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Tsutomu Wada Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Akari Ishikawa Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Eri Watanabe Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Yuto Nakamura Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Yusuke Aruga Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Hayate Hasegawa Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Yasuhiro Onogi Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Hiroe Honda Department of Immunobiology and Pharmacological Genetics, University of Toyama, Toyama, Japan
Toyama Prefectural Institute for Pharmaceutical Research, Toyama, Japan

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Yoshinori Nagai Department of Immunobiology and Pharmacological Genetics, University of Toyama, Toyama, Japan
JST, PRESTO, Saitama, Japan

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Kiyoshi Takatsu Department of Immunobiology and Pharmacological Genetics, University of Toyama, Toyama, Japan
Toyama Prefectural Institute for Pharmaceutical Research, Toyama, Japan

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Yoko Ishii Department of Pathology, University of Toyama, Toyama, Japan

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Masakiyo Sasahara Department of Pathology, University of Toyama, Toyama, Japan

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Daisuke Koya Department of Internal Medicine, Kanazawa Medical University, Ishikawa, Japan

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Hiroshi Tsuneki Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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Toshiyasu Sasaoka Department of Clinical Pharmacology, University of Toyama, Toyama, Japan

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maintenance of host homeostasis. Accumulating evidence has been untangling the complex link between insulin resistance in obesity and innate immunity, particularly via macrophages ( Lackey & Olefsky 2016 ). The macrophage is known to express at least two types

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0351
Volume/Issue:
Volume 235: Issue 3
Free access
Eun Soo Lee Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea

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Mi-Hye Kwon The East Coast Research Institute of Life Science, Gangneung-Wonju National University, Gangneung, Korea

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Hong Min Kim Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea

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Nami Kim Department of Anatomy, Korea University College of Medicine, Seoul, Korea

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You Mi Kim Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea

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Hyeon Soo Kim Department of Anatomy, Korea University College of Medicine, Seoul, Korea

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Eun Young Lee Department of Internal Medicine and Institute of Tissue Regeneration, Soonchunhyang University, Cheonan, Korea

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Choon Hee Chung Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea

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-induced excessive cellular stress conditions, NADPH oxidase (NOX)-derived reactive oxygen species (ROS) are increased and accelerate macrophage polarization to proinflammatory macrophage M1 and activation. In particular, activated macrophages are recognized as

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0206
Volume/Issue:
Volume 240: Issue 2
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Anne H van der Spek Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands

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Eric Fliers Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands

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Anita Boelen Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands

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metabolism present in innate immune cells and the role and effects of intracellular TH metabolism in these cells. It focuses specifically on the phagocytic innate immune cells: neutrophils, macrophages and dendritic cells. Thyroid hormone production and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-16-0462
Volume/Issue:
Volume 232: Issue 2
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Yuriko Sakai Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Hideyuki Arie Division of Health Sciences, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan

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Yinhua Ni Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Fen Zhuge Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Liang Xu Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Guanliang Chen Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Naoto Nagata Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Takuya Suzuki Department of Biofunctional Science and Technology, Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan

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Shuichi Kaneko Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Tsuguhito Ota Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

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Mayumi Nagashimada Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
Division of Health Sciences, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan

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) activation promote steatosis–NASH progression ( Tilg & Moschen 2010 ). Lipid overload in the liver enhances lipid peroxidation, leading to reactive oxygen species (ROS) production. Enhanced lipid peroxidation and ROS production activates T cells, macrophages

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0105
Volume/Issue:
Volume 247: Issue 2
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Vinicius Fernandes Cruzat School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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Kevin Noel Keane School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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Anita Lavarda Scheinpflug School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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Robson Cordeiro School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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Mario J Soares School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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Philip Newsholme School of Biomedical Sciences, Directorate of Nutrition, Dietetics and Food Technology, School of Public Health, Curtin Health Innovation Research Institute of Ageing and Chronic Disease - Curtin University, GPO Box U1987, Perth, Western Australia, Australia 6845

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, Kim et al . 2014 ). Chronic inflammation is characterised by enhanced cytokine levels (e.g. interleukin 1β (IL1β), IL6, IL10 and tumour necrosis factor alpha (TNFα)), and oxygen free radicals generated by immune cells, such as activated macrophages

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0677
Volume/Issue:
Volume 224: Issue 3
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Bo-Kyung Son Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
Institute of Gerontology, The University of Tokyo, Tokyo, Japan

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Taro Kojima Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

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Sumito Ogawa Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

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Masahiro Akishita Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

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, in the present study, we sought to unravel the effects of testosterone on AAA formation and found that castration promoted AAA formation through exacerbated infiltration of inflammatory macrophages and Il-6 and Il-1b upregulation. Conversely

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0646
Volume/Issue:
Volume 241: Issue 3
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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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pancreata were double stained and counted as described for grafts. CD68, IL-1β, and iNOS immunohistochemistry To identify the presence of macrophages, we stained CD68-expressing cells (monocyte/macrophage lineage

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06968
Volume/Issue:
Volume 192: Issue 1
Free access
Mark A Exley Department of Medicine, Faculty of Medical and Human Sciences, Department of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
Department of Medicine, Faculty of Medical and Human Sciences, Department of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA

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Laura Hand Department of Medicine, Faculty of Medical and Human Sciences, Department of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA

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Donal O'Shea Department of Medicine, Faculty of Medical and Human Sciences, Department of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA

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Lydia Lynch Department of Medicine, Faculty of Medical and Human Sciences, Department of Endocrinology, Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA

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( Wu et al . 2011 ), and macrophages ( Weisberg et al . 2003 , Lumeng et al . 2007 , Wentworth et al . 2010 ). Resident adipose leukocyte populations represent distinct subsets, with particular functions compared with their equivalent populations

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0516
Volume/Issue:
Volume 223: Issue 2
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Leke Wiering Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hepatology and Gastroenterology, Campus Virchow-Klinikum and Campus Charité Mitte, Berlin, Germany
Berlin Institute of Health at Charité – Universitätsmedizin Berlin, BIH Biomedical Innovation Academy, BIH Charité Junior Clinician Scientist Program, Berlin, Germany

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Frank Tacke Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hepatology and Gastroenterology, Campus Virchow-Klinikum and Campus Charité Mitte, Berlin, Germany

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progresses, Kupffer cells are replaced by monocyte-derived macrophages. Also, other immune cells as neutrophils and Type 1 T helper cells contribute to the inflammatory environment in NASH. However, also anti-inflammatory effects of immune cells in NASH are

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-22-0194
Volume/Issue:
Volume 256: Issue 1
Free access
James C Needell Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado, USA

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Madalyn N Brown Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado, USA

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Danny Zipris Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado, USA

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-induced adipose tissue inflammation in the development of T1D in the LEW1.WR1 rat. Our data demonstrate for the first time that infection with a diabetogenic virus leads to CD68 + macrophage infiltration into visceral but not subcutaneous adipose tissue observed

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0131
Volume/Issue:
Volume 238: Issue 1
Free access