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Sian J S Simpson Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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Lorna I F Smith Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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Peter M Jones Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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James E Bowe Department of Diabetes, School of Life Course Sciences, Faculty of Life Science and Medicine, King’s College London, London, UK

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of β-cell adaptations in rodent pregnancy ( Rieck & Kaestner 2010 ). Similarly, in human pregnancy, levels of CRH in the peripheral circulation increase as gestation progresses ( Campbell et al . 1987 , Sasaki et al . 1987 ) and CRH

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0568
Volume/Issue:
Volume 245: Issue 2
Open access
Liselotte Fransson Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Stephanie Franzén Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Victoria Rosengren Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Petra Wolbert Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Åke Sjöholm Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Henrik Ortsäter Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden

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Glucocorticoids (GCs) are stress hormones primarily responsible for mobilizing glucose to the circulation. Due to this effect, insulin resistance and glucose intolerance are concerns in patients with endogenous overproduction of GCs and in patients prescribed GC-based therapy. In addition, hypercortisolemic conditions share many characteristics with the metabolic syndrome. This study reports on a thorough characterization, in terms of glucose control and lipid handling, of a mouse model where corticosterone is given via the drinking water. C57BL/6J mice were treated with corticosterone (100 or 25 μg/ml) or vehicle in their drinking water for 5 weeks after which they were subjected to insulin or glucose tolerance tests. GC-treated mice displayed increased food intake, body weight gain, and central fat deposit accumulations. In addition, the GC treatment led to dyslipidemia as well as accumulation of ectopic fat in the liver and skeletal muscle, having a substantial negative effect on insulin sensitivity. Also glucose intolerance and hypertension, both part of the metabolic syndrome, were evident in the GC-treated mice. However, the observed effects of corticosterone were reversed after drug removal. Furthermore, this study reveals insights into β-cell adaptation to the GC-induced insulin resistance. Increased pancreatic islet volume due to cell proliferation, increased insulin secretion capacity, and increased islet chaperone expression were found in GC-treated animals. This model mimics the human metabolic syndrome. It could be a valuable model for studying the complex mechanisms behind the development of the metabolic syndrome and type 2 diabetes, as well as the multifaceted relations between GC excess and disease.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0189
Volume/Issue:
Volume 219: Issue 3
Free access
J Han The Research Institute for Children, Department of Pediatrics, Children's Hospital at New Orleans, 200 Henry Clay Avenue, New Orleans, Louisiana 70118, USA

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Y Q Liu The Research Institute for Children, Department of Pediatrics, Children's Hospital at New Orleans, 200 Henry Clay Avenue, New Orleans, Louisiana 70118, USA
The Research Institute for Children, Department of Pediatrics, Children's Hospital at New Orleans, 200 Henry Clay Avenue, New Orleans, Louisiana 70118, USA

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, pancreatic β-cells must secrete more insulin to maintain normal glucose levels. Increased insulin secretion requires β-cell adaptation, a process that includes both enhanced insulin secretion and β-cell proliferation. During compensated obesity, islet PDH

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0391
Volume/Issue:
Volume 204: Issue 2
Free access
B T Layden
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V Durai
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M V Newman
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A M Marinelarena
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C W Ahn
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G Feng Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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S Lin Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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X Zhang Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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D B Kaufman Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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N Jafari Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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G L Sørensen Division of Endocrinology, Northwestern University Biomedical Informatics Center, Division of Transplantation Surgery, Genomics Core, Medical Biotechnology Center, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611, USA

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W L Lowe Jr
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resistant states of pregnancy and obesity ( Butler et al . 2007 ). Studying states in which insulin needs change can provide insight into pathways mediating β cell adaptations. In mice, β cell mass increases about twofold during pregnancy, with a maximum

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-10-0298
Volume/Issue:
Volume 207: Issue 3
Free access
Gustavo Canul-Medina Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México/Instituto Nacional de Pediatría, Mexico City, Mexico

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Leticia Riverón-Negrete Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México/Instituto Nacional de Pediatría, Mexico City, Mexico

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Karina Pastén-Hidalgo Cátedra CONACYT, Instituto Nacional de Pediatría, Mexico City, Mexico

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Paulina Morales-Castillo Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México/Instituto Nacional de Pediatría, Mexico City, Mexico

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Francisco García-Vázquez Laboratorio de Immunología y Alergia, Departamento de Análisis Clínicos y Estudios Especiales, Instituto Nacional de Pediatría, Mexico City, Mexico

