Steroid hormones exert their action on target cells by binding to

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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.

Cortisol - Cortisol is important for maintaining blood sugar levels, maintenance of body fluids and electrolytes, and protecting the body from stress. Cortisol has anti-inflammatory action, maintains blood sugar level, blood pressure, and muscle strength.

Dehydroepiandrosterone (DHEA) - Dehydroepiandrosterone is a steroid precursor produced by the adrenal gland and converted to testosterone or the estrogens by the body's tissues. DHEA appears to facilitate improved cholesterol profiles, loss of body fat, increased muscle gain.

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

Boys with too little androstenedione may fail to develop the sexual characteristics associated with puberty, including pubic and body hair, growth of the sexual organs and deepening of the voice. Similarly, girls may fail to start their periods and may not undergo many of the changes usually seen in puberty. In addition, if a male foetus has too little androstenedione, he may be born with abnormal genitalia. Too little androstenedione in later life would cause the same changes for both men and women as too little testosterone and oestrogen.

Steroid hormones exert their action on target cells by binding to

steroid hormones exert their action on target cells by binding to

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

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