J
Jonathan R. Seckl
Researcher at University of Edinburgh
Publications - 560
Citations - 57721
Jonathan R. Seckl is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Glucocorticoid & Glucocorticoid receptor. The author has an hindex of 114, co-authored 556 publications receiving 54990 citations. Previous affiliations of Jonathan R. Seckl include Queen's University & Charing Cross Hospital.
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Journal ArticleDOI
Epigenetic programming by maternal behavior.
Ian C. G. Weaver,Nadia Cervoni,Frances A. Champagne,Ana C. D'Alessio,Shakti Sharma,Jonathan R. Seckl,Sergiy Dymov,Moshe Szyf,Michael J. Meaney +8 more
TL;DR: It is shown that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible, suggesting a causal relation among epigenomicState, GR expression and the maternal effect on stress responses in the offspring.
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A Transgenic Model of Visceral Obesity and the Metabolic Syndrome
Hiroaki Masuzaki,Janice M. Paterson,Hiroshi Shinyama,Nicholas M. Morton,John J. Mullins,Jonathan R. Seckl,Jeffrey S. Flier +6 more
TL;DR: Increased adipocyte 11β HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.
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Early environmental regulation of forebrain glucocorticoid receptor gene expression: implications for adrenocortical responses to stress.
Michael J. Meaney,Josie Diorio,Darlene D. Francis,Judith Widdowson,Patricia Laplante,Christian Caldji,Shakti Sharma,Jonathan R. Seckl,Paul M. Plotsky +8 more
TL;DR: The findings indicate that the early postnatal environment alters the differentiation of hippocampal neurons, and these data provide examples of early environmental programming of neural systems.
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Prenatal Stress, Glucocorticoids and the Programming of the Brain
Leonie Welberg,Jonathan R. Seckl +1 more
TL;DR: The data suggest that key targets for programming include glucocorticoid receptor gene expression and the corticotrophin‐releasing hormone system, and that approaches to minimize or reverse the consequences of such early life events may have therapeutic importance.
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11beta-hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress.
Yuri Kotelevtsev,Megan C. Holmes,Ann Burchell,Pamela Houston,Dieter Schmoll,Pauline Jamieson,Ruth Best,Roger W. Brown,Christopher R. W. Edwards,Jonathan R. Seckl,John J. Mullins +10 more
TL;DR: Attenuation of hepatic 11beta-HSD-1 may provide a novel approach to the regulation of gluconeogenesis, which involves regenerating active glucocorticoids from circulating inert 11-keto forms in specific tissues, notably the liver.