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Cristina Fernandez-Mejia Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México/Instituto Nacional de Pediatría, Mexico City, Mexico

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.1097/00006676-199305000-00006 ) Baeyens L Hindi S Sorenson RL German MS 2016 β-Cell adaptation in pregnancy . Diabetes, Obesity and Metabolism 18 (Supplement 1) 63 – 70 . ( https://doi.org/10.1111/dom.12716 ) Beamish CA Zhang L Szlapinski SK Strutt BJ Hill DJ

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0184
Volume/Issue:
Volume 248: Issue 1
Restricted access
Sandra K Szlapinski Department of Physiology and Pharmacology, Western University, London, Ontario, Canada
Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Anthony A Botros Department of Physiology and Pharmacology, Western University, London, Ontario, Canada
Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Sarah Donegan Department of Physiology and Pharmacology, Western University, London, Ontario, Canada
Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Renee T King Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Gabrielle Retta Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Brenda J Strutt Department of Physiology and Pharmacology, Western University, London, Ontario, Canada
Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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David J Hill Department of Physiology and Pharmacology, Western University, London, Ontario, Canada
Lawson Health Research Institute, St Joseph’s Health Care, London, Ontario, Canada

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Introduction Pregnancy presents as a unique situation of endocrine pancreas β-cell adaptation that reverses after parturition. Late pregnancy is characterized by a state of peripheral maternal insulin resistance mediated by placental hormones

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0012
Volume/Issue:
Volume 245: Issue 2
Restricted access
Andrew T Templin Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Christine Schmidt Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Meghan F Hogan Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Nathalie Esser Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Richard N Kitsis Departments of Medicine and Cell Biology and Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, New York, USA

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Rebecca L Hull Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Sakeneh Zraika Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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Steven E Kahn Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veteran Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA

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first to show that ARC is required for β-cell survival and sufficient insulin secretion in vivo in response to a genetic model of diabetogenic stress. The role of ARC in β-cell adaptation to high fat diet (HFD) feeding, a physiologically relevant

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0612
Volume/Issue:
Volume 251: Issue 2
Restricted access
Kaiyuan Yang Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada

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Jonathan Gotzmann Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

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Sharee Kuny Department of Ophthalmology and Visual Sciences, University of Alberta, Edmonton, Alberta, Canada

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Hui Huang Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

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Yves Sauvé Department of Physiology, University of Alberta, Edmonton, Alberta, Canada
Department of Ophthalmology and Visual Sciences, University of Alberta, Edmonton, Alberta, Canada

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Catherine B Chan Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada
Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

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relative insulin deficiency in insulin-resistant individuals. In stage 2, glucose levels start to rise due to loss of β-cell mass and an initial disruption of β-cell function. This stage represents a stable state of β-cell adaptation. Stage 3 consists of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0517
Volume/Issue:
Volume 229: Issue 3
Free access
B Maiztegui CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CCT LA PLATA-CONICET, Centro Colaborador OPS/OMS en Diabetes), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina

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M I Borelli CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CCT LA PLATA-CONICET, Centro Colaborador OPS/OMS en Diabetes), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina

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M A Raschia CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CCT LA PLATA-CONICET, Centro Colaborador OPS/OMS en Diabetes), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina

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H Del Zotto CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CCT LA PLATA-CONICET, Centro Colaborador OPS/OMS en Diabetes), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina

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J J Gagliardino CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CCT LA PLATA-CONICET, Centro Colaborador OPS/OMS en Diabetes), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina

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( Marynissen et al . 1990 , Chen et al . 1993 ), whereas the mechanism of the latter has not been completely elucidated. Failure of β-cell adaptation to the increased demand of insulin will result in impaired glucose homeostasis and, in time, development of

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0386
Volume/Issue:
Volume 200: Issue 2
Free access
Bethany P Cummings Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA
Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Andrew A Bremer Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Timothy J Kieffer Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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David D'Alessio Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Peter J Havel Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA
Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Cell adaptation to dexamethasone-induced insulin resistance in rats involves increased glucose responsiveness but not glucose effectiveness . Pancreas 22 148 – 156 . ( doi:10.1097/00006676-200103000-00007 ) Kim SJ Winter K Nian C Tsuneoka M

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0459
Volume/Issue:
Volume 216: Issue 2
Free access