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Glucocorticoids (or, less commonly, ... deficiency or to suppress the body's immune system. ... or hyperadrenocorticism have effects on many systems. Some examples ...
Steroid ring system.. This is a list of corticosteroids (glucocorticoids and mineralocorticoids) or derivatives of cortisol (hydrocortisone).Most esters of these corticosteroids are not included in this list; for esters, see here instead.
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones.Two main classes of corticosteroids, glucocorticoids and mineralocorticoids, are involved in a wide range of physiological processes, including stress response, immune response, and regulation of inflammation, carbohydrate metabolism ...
In many species, including amphibians, reptiles, rodents and birds, corticosterone is a main glucocorticoid, [3] involved in regulation of energy, immune reactions, and stress responses. [4] However, in humans, cortisol is the primary glucocorticoid that is produced primarily in the zona fasciculata of the adrenal cortex.
The following is a list of hormones found in Homo sapiens.Spelling is not uniform for many hormones. For example, current North American and international usage uses [citation needed] estrogen and gonadotropin, while British usage retains the Greek digraph in oestrogen and favours the earlier spelling gonadotrophin.
The glucocorticoid receptor (GR or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind. The GR is expressed in almost every cell in the body and regulates genes controlling the development , metabolism , and immune response .
Abnormally high amounts of a hormone can result in atypical effects. Glucocorticoids function by attaching to cytoplasmic receptors to either enhance or suppress changes in the transcription of DNA and thus the synthesis of proteins. Glucocorticoids also inhibit the secretion of cytokines via post-translational modification effects. [4]
Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue ...