11-beta hidroxiesteroide deshidrogenasa tipo ii

Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and hence may explain why aspirin improves glycemic control in type 2 diabetes. [8] Epigallocatechin gallate from green tea can also potently inhibit this enzyme, [9] green tea is a complex mixture of various phenolics with contents varying with production and processing, some of the phenolics are known HDAC inhibitors that alter genetic expression. EGCG as usually consumed in green tea is poorly absorbed into the bloodstream, more research is needed to reach firm conclusions.

In contrast, the 41-kD type 2 enzyme 281 catalyzes the oxidation of cortisol and corticosterone using NAD + , and, although this enzyme has a high affinity for its steroid substrates ( K m to μM), 282 catalysis of the reductive reactions by 11βHSD2 has not been conclusively demonstrated. Cortisol is a potent agonist at the mineralocorticoid (glucocorticoid type 2) receptor in the distal nephron, but its oxidized 11-keto derivative, cortisone, is not a mineralocorticoid. The reason cortisol does not act as a mineralocorticoid in vivo, even though cortisol concentrations can exceed aldosterone concentrations by three orders of magnitude, is because cortisol is enzymatically converted to cortisone in the cells lining the cortical and medullary collecting ducts. Thus, the type 2 enzyme inactivates the mineralocorticoid activity of cortisol in the kidney tubule, 283 and inactivating mutations in the type 2 enzyme cause a syndrome of apparent mineralocorticoid excess 284 (see Chapter 108 ). The presence of the type 2 enzyme in the placenta 285 also inactivates endogenous and synthetic corticosteroids such as prednisolone, allowing the use of these agents during pregnancy without affecting the fetus. In contrast, 9α-fluorinated steroids such as dexamethasone are minimally inactivated by the type 2 enzyme, primarily because of a shift in the oxidation/reduction preference rather than a reduction in affinity for the enzyme. 288 It is this resistance to inactivation by placental 11βHSD2 that is essential for synthetic glucocorticoids to “cross the placenta” and to exert a pharmacologic effect on the fetus. Furthermore, the relatively high placental concentrations of NADP + may also favor the oxidative action of 11βHSD1, so that both placental enzymes protect the fetus from the high maternal concentrations of cortisol that occur during pregnancy. 270

Cortisol , a glucocorticoid, binds the glucocorticoid receptor. However, because of its molecular similarity to aldosterone it is also capable of binding the mineralcorticoid receptor. Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor; however, there is vastly more cortisol in circulation than aldosterone. To prevent over-stimulation of the mineralocorticoid receptor by cortisol, 11β-HSD converts the biologically active cortisol to the inactive cortisone, which can no longer bind to the mineralocorticoid receptor. 11β-HSD co-localizes with intracellular adrenal steroid receptors. Licorice , which contains glycyrrhetinic acid , or enoxolone , can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome .

11-beta hidroxiesteroide deshidrogenasa tipo ii

11-beta hidroxiesteroide deshidrogenasa tipo ii

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