Jonathan R. Seckl

ORCID: 0000-0001-5150-6624
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About
Contact & Profiles
Research Areas
  • Hormonal Regulation and Hypertension
  • Stress Responses and Cortisol
  • Birth, Development, and Health
  • Adrenal Hormones and Disorders
  • Apelin-related biomedical research
  • Neuroendocrine regulation and behavior
  • Pregnancy and preeclampsia studies
  • Estrogen and related hormone effects
  • Adipose Tissue and Metabolism
  • Electrolyte and hormonal disorders
  • Neonatal Respiratory Health Research
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Diet and metabolism studies
  • Gestational Diabetes Research and Management
  • Aldose Reductase and Taurine
  • Pharmacological Effects of Natural Compounds
  • Hormonal and reproductive studies
  • Anesthesia and Neurotoxicity Research
  • Nuclear Receptors and Signaling
  • Infant Nutrition and Health
  • Neuropeptides and Animal Physiology
  • Eicosanoids and Hypertension Pharmacology
  • Pancreatic function and diabetes
  • Diabetes and associated disorders
  • Ion Transport and Channel Regulation

University of Edinburgh
2016-2025

The Queen's Medical Research Institute
2014-2025

Diabetes UK
2023

Queen's Medical Centre
2011-2020

Medical Research Institute
2020

Edinburgh Royal Infirmary
2016-2019

British Heart Foundation
2011-2018

University of Helsinki
2010-2016

University of Southern Denmark
2016

Queen Margaret University
2016

The adverse metabolic consequences of obesity are best predicted by the quantity visceral fat. Excess glucocorticoids produce and diabetes, but circulating glucocorticoid levels normal in typical obesity. Glucocorticoids can be produced locally from inactive 11-keto forms through enzyme 11beta hydroxysteroid dehydrogenase type 1 (11beta HSD-1). We created transgenic mice overexpressing HSD-1 selectively adipose tissue to an extent similar that found obese humans. These had increased...

10.1126/science.1066285 article EN Science 2001-12-07

Glucocorticoid hormones, acting via nuclear receptors, regulate many metabolic processes, including hepatic gluconeogenesis. It recently has been recognized that intracellular glucocorticoid concentrations are determined not only by plasma hormone levels, but also 11β-hydroxysteroid dehydrogenases (11β-HSDs), which interconvert active corticosterone (cortisol in humans) and inert 11-dehydrocorticosterone (cortisone humans). 11β-HSD type 2, a dehydrogenase, thus excludes glucocorticoids from...

10.1073/pnas.94.26.14924 article EN Proceedings of the National Academy of Sciences 1997-12-23

Context: Reduced cortisol levels have been linked with vulnerability to posttraumatic stress disorder (PTSD) and the risk factor of parental PTSD in adult offspring Holocaust survivors.

10.1210/jc.2005-0550 article EN The Journal of Clinical Endocrinology & Metabolism 2005-07-01

Eosinophils and neutrophils are closely related, terminally differentiated cells that in vitro undergo constitutive cell death by apoptosis. The onset of apoptosis both types can be delayed hemopoietins inflammatory mediators. Although there have been a number reports demonstrating glucocorticoids (in particular dexamethasone) antagonize the eosinophil life-prolonging effects hemopoietins, direct dexamethasone on not documented. In this study we examined neutrophil light their common...

10.4049/jimmunol.156.11.4422 article EN The Journal of Immunology 1996-06-01

Abstract A large body of human epidemiological data, as well experimental studies, suggest that environmental factors operating early in life potently affect developing systems, permanently altering structure and function throughout life. This process with its persistent organizational effects has been called ‘programming’. The brain is a key target for such effects. review focuses on the adverse environments, notably exposure to stress or glucocorticoids, upon subsequent adult...

10.1111/j.1365-2826.2001.00601.x article EN Journal of Neuroendocrinology 2001-02-01

Gout is a common disease both in primary care and hospital practice [1]. Although drug therapy for gout has become paradigm the effective management prevention of an acute potentially chronic rheumatic disease, many recommendations treatment are based on expert consensus rather than research evidence audits suggest that very variable. Evidence-based guidelines needed at present time:

10.1093/rheumatology/kem056a article EN Lara D. Veeken 2007-05-23

Human epidemiological data show a strong association between low birth weight and hypertension in adulthood, an effect that has been ascribed to 'fetal programming'. In rats, fetoplacental exposure maternally administered dexamethasone throughout gestation reduces produces hypertensive adult offspring, though the mechanism is unclear. Pre- postnatal stress programmes hypothalamic-pituitary-adrenal (HPA) axis responses lifespan, thought be mediated via permanent effects on glucocorticoid...

10.1159/000127146 article EN Neuroendocrinology 1996-01-01

Background— The causes of metabolic syndrome (MS), which may be a precursor coronary disease, are uncertain. We hypothesize that disturbances in neuroendocrine and cardiac autonomic activity (CAA) contribute to development MS. examine reversibility the power psychosocial behavioral factors explain adaptations accompany Methods Results— This was double-blind case-control study working men aged 45 63 years drawn from Whitehall II cohort. MS cases (n=30) were compared with healthy controls...

10.1161/01.cir.0000038364.26310.bd article EN Circulation 2002-11-18

OBJECTIVE Placental 11β‐hydroxysteroid dehydrogenase (11β‐HSD), which converts active cortisol to inactive cortisone, has been proposed be the mechanism guarding fetus from growth retarding effects of maternal glucocorticoids; however, other placental enzymes have also implicated. 11β‐HSD is unstable in vitro , and enzyme activity thus detected may not relevant barrier role. We therefore examined glucocorticoid metabolism dually perfused freshly isolated intact human placentas. DESIGN...

10.1046/j.1365-2265.1997.1230939.x article EN Clinical Endocrinology 1997-02-01

The metabolic syndrome (visceral obesity, insulin resistance, type 2 diabetes, and dyslipidemia) resembles Cushing's Syndrome, but without elevated circulating glucocorticoid levels. An emerging concept suggests that the aberrantly levels of intracellular reamplifying enzyme 11 beta-hydroxysteroid dehydrogenase 1 (11 beta-HSD-1) found in adipose tissue obese humans rodents underlies phenotypic similarities between idiopathic "Cushingoid" obesity. Transgenic overexpression beta-HSD-1...

10.2337/diabetes.53.4.931 article EN Diabetes 2004-04-01

Excess tissue glucocorticoid action may underlie the dyslipidemia, insulin resistance, and impaired glucose tolerance of metabolic syndrome. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD-1) catalyzes conversion circulating inert 11-dehydrocorticosterone into active corticosterone, thus amplifying local intracellular action, particularly in liver. The importance 11β-HSD-1 homeostasis is suggested by resistance 11β-HSD-1<sup>−/−</sup> mice to hyperglycemia upon stress or obesity, due...

10.1074/jbc.m103676200 article EN cc-by Journal of Biological Chemistry 2001-11-01
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