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permanently alter some functional aspect normally responsive to the hormone and often establishing a sexual dimorphism ( Csaba 2008 ). Moreover, the tissue is programmable for only a brief developmental period, after which time the tissue becomes permanently
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
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Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
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Department of Psychology, 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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) ( Schmidt et al. 2003 ). There is a similar developmental period in humans, from ~4 months to ~5 years ( Gunnar & Donzella 2002 ). Studies of the SHRP in mice and rats demonstrate that some stressors such as ether, shock, cold, and novelty produce little
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role in the imprinting of gene(s). Thus, when a gene programmed to respond to oestrogen at puberty is misprogrammed by developmental exposure to an endocrine disruptor, it will respond abnormally and the possibility exists that abnormalities in the
Graduate School for Biomedical Science and Engineering, University of Maine, Orono, Maine, USA
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts, USA
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differentiation and could also influence their epigenetic information. Much work is needed to understand the molecular and cellular mechanisms underlying T3-driven germ line epigenetics, and to delineate the developmental gene expression programs and disease
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nutritional or hormonal factors during critical periods of life (such as pregnancy and/or lactation) with the development of chronic diseases in adulthood, such as obesity and type 2 diabetes. This biological phenomenon is known as metabolic programming
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Pilgaard K Grunnet L Vielwerth S Alibegovic A 2006 Metabolic aspects of insulin resistance in individuals born small for gestational age . Hormone Research 65 137 – 143 . Vickers MH 2007 Developmental programming and adult obesity
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and life-long immunosuppression. There are, however, specific problems when considering β-cell transplantation into patients with Type 1 diabetes since their immune systems are programmed to destroy primary β-cells, and will presumably target even the
Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA
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mean ± s.e.m. Reproduced, with permission, from Thornburg KL; 2015; The programming of cardiovascular disease; Journal of Developmental Origins of Health and Disease ; volume 6, pages 366–376. Signaling pathways Extracellular control
Nottingham Digestive Disease Centre and Biomedical Research Centre, School of Medicine, University of Nottingham, Nottingham, UK
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-1055 Symonds ME 2013 Brown adipose tissue growth and development . Scientifica 2013 14 . ( https://doi.org/10.1155/2013/305763 ) Symonds ME Budge H 2009 Nutritional models of the developmental programming of adult health and disease
Early Life Research Unit, INRA and University of Nantes, School of Veterinary Medicine and Science, Institute of Health Sciences, Oniris, Department of Animal Science, Academic Division of Child Health, Obstetrics and Gynaecology, School of Medicine, Queen's Medical Centre, The University of Nottingham, Nottingham NG7 2UH, UK
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Early Life Research Unit, INRA and University of Nantes, School of Veterinary Medicine and Science, Institute of Health Sciences, Oniris, Department of Animal Science, Academic Division of Child Health, Obstetrics and Gynaecology, School of Medicine, Queen's Medical Centre, The University of Nottingham, Nottingham NG7 2UH, UK
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Introduction There is increasing evidence to support the early life programing of adult obesity, type 2 diabetes, and hypertension. The influence of prenatal environment depends on organ-specific windows of susceptibility with some, but not all