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. 2000 ), arterial stiffness ( Smith et al. 2002 ), endothelial and/or endothelium-independent vasodilation ( Rossoni et al. 1999 , Evans et al. 2000 , Capaldo et al. 2001 ), and may reverse markers of early atherosclerosis ( Pfeifer et al
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Introduction Type 2 diabetes is characterized by accelerated atherosclerosis ( Hobb 2006 ). Elevated tumour necrosis factor α (TNF) levels and hyperglycaemia are implicated in diabetes-associated endothelial cell dysfunction and may be causal in
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Introduction Type 2 diabetes is characterised by accelerated atherosclerosis ( Hobb 2006 ). Elevated tumour necrosis factor α (TNFα) levels and hyperglycaemia are implicated in diabetes-associated endothelial cell dysfunction and may be causal in
CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland
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Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain
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Gonadal steroids strongly contribute to the metabolic programming that shapes the susceptibility to the manifestation of diseases later in life, and the effect is often sexually dimorphic. Microbiome signatures, together with metabolic traits and sex steroid levels, were analyzed at adulthood in neonatally androgenized female rats, and compared with those of control male and female rats. Exposure of female rats to high doses of androgens on early postnatal life resulted in persistent alterations of the sex steroid profile later on life, namely lower progesterone and higher estradiol and estrone levels, with no effect on endogenous androgens. Neonatally androgenized females were heavier (10% at early adulthood and 26% at adulthood) than controls and had impaired glucose homeostasis observed by higher AUC of glucose in GTT and ITT when subjected to obesogenic manipulations. Androgenized female displayed overt alterations in gut microbiota, indicated especially by higher Bacteroidetes and lower Firmicutes abundance at early adulthood, which disappeared when animals were concurrently overfed at adulthood. Notably, these changes in gut microbiota were related with the intestinal expression of several miRNAs, such as miR-27a-3p, miR-29a-5p, and miR-100-3p. Our results suggest that nutritional and hormonal disruption at early developmental periods not only alters the metabolic programming of the individual later in life but also perturbs the architecture of gut microbiota, which may interact with the host by a cross-talk mediated by intestinal miRNAs; phenomena that may contribute to amplify the metabolic derangement caused by obesity, as seen in neonatally androgenized female rats.
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Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK
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type 2 diabetes mellitus (T2DM)) that are well known to be associated with an increased incidence of CVD. Atherosclerosis is a complex disease of the arteries characterised by endothelial dysfunction, vascular inflammation and the build-up of lipids
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Departamento de Biofísica, Departmento de Microbiologia, Departamento de Fisiologia, Department of Oral Biological and Medical Sciences, Centro de Ciências Naturais e Humanas, Departamento de Ciências Exatas e da Terra, Universidade Federal de São Paulo, Rua Pedro de Toledo 669, São Paulo, São Paulo 04039-032, Brazil
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( Thomas et al . 2004 ), immune response, inflammation ( Lago et al . 2007 ), and atherosclerosis ( Taleb et al . 2007 ). The activities of leptin are mediated through its receptor (OB-R), which is encoded by the diabetes ( db ( Lepr )) gene on
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). Furthermore, the adipo-cytokine adiponectin has been established as both an endogenous insulin sensitizer and a protector of endothelial function diminishing the development of atherosclerosis ( Kubota et al. 2002 ). Moreover, various acute-phase reactants
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vascular remodeling & Stroke Unclear Vascular remodeling and vascular stiffness Lumen diameter reduction ( Dorrance et al. 2001 , McClain & Dorrance 2014 , Rigsby et al. 2007 ) Atherosclerosis & Myocardial Infarction EC Upregulation of
Department of Experimental Physiology, Department of Internal Medicine III and Institute of Physiology, Department of Biological Chemistry, Endocrine Unit, Experimental Research Centre, University of Athens Medical School, Athens, Greece
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Department of Experimental Physiology, Department of Internal Medicine III and Institute of Physiology, Department of Biological Chemistry, Endocrine Unit, Experimental Research Centre, University of Athens Medical School, Athens, Greece
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pathogenesis of other diseases such as atherosclerosis, chronic renal failure, polycystic ovary syndrome (PCOS) and Alzheimer's disease ( Mukhopadhyay & Mukherjee 2005 , Tan et al . 2011 ). Furthermore, data obtained from humans and experimental animals
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Severance Biomedical Research Institute, Department of Internal Medicine, Yonsei University College of Medicine, 50 Yonsei‐ro, Seodaemun‐gu, Seoul 120-752, Korea
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disease (CAD) and atherosclerosis. It has been reported that FGF21 was increased in the serum of human subjects with CAD and carotid artery plaques, and increased FGF21 levels were associated with adverse lipid profiles in CAD subjects ( Lin et al . 2010