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Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark
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have been linked to states of low-grade inflammation such as diabetes, obesity, liver disease, and atherosclerosis (5, 6, 7, 8, 9, 10, 11) , underscoring the important role of macrophages in initiating and propagating these conditions. Previously, we
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
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Department of Medicine, Karlstad Hospital, Karlstad, Sweden
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shown that GH treatment improves the above-mentioned risk factors for CVD ( 1 , 2 , 3 , 5 , 6 , 7 , 12 , 13 , 14 ), but it is currently unknown if GHD and long-term GHD treatment influences the level of low-grade inflammation. Urokinase
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in sCD163 are seen in conditions of low-grade inflammation, such as obesity, insulin resistance and type 2 diabetes mellitus (T2D) ( 17 , 18 , 19 , 20 ), but it is not known if these changes are directly linked to low-grade endotoxinemia or they
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
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Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
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Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
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Department of Biomedicine, University of Basel, Basel, Switzerland
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Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland
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/m 2 with nearly all patients having visceral obesity. Around 70% of the patients presented with chronic low-grade inflammation (defined by a CRP level of ≥2 mg/L). In study A, 86.3% of the patients suffered from either prediabetes or type 2 diabetes
Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
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Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
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Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
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Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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and dyslipidemia, as well as insulin resistance ( 3 ). The abdominal obesity is characterized by a state of low-grade inflammation. Visceral adipose tissue secretes pro-inflammatory adipokines promoting an inflammatory state, contributing to
Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
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Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
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Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
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Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
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Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
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Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
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pathway in the development of metabolic complications and atherosclerosis is the release of pro-inflammatory cytokines from adipose tissue promoting a state of chronic low-grade inflammation ( 3 , 4 , 5 ). It has been suggested that inflammation in turn
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, and waist circumference. These findings suggest that the decreased frequencies of PD-L2 + M-MDSCs and PD-1 + Tregs may contribute to the activation of effector T cells and the development of chronic low-grade inflammation in type 2 diabetes. Our
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The global epidemic of obesity is closely linked to the development of serious co-morbidities, including many forms of cancer. Epidemiological evidence consistently shows that obesity is associated with a similar or mildly increased incidence of prostate cancer but, more prominently, an increased risk for aggressive prostate cancer and prostate cancer-specific mortality. Studies in mice demonstrate that obesity induced by high-fat feeding increases prostate cancer progression; however, the mechanisms underpinning this relationship remain incompletely understood. Adipose tissue expansion in obesity leads to local tissue dysfunction and is associated with low-grade inflammation, alterations in endocrine function and changes in lipolysis that result in increased delivery of fatty acids to tissues of the body. The human prostate gland is covered anteriorly by the prominent peri-prostatic adipose tissue and laterally by smaller adipose tissue depots that lie directly adjacent to the prostatic surface. We discuss how the close association between dysfunctional adipose tissue and prostate epithelial cells might result in bi-directional communication to cause increased prostate cancer aggressiveness and progression. However, the literature indicates that several ‘mainstream’ hypotheses regarding obesity-related drivers of prostate cancer progression are not yet supported by a solid evidence base and, in particular, are not supported by experiments using human tissue. Understanding the links between obesity and prostate cancer will have major implications for the health policy for men with prostate cancer and the development of new therapeutic or preventative strategies.
Frontier Science Research Center, Circulatory and Body Fluid Regulation, AIA Research Group, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan
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, low-grade inflammation in fat tissues associated with obesity is assumed to be involved in the increased expression of AM (6, 8, 11) . When evaluating plasma levels of endogenous bioactive substances, we sometimes need to take gender
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associated with a chronic low-grade inflammation ( 5 ) that has been implicated as a crucial factor for insulin resistance ( 6 ) and also beta-cell dysfunction ( 7 , 8 ). Patients diagnosed with latent autoimmune diabetes of the adults (LADA) ( 9