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Introduction The fetal adrenal gland and hypothalamic–pituitary axis (HPA) play important roles during pregnancy. Between weeks 32 and 34 of gestation, there is a rapid maturation of the fetal adrenal cortex, allowing development of a variety of
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Faculty of Life Sciences and Medicine, School of Life Course Sciences, King’s College London, London, UK
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Quebec Heart and Lung Institute, Laval University, Quebec, Canada
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Barts and the London School of Medicine, Centre for Endocrinology, William Harvey Institute, London, UK
Neuroendocrine Tumour Unit, Royal Free Hospital, London, UK
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Obesity, Type 2 Diabetes and Immunometabolism Research Group, School of Cardiovascular and Metabolic Medicine & Sciences, Faculty of Life Course Sciences, King’s College London, London, UK
Division of Reproductive Health, Warwick Medical School, University of Warwick, Coventry, UK
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no clinical utility when evaluating hypothalamic–pituitary–adrenal (HPA) axis capacity in patients on mitotane ( 13 ). The relationship between cortisol and CBGs was assessed in patients on mitotane therapy; the rank revealed a negative correlation
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
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Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
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Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
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Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK
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Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
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Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK
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–pituitary–adrenal (HPA) axis during the follow-up period after being switched from hydrocortisone to prednisolone. Endogenous cortisol production only became apparent when they were switched to prednisolone. These individuals had a diagnosis of SAI and showed evidence of
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Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
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negative feedback on the hypothalamus–pituitary–adrenal (HPA) axis, resulting in the over-production of adrenocorticotropic hormone (ACTH). The excess ACTH is shunted towards the androgen production pathways in the adrenal cortex and thus leads to an
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the underlying inflammatory pathology per se or could be due to suppression of the HPA axis by supraphysiological dose of exogenous glucocorticoids. It is difficult to differentiate between the two; however, radiological evaluation with MRI may
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
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inflammatory response is the local release of a number of inflammatory mediators such as cytokines (interleukin 1 (IL1), IL6, and tumor necrosis factor α (TNFα)), which then act in the CNS activating the hypothalamic–pituitary–adrenal (HPA) axis, the main
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Hypothalamo–pituitary–adrenal axis The hypothalamo–pituitary–adrenal (HPA) axis dictates the production of glucocorticoids secreted from the adrenal gland. Parvocellular neurosecretory neurons within the hypothalamic paraventricular nucleus
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affecting neurons of the HPA axis, which in turn can trigger pituitary TSH stimulation ( 48 , 49 ). The same mechanisms may be at play in both NORM:HCHF sheep and HIGH:CONV sheep. The adult sheep in our study could not be characterized as obese, but had a
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Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
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and OST were indicative of normal HPA axis function at the time the response to desmopressin changed and became clearly altered only months to years after this first response ( Table 2 ). Figure 3 ACTH response to desmopressin at long
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class of steroid hormones present in almost every cell of the body and are essential for survival ( 13 ). Glucocorticoid release is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. The suprachiasmatic nucleus of the hypothalamus releases