secretion is implicated in the development of atherosclerosis, CVD and CV mortality ( 15 , 16 , 17 ). Several disturbances of the hypothalamus–pituitary–adrenal (HPA) axis in patients with T1D have been demonstrated. The disturbances include increased
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Eva Olga Melin, Magnus Hillman, and Mona Landin-Olsson
Ermina Bach, Niels Møller, Jens Otto L Jørgensen, Mads Buhl, and Holger Jon Møller
are indirect, since LPS acts through a number of cytokines and also activates the hypothalamo-pituitary axis (HPA) and stimulates the release of stress hormones (e.g. cortisol) into the blood ( 21 , 22 , 23 ). Since CD163 is strongly expressed in
Dorte Glintborg, Magda Lambaa Altinok, Pernille Ravn, Kurt Bjerregaard Stage, Kurt Højlund, and Marianne Andersen
increased hypothalamic–pituitary–adrenal (HPA) axis activity in PCOS. Increased adrenal activity was also found in patients with major depression and their first-degree relatives compared to healthy controls ( 9 , 10 ). Therefore, decreased quality of life
Fiona Broughton Pipkin, Hiten D Mistry, Chandrima Roy, Bernhard Dick, Jason Waugh, Rebecca Chikhi, Lesia O Kurlak, and Markus G Mohaupt
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
Annelies van’t Westeinde, Leif Karlsson, Valeria Messina, Lena Wallensteen, Manuela Brösamle, Giorgio Dal Maso, Alessandro Lazzerini, Jette Kristensen, Diana Kwast, Lea Tschaidse, Matthias K Auer, Hanna F Nowotny, Luca Persani, Nicole Reisch, and Svetlana Lajic
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
Brijesh Krishnappa, Ravikumar Shah, Saba Samad Memon, Chakra Diwaker, Anurag R Lila, Virendra A Patil, Nalini S Shah, and Tushar R Bandgar
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
Tatiana V Novoselova, Peter J King, Leonardo Guasti, Louise A Metherell, Adrian J L Clark, and Li F Chan
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
Fernando Aprile-Garcia, María Antunica-Noguerol, Maia Ludmila Budziñski, Ana C Liberman, and Eduardo Arzt
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
L Johnsen, N B Lyckegaard, P Khanal, B Quistorff, K Raun, and M O Nielsen
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
Alberto Giacinto Ambrogio, Massimiliano Andrioli, Martina De Martin, Francesco Cavagnini, and Francesca Pecori Giraldi
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
