-1β and iNOS

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06968
Volume/Issue:
Volume 192: Issue 1
Free access