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Laboratory of Pharmacological Neuroendocrinology, Department of Pharmacology and Toxicology, Biotechnology Center, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia
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during stress conditions is limited. The activation of release of anterior pituitary hormones, such as adrenocorticotropic hormone (ACTH) or prolactin, is one of the main characteristics of the stress response ( Jezova & Hlavacova 2008 ). Knowledge
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experiences to type 2 diabetes in humans and type 2 diabetes models in mice, even if no inferences should be allowed between animal studies and human studies. Here, we evidence step-by-step trajectories from cause (postnatal stress) to effect (adult type-2
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expression is independent of circulating TH concentration ( Zoeller et al . 1990 ) or of nutritional status ( Jaimes-Hoy et al . 2008 ), but is inhibited by a previous stress exposure ( Uribe et al . 2011 ) or corticosterone injection ( Sotelo-Rivera et
Departments of Obstetrics & Gynaecology and Medicine, University of Toronto, Toronto, Ontario, Canada
Lunenfeld Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada
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Department of Biological Sciences and Center for Environmental Epigenetics and Development, University of Toronto, Scarborough, Ontario, Canada
Department of Cell and Systems Biology, Department of Psychology, University of Toronto, Toronto, Ontario, Canada
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maternal stress/anxiety/depression, maternal obesity, maternal glucocorticoid exposure and altered level of maternal care. While early studies in the field were confined to animal models, more recently, they have been extended to include humans. The
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dexamethasone ( Holsboer-Trachsler et al . 1987 , Hoshino et al . 1987 , Vreeburg et al . 2009 , Hempel et al . 2010 ), and abnormal adrenocorticotropin (ACTH) and cortisol responses to corticotropin-releasing factor (CRF) or stress ( Young et al . 2000
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Glycation and Diabetes Group, Mater Clinical School, Mater Research Institute - The University of Queensland, Translational Research Institute, 37 Kent Street, Woolloongabba, South Brisbane, Queensland, Australia
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develop a detrimental condition referred to as ER stress. The principles of the UPR are now relatively well defined ( Ron & Walter 2007 , Hasnain et al . 2012 , Hetz 2012 ), and the mechanisms of the signal transducers involved in the activation of this
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Introduction The global prevalence of obesity is rising ( Yach et al . 2006 ), emphasizing the need to decipher the complex regulatory mechanisms underlying energy balance. Evidence indicates that chronic stress is a risk factor for obesity
Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada
Graduate Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada
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Introduction The effects of early-life stress (ELS) are profound, long lasting, and diverse. ELS impacts growth, metabolism, immunity, brain physiology, and behavior ( Meaney & Plotsky 2000 , Lehmann et al. 2002 , Levine 2002 , Bilbo et
ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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ZBSA – Freiburg Center for Systems Biology, University of Freiburg, Germany
Renal Division, University Hospital Freiburg, Germany
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in lipid biosynthesis and storage ( Mak et al. 2006 ), regulatory micro-RNAs ( Mansfield et al. 2004 ), neurotrans-mission, and the control of developmental decisions, stress response, and lifespan ( Lee et al. 2003 , Hamilton et al. 2005
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of excessive oxidative stress ( Hubel 1999 , Burton & Jauniaux 2004 , Myatt & Cui 2004 ), thought to result from either hypoxia-reperfusion injury ( Burton & Hung 2003 ) and/or deficient antioxidant defences ( Perkins 2006 ). In turn, increased