| Mechanism of action and elimination of the steroid hormones
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| Steroid hormones act via nuclear receptors
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| All the steroid hormones act by binding to nuclear receptors and stimulating transcription. which results in specific protein synthesis (see Chapter 33, Fig. 33.4). Steroid hormone receptors belong to a super-family of hormone receptors, which include receptors to the thyroid hormone T3 and the active forms of vitamins A and D. The specificity of each receptor is being achieved through differing hydrophobic pockets in a small hormone-binding domain situated towards the C-terminus of the receptor. Adjacent to the hormone-binding domain is a highly conserved DNA-binding domain, which is characterized by the presence of two zinc fingers (see Fig. 33.3). Binding of the steroid ligand facilitates translocation to the nucleus, dimerization and binding to a specific steroid response element within the nuclear DNA, leading to transcription. Genetic variability in steroid hormone receptors' structure is well described, conveying a variable degree of steroid hormone resistance and diverse clinical presentations.
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| The biological actions of the steroid hormones are are best considered as part of the trophic hormone system to which they belong. This system is described in Chapter 37.
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| Steroid hormones are excreted in the urine
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| Most steroid hormones are excreted via the kidney. In general there are two main steps in this process. First, the biological potency of the steroid must be removed and this is achieved by a series of reduction reactions. Second, the steroid structure must be rendered water-soluble by conjugation to a glucuronide or sulfate moiety, usually through the hydroxyl group at C-3. These steps occur predominantly within the liver. As a result there are many different steroid hormone conjugates in urine, some of them present in high concentrations. Urinary steroid profiling by gas chromatography-mass spectrometry typically identifies more than 30 such steroids and the relative concentrations of these may be used to pinpoint specific defects in the steroidogenic pathway (see box on p. 222).
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