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Virginia Rider Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Alex Talbott Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Anuradha Bhusri Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Zach Krumsick Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Sierra Foster Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Joshua Wormington Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA

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Bruce F Kimler Department of Radiation Oncology, The University of Kansas Medical Center, Kansas City, Kansas, USA

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adult mammals, female sex steroids direct changes that alter the uterus from a hostile to a receptive state for embryo implantation ( Franco et al . 2012 , Fritz et al. 2014 , Pawar et al. 2014 ). Hormones stimulate uterine cell proliferation by a

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0523
Volume/Issue:
Volume 229: Issue 2
Open access
Romain Fontaine Department of Basic Sciences and Aquatic Medicine, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Oslo, Norway

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Eirill Ager-Wick Department of Basic Sciences and Aquatic Medicine, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Oslo, Norway

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Kjetil Hodne Department of Basic Sciences and Aquatic Medicine, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Oslo, Norway

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Finn-Arne Weltzien Department of Basic Sciences and Aquatic Medicine, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Oslo, Norway

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both genders. We investigated whether LH cell plasticity may be due to both recruitment of existing pituitary cells and cell proliferation. Materials and methods Animal maintenance and sexing Wild-type (WT, d-rR strain) and tg ( lhb -hrGfpII

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0412
Volume/Issue:
Volume 240: Issue 2
Free access
Tatiana Dorfman Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Yulia Pollak Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Rima Sohotnik Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Arnold G Coran Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Jacob Bejar Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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Igor Sukhotnik Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel

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). The understanding of the mechanisms by which diabetes stimulates intestinal cell proliferation may have important clinical implications. The results of many trials have indicated that diabetic patients have an increased risk of malignant disease

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0725
Volume/Issue:
Volume 226: Issue 3
Free access
G M Ledda-Columbano Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy

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A Perra Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy

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M Pibiri Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy

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F Molotzu Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy

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A Columbano Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Via Porcell 4, 09124 Cagliari, Italy

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respond to direct mitogenic stimuli such as those elicited by primary mitogens, such as ligands of nuclear receptors, namely agents that, in other organs, induce cell proliferation in the absence of cell death. In the current study, we have

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06110
Volume/Issue:
Volume 185: Issue 3
Free access
Yan Cao Department of Endocrinology, First Affiliated Hospital of Harbin Medical University, Harbin, China
Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Zijie Feng Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Xin He Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Xuyao Zhang Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Bowen Xing Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Yuan Wu Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Taylor Hojnacki Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Bryson W Katona Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
Division of Gastroenterology and Hepatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Jian Ma Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Xiaorong Zhan Department of Endocrinology, First Affiliated Hospital of Harbin Medical University, Harbin, China
Department of Endocrinology, Southern University of Science and Technology Hospital, Shenzhen, China

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Xianxin Hua Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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of GDM. Previous studies in mice have shown that this adaptive increase in insulin production during pregnancy is accomplished both through enhanced insulin secretion by β-cells proliferation and expansion ( Sorenson & Brelje 1997 ). During

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-21-0114
Volume/Issue:
Volume 252: Issue 2
Restricted access
Tao Xie Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA

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Min Chen Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA

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Lee S Weinstein Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA

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Introduction Both type 1 and type 2 diabetes have been associated with pancreatic β-cell dysfunction, with reduced glucose-stimulated insulin secretion and decreased β-cell mass due to impaired β-cell proliferation and survival ( Butler et al

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-10-0030
Volume/Issue:
Volume 206: Issue 3
Free access
Haifan Zhang Center for the Study for Reproductive Biology and Women’s Health, Departments of Developmental and Molecular Biology and OB/GYN and Women’s Health,, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA

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Tim McElrath Center for the Study for Reproductive Biology and Women’s Health, Departments of Developmental and Molecular Biology and OB/GYN and Women’s Health,, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA

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Wei Tong Center for the Study for Reproductive Biology and Women’s Health, Departments of Developmental and Molecular Biology and OB/GYN and Women’s Health,, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA

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Jeffrey W Pollard Center for the Study for Reproductive Biology and Women’s Health, Departments of Developmental and Molecular Biology and OB/GYN and Women’s Health,, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA

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Introduction Estrogen induces cell proliferation in the uterine and mammary gland epithelium ( Martin et al. 1973 , Tong & Pollard 2002 ). Exposure to estrogen is also the major risk factor in the development of adenocarcinomas of

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.05987
Volume/Issue:
Volume 184: Issue 1
Free access
A Sengupta Endocrinology Program and Department of Animal Sciences, Rutgers, The State University of New Jersey, 67 Poultry Farm Road, New Brunswick, New Jersey 08901, USA

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D K Sarkar Endocrinology Program and Department of Animal Sciences, Rutgers, The State University of New Jersey, 67 Poultry Farm Road, New Brunswick, New Jersey 08901, USA

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PRL production and cell proliferation of lactotropes ( Ben-Jonathan & Hnasko 2001 ). Abnormalities in DA secretion, D2 receptors, and DA transporter functions lead to hyperplasia of lactotropes and the development of PRL-secreting prolactinomas

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0125
Volume/Issue:
Volume 214: Issue 1
Free access
Wenjuan Liu Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Harry Kevin Lau Division of Endocrinology and Metabolism, The Keenan Research Centre in the Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Ontario, Canada

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Dong Ok Son Division of Endocrinology and Metabolism, The Keenan Research Centre in the Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Ontario, Canada

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Tianru Jin Department of Physiology, University of Toronto, Toronto, Ontario, Canada
Division of Advanced Diagnostics, Toronto General Research Institutes, University Health Network, Toronto, Ontario, Canada
Banting and Best Diabetes Centre, University of Toronto, Toronto, Ontario, Canada

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Yehong Yang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Zhaoyun Zhang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Yiming Li Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Gerald J Prud’homme Department of Laboratory Medicine and Pathobiology, Keenan Research Centre for Biomedical Science of St. Michael’s Hospital, University of Toronto, Toronto, Ontario, Canada

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Qinghua Wang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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) ( Pettus et al. 2013 , Jin & Weng 2016 ). Thus, it is of critical importance to investigate new therapeutic methods that have two actions: to increase human β-cell proliferation and/or regeneration, and to reduce apoptosis. However, no single therapy has

Article Type:
Research Article
Collections:
Top-cited articles of 2023
DOI:
https://doi.org/10.1530/JOE-20-0315
Volume/Issue:
Volume 248: Issue 2
Restricted access
N David Åberg Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden
Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Inger Johansson Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Maria A I Åberg Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Johan Lind Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Ulf E Johansson Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Christiana M Cooper-Kuhn Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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H Georg Kuhn Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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Jörgen Isgaard Center of Brain Research and Rehabilitation, Laboratory of Experimental Endocrinology, Institute of Physiology and Neuroscience, University of Gothenburg, Gothenburg, Sweden

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′-cyclic nucleotide 3′ phosphohydrolase (CNPase) activity as well as in cell proliferation have been observed during postnatal development, while neuron numbers were not studied. Also, GH treatment restored CNPase activity and cell numbers. Conversely, in

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0495
Volume/Issue:
Volume 201: Issue 1
Free access