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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Pharmacogenomics
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<blockquote data-quote="Cataceous" data-source="post: 221671" data-attributes="member: 38109"><p>Metabolism of testosterone is perhaps simpler than that of many other drugs, though no doubt genes still have some influence via the relative amounts of the necessary enzymes in the liver. Wikipedia describes it this way:</p><p></p><p style="margin-left: 20px"><em>Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine.</em></p><p>[<a href="https://en.wikipedia.org/wiki/Testosterone#Metabolism" target="_blank">R</a>]</p><p></p><p>The basic model for steady-state is:</p><p></p><p>Production_Rate(free testosterone) = Clearance_Rate(free testosterone) = MCR * Concentration(free testosterone)</p><p></p><p>The metabolic rate constant MCR represents the total action of the various enzymes that metabolize testosterone. The law of mass action explains the linear relationship. In any case, someone like you has a relatively lower value for MCR. Thus for a given production rate of testosterone—or total dose given over time—you must have a higher concentration of testosterone than someone with a higher MCR getting testosterone at the same rate.</p></blockquote><p></p>
[QUOTE="Cataceous, post: 221671, member: 38109"] Metabolism of testosterone is perhaps simpler than that of many other drugs, though no doubt genes still have some influence via the relative amounts of the necessary enzymes in the liver. Wikipedia describes it this way: [INDENT][I]Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[/I][/INDENT] [[URL='https://en.wikipedia.org/wiki/Testosterone#Metabolism']R[/URL]] The basic model for steady-state is: Production_Rate(free testosterone) = Clearance_Rate(free testosterone) = MCR * Concentration(free testosterone) The metabolic rate constant MCR represents the total action of the various enzymes that metabolize testosterone. The law of mass action explains the linear relationship. In any case, someone like you has a relatively lower value for MCR. Thus for a given production rate of testosterone—or total dose given over time—you must have a higher concentration of testosterone than someone with a higher MCR getting testosterone at the same rate. [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Pharmacogenomics
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