Testosterone can either directly exert effects on target tissues or be metabolized by 5α-reductase into dihydrotestosterone (DHT) or aromatized to estradiol (E2). In general, androgens such as testosterone promote protein synthesis and thus growth of tissues with androgen receptors. Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. In addition to its role as a natural hormone, testosterone is used as a medication to treat hypogonadism and breast cancer. As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men.
Common side effects from testosterone medication include acne, swelling, and breast enlargement in males. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. The brain is also affected by this sexual differentiation; the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. Some of these effects may decline as testosterone levels might decrease in the later decades of adult life. Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes.
The effect of testosterone on blood pressure is often controversial. For these patients, testosterone replacement therapy might restore the protective influence of EPHB6 mutation in lowering catecholamine secretion and hence, blood pressure. Abolished expression of EPHB6 in KO mice alleviates the inhibitory influence of testosterone over BK channels, leading to a larger K+ efflux. Testosterone enhances BK currents either through direct binding with the ion channel33, by non-genomic signaling through Src kinases27 or its cell surface androgen receptors28.
Despite substantially lower risk of mortality compared to commonplace activities such as driving (Hart, Griffith, & Randell, 2006), skydiving generates a substantial physiological response. Testosterone re- sponsivity to skydiving was predicted by increased cortisol, increased sympathetic activity (heart rate) and reduced parasympathetic activity (RMSSD). Testosterone reactivity/recovery to skydiving was significantly greater than basal day measurements. It also increases blood pressure and helps break down fat and increase blood sugar levels to provide more energy to the body.
Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. It is bound 65% to sex hormone-binding globulin (SHBG) and 33% bound weakly to albumin. The plasma protein binding of testosterone is 98.0 to 98.5%, with 1.5 to 2.0% free or unbound. The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (Figure 2). In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone. In contrast to testosterone, DHEA and DHEA sulfate have been found to act as high-affinity agonists of these receptors. Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor (NGF), with high affinity (around 5 nM).

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