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Liting Wu Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Li Xiong Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Jin Li Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Department of Geriatrics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Zishan Peng Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Luyao Zhang Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Peijie Shi Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Yingying Gong Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Department of Geriatrics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Haipeng Xiao Department of Endocrinology and Metabolism, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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and disease ( Zhang et al. 2013 , 2018 b , Du et al. 2016 , 2017 ). In diabetes, circHIPK3 and CDR1as have been shown to regulate β-cell proliferation and insulin secretion in mouse islets by sponging multiple miRNA and modulating the activity

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-20-0079
Volume/Issue:
Volume 65: Issue 4
Open access
Amanda M Ackermann Departments of Medicine,
Molecular Physiology and Biophysics and
Program in Developmental Biology, Vanderbilt University Medical Center, 2220 Pierce Avenue 746 PRB, Nashville, Tennessee 37232, USA

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Maureen Gannon Departments of Medicine,
Molecular Physiology and Biophysics and
Program in Developmental Biology, Vanderbilt University Medical Center, 2220 Pierce Avenue 746 PRB, Nashville, Tennessee 37232, USA

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by β-cell neogenesis (differentiation from precursor cells), β-cell proliferation, and β-cell hypertrophy (increased cell size), and is decreased by β-cell death, primarily through apoptosis, and β-cell atrophy (decreased cell size; Fig. 3 ). From

Article Type:
Review Article
DOI:
https://doi.org/10.1677/JME-06-0053
Volume/Issue:
Volume 38: Issue 2
Free access
M Blandino-Rosano Investigation Unit and Endocrinology and Nutrition Service, Puerta del Mar Hospital, Ana de Viya, 21, Cadiz 11009, Spain

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G Perez-Arana Investigation Unit and Endocrinology and Nutrition Service, Puerta del Mar Hospital, Ana de Viya, 21, Cadiz 11009, Spain

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J M Mellado-Gil Investigation Unit and Endocrinology and Nutrition Service, Puerta del Mar Hospital, Ana de Viya, 21, Cadiz 11009, Spain

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C Segundo Investigation Unit and Endocrinology and Nutrition Service, Puerta del Mar Hospital, Ana de Viya, 21, Cadiz 11009, Spain

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M Aguilar-Diosdado Investigation Unit and Endocrinology and Nutrition Service, Puerta del Mar Hospital, Ana de Viya, 21, Cadiz 11009, Spain

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et al . 2001 ) and diet-inducing hyperglycemia has been shown to be associated with a transient proliferative response ( Donath et al . 1999 ). However, no increased β-cell proliferation has been observed associated with the recent onset of DM1 in

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-07-0154
Volume/Issue:
Volume 41: Issue 1
Free access
Jianling Xie Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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Norhan M El Sayed Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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Cheng Qi Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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Xuechan Zhao Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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Claire E Moore Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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Terence P Herbert Department of Cell Physiology and Pharmacology, University of Leicester, Henry Wellcome Building, University Road, Leicester LE1 9HN, UK

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investigate how exendin-4 stimulates β-cell proliferation. To these ends, we have demonstrated, in rat islets of Langerhans, that in the presence of glucose, exendin-4 acutely activates mTORC1 via the autocrine/paracrine activation of the IGF1R, whereas EGFR

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-13-0200
Volume/Issue:
Volume 53: Issue 1
Free access
K Lindberg Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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S G Rønn Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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D Tornehave Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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H Richter Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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J A Hansen Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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J Rømer Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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M Jackerott Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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N Billestrup Department of Signal Transduction,
Department of Pharmacology, Novo Nordisk A/S, Bagsværd, Denmark
Steno Diabetes Center, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark
Institute of Medical Biochemistry and Genetics, Panum Institute, University of Copenhagen, Denmark

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shown to be important growth factors for the β-cell as they stimulate insulin synthesis as well as β-cell proliferation ( Nielsen 1982 , 1985 , Nielsen et al. 1992 , Brelje et al. 1993 ). Specific receptors for both PRL and GH are present on β

Article Type:
Research Article
DOI:
https://doi.org/10.1677/jme.1.01840
Volume/Issue:
Volume 35: Issue 2
Free access
Kay E Garnett School of Biological Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK
AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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Philip Chapman School of Biological Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK
AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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Julie A Chambers School of Biological Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK
AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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Ian D Waddell School of Biological Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK
AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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David S W Boam School of Biological Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK
AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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Egr-1 expression is strikingly enriched in islets and that its small interfering RNA (siRNA)-mediated silencing inhibits β-cell proliferation. Taken together, these findings suggest a significant role for Egr-1 in β-cell proliferation

Article Type:
Research Article
DOI:
https://doi.org/10.1677/jme.1.01792
Volume/Issue:
Volume 35: Issue 1
Free access
Xianjie Wen Division of Endocrinology, Department of Medicine, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio, USA
Department of Anesthesiology, The First People’s Hospital of Foshan & Foshan Hospital of Sun Yat-sen University, Guangdong, China

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Yisheng Yang Division of Endocrinology, Department of Medicine, MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio, USA

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secretion per se in Glis3 − / − mice. GLIS3 is required for obesity-induced β cell proliferation and mass expansion In states of insulin resistance, such as obesity and pregnancy, the expansion of β cell mass in accordance with the requirements

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-16-0232
Volume/Issue:
Volume 58: Issue 2
Free access
Riccarda Granata Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism
Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism

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Alessandra Baragli Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism
Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism

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Fabio Settanni Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism
Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism

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Francesca Scarlatti Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism
Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism

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Ezio Ghigo Laboratory of Molecular, Division of Endocrinology, Cellular Endocrinology and Metabolism

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. 2010 ). Both AG and UAG promote HIT-T15 and INS-1E β-cell proliferation, and inhibit apoptotic events induced by serum starvation and treatment with cytokines ( Granata et al . 2006 , 2007 ), a major cause of β-cell loss particularly in type 1

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-10-0019
Volume/Issue:
Volume 45: Issue 3
Free access
Laura de Miguel-Santos Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain
Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain

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Elisa Fernández-Millán Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain

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María Ángeles Martín Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain
Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain

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Fernando Escrivá Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain
Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain

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Carmen Álvarez Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain
Departamento de Bioquímica y Biología Molecular II, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Departamento de Metabolismo y Nutrición, Facultad de Farmacia, Universidad Complutense de Madrid, UCM, 28040 Madrid, Spain

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al . 1997 ), associated to the stimulation of β-cell proliferation due to locally increased pancreatic IGF-1 and islet IRS-2 production ( Martín et al . 2005 , Fernández et al . 2007 ). Nevertheless, food restriction continued after birth induced a

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-09-0045
Volume/Issue:
Volume 44: Issue 1
Free access
Maria Sörhede Winzell Division of Medicine, Department of Clinical Sciences, Lund University, BMC, B11, SE-221 84 Lund, Sweden

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Bo Ahrén Division of Medicine, Department of Clinical Sciences, Lund University, BMC, B11, SE-221 84 Lund, Sweden

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studies have suggested that GLP-1 receptor activation inhibits islet apoptosis and stimulates β-cell proliferation ( Xu et al . 1999 , Perfetti et al . 2000 , Stoffers et al . 2000 , Wang & Brubaker 2002 , Egan et al . 2003 , Li et al . 2003

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-07-0121
Volume/Issue:
Volume 40: Issue 2
Free access