Acth steroid synthesis

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

As indicated above, ACTH is a cleavage product of the pro-hormone, proopiomelanocortin (POMC), which also produces other hormones including α-MSH that stimulates the production of melanin . A family of related receptors mediates the actions of these hormones, the MCR, or melanocortin receptor family. These are mainly not associated with the pituitary - adrenal axis. MC2R is the ACTH receptor . While it has a crucial function in regulating the adrenal, it is also expressed elsewhere in the body, specifically in the osteoblast , which is responsible for making new bone, a continual and highly regulated process in the bodies of air-breathing vertebrates. [10] The functional expression of MC2R on the osteoblast was discovered by Isales et alia in 2005. [11] Since that time, it has been demonstrated that the response of bone forming cells to ACTH includes production of VEGF , as it does in the adrenal. This response might be important in maintaining osteoblast survival under some conditions. [12] If this is physiologically important, it probably functions in conditions with short-period or intermittent ACTH signaling, since with continual exposure of osteoblasts to ACTH, the effect was lost in a few hours.

Acth steroid synthesis

acth steroid synthesis


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