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Rubén Marín-Juez
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Susanne Jong-Raadsen
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Shuxin Yang ZF‐Screens BV, Institute of Biology, J.H. Oortweg 19, 2333 CH Leiden, The Netherlands

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Herman P Spaink ZF‐Screens BV, Institute of Biology, J.H. Oortweg 19, 2333 CH Leiden, The Netherlands

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hypoglycemia In order to study whether zebrafish are sensitive to human insulin, we analyzed phosphoenolpyruvate carboxykinase 1 ( pck1 ) expression levels because the transcription of this gene is well known to be inhibited by insulin ( O'Brien & Granner 1990

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0178
Volume/Issue:
Volume 222: Issue 2
Free access
Pouneh K Fazeli Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit Street, Bulfinch 457, Boston, Massachusetts 02114, USA

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Anne Klibanski Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit Street, Bulfinch 457, Boston, Massachusetts 02114, USA

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able to rescue the Goat knockout mice from hypoglycemia and normalize blood sugars, suggesting that an important role of elevated GH levels in states of malnutrition is to maintain euglycemia ( Zhao et al . 2010 ). Although there is recent

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0477
Volume/Issue:
Volume 220: Issue 3
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Laura B Lemke Department of Biological Engineering, Division of Comparative Medicine

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Arlin B Rogers Department of Biological Engineering, Division of Comparative Medicine

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Prashant R Nambiar Department of Biological Engineering, Division of Comparative Medicine

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James G Fox Department of Biological Engineering, Division of Comparative Medicine
Department of Biological Engineering, Division of Comparative Medicine

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euglycemia or hypoglycemia in some mice with previously noted hyperglycemia. Figure 4 Glucose tolerance testing in aged dSW and ndSW at 12 months of age. (A) Glucose tolerance curves revealed elevated baseline with delayed return to baseline in diabetic males

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0588
Volume/Issue:
Volume 199: Issue 1
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Ulrika Bergström Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Charlotte Lindfors Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Marie Svedberg Department of Clinical Neuroscience, Center for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden

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Jeanette E Johansen Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Jenny Häggkvist Department of Clinical Neuroscience, Center for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden

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Martin Schalling Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Rolf Wibom Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden

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Abram Katz Department of Physical Therapy, Ariel University, Ariel, Israel

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Ida A K Nilsson Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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. Noteworthy is that large increases in blood glucose can be associated with significant reductions in mouse brain glucose utilization ( Vannucci et al . 1997 , Toyama et al . 2004 ) and, conversely, chronic hypoglycemia can result in increased brain glucose

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0383
Volume/Issue:
Volume 233: Issue 1
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Xiwen Xiong Department of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, China

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Xupeng Sun Department of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, China

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Qingzhi Wang Department of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, China

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Xinlai Qian Department of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, China

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Yang Zhang Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA

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Xiaoyan Pan Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA
Department of Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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X Charlie Dong Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA

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processes, such as DNA repair, tumor suppression, anti-inflammation and metabolism. Sirt6 -deficient mice display severe hypoglycemia and a multisystemic aging phenotype and died around 4 weeks after birth ( Mostoslavsky et al . 2006 , Xiao et al . 2010

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0317
Volume/Issue:
Volume 231: Issue 2
Free access
Yusuke Seino Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Takashi Miki Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Wakako Fujimoto Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Eun Young Lee Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Yoshihisa Takahashi Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Kohtaro Minami Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Yutaka Oiso Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Susumu Seino Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

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Investigation 119 80 – 90 . ( doi:10.1172/JCI35772 ) Havel PJ Akpan JO Curry DL Stern JS Gingerich RL Ahren B 1993 Autonomic control of pancreatic polypeptide and glucagon secretion during neuroglucopenia and hypoglycemia in mice . American

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0579
Volume/Issue:
Volume 218: Issue 1
Free access
S Ö Íşeri Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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G Şener Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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M Yüksel Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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G Contuk Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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Ş Çetinel Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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N Gedik Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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B Ç Yeğen Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey
School of Pharmacy, Department of Pharmacology, Marmara University School of Medicine, Istanbul, Turkey
Department of Histology and Embryology, Marmara University School of Medicine, Istanbul, Turkey
Vocational School of Health Related Professions, Marmara University School of Medicine, Istanbul, Turkey
Division of Biochemistry, Kasimpasa Military Hospital, Istanbul, Turkey

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, Tschop et al. 2001 ). Ghrelin secretion is pulsatile and directly related to feeding behavior ( Tolle et al. 2002 ) and it is upregulated during negative nutritional status, fasting and insulin-induced hypoglycemia (Toshiani et al. 2001), suggesting

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06432
Volume/Issue:
Volume 187: Issue 3
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Jennifer M Ikle Division of Endocrinology, Department of Pediatrics, Stanford University School of Medicine, Stanford, California, USA

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Anna L Gloyn Division of Endocrinology, Department of Pediatrics, Stanford University School of Medicine, Stanford, California, USA
Stanford Diabetes Research Center, Stanford University, Stanford, California, USA

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mutations lead to over-secretion of insulin and hypoglycemia, and given the lack of compensation by the WT allele, the phenotype is more varied ( Glaser et al. 1998 , Gloyn 2003 , Cuesta-Muñoz et al. 2004 ). Patients with GCK-MODY have stable mild

Article Type:
Review Article
Collections:
100 years of insulin: A special collection
DOI:
https://doi.org/10.1530/JOE-21-0067
Volume/Issue:
Volume 250: Issue 3
Free access
Elliott P Brooks Barbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, USA

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Lori Sussel Barbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, USA

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endoderm did not affect early pancreas development but instead caused a decrease in glucagon+ cells and severe hypoglycemia. The authors concluded FOXA2 was essential for the differentiation and maturation of the α cell lineage. Transcriptomics of α

Article Type:
Review Article
Collections:
100 years of glucagon: Anniversary collection
DOI:
https://doi.org/10.1530/JOE-22-0297
Volume/Issue:
Volume 258: Issue 2
Free access
Brit H Boehmer Department of Pediatrics, Perinatal Research Center, University of Colorado School of Medicine, Aurora, Colorado, USA

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Sean W Limesand School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona, USA

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Paul J Rozance Department of Pediatrics, Perinatal Research Center, University of Colorado School of Medicine, Aurora, Colorado, USA

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attenuation of GSIS ( Lavezzi et al. 2013 ). β-cell mass, however, was significantly lower in these hypoglycemic fetuses compared to controls, thus showing that chronic experimental fetal hypoglycemia can mimic the two main pancreatic islet defects seen in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-17-0076
Volume/Issue:
Volume 235: Issue 2
Free access