83 research outputs found
Cortisol exposure and sensitivity in health and disease
Cortisol, the main glucocorticoid (GC) in man, is produced by the adrenal glands
and its secretion is under control of the Hypothalamic-Pituitary-Adrenal (HPA)
axis. Activation of the HPA-axis begins with the release of corticotrophinreleasing
hormone (CRH) from neurons in the paraventricular nucleus (PVN) of
the hypothalamus (1). CRH is released in the hypophysial-portal circulation and
binds to the type 1 corticotrophin releasing hormone receptors (CRH-R1) on the
anterior pituitary corticotroph cells. This stimulates the biosynthesis and secretion
of adrenocorticotropic hormone (ACTH) (2). This hormone is produced by cleavage
of pro-opiomelanocortin (POMC). ACTH is released in the peripheral circulation
and stimulates glucocorticoid production by the zona fasciculate cells of the adrenal
cortex, by binding to the type 2 melanocortin receptor (MC2-R). Binding of ACTH
to its receptor results in elevated intracellular levels of cyclic AMP (cAMP), which
ultimately leads to activation of steroidogenic enzymes, which are required for the
cortisol synthesis from cholesterol (3-4). There are three regulatory mechanisms of
cortisol secretion, namely 1) the inhibition of ACTH and CRH production by cortisol
itself (negative feedback), 2) the circadian rhythm of ACTH and cortisol secretion
and 3) the response to stress of the HPA-axis. A simplified version of the HPA-axis
is shown in figure 1
Increased Hair Cortisol Concentrations and BMI in Patients With Pituitary-Adrenal Disease on Hydrocortisone Replacement
Diabetes mellitus: pathophysiological changes and therap
Recent negative life events increase hair cortisol concentrations in patients with bipolar disorder
Stress-related psychiatric disorders across the life spa
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