11beta hydroxysteroid

When tested in vitro , 7-keto appears to activate the beta subset of the estrogen receptor (ERβ) with an EC 50 around 500μM which is partially blocked by exemestane (aromatase inhibitor or AI); there was no apparent activity on the classical subset (ERα) and parent DHEA and DHEAS were eqipotent. [45] As activity was hindered with an AI and there was efficacy in HepG2 cells but not Hep293 (expressing [46] and not expressing [47] aromatase, respectively) it is though that 7-oxo can be metabolized into an estrogen. [45]

Biosynthesis of steroid hormones requires a battery of oxidative enzymes located in both mitochondria and endoplasmic reticulum. The rate-limiting step in this process is the transport of free cholesterol from the cytoplasm into mitochondria. Within mitochondria, cholesterol is converted to pregnenolone by an enzyme in the inner membrane called CYP11A1. Pregnenolone itself is not a hormone, but is the immediate precursor for the synthesis of all of the steroid hormones. The following table delineates the enzymes required to synthesize the major classes of steroid hormones.

This gene encodes a member of the aldo/keto reductase superfamily , which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ), and the oxidation of 9alpha,11beta-PGF2 to PGD2. It may play an important role in the pathogenesis of allergic diseases such as asthma, and may also have a role in controlling cell growth and/or differentiation. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14. [7]

Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)

11beta hydroxysteroid

11beta hydroxysteroid

Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)

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