Summary of androgen physiology Mechanism of action and conversions in VS .NET

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Summary of androgen physiology Mechanism of action and conversions
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The testis has a dual function: spermatogenesis and the production of T The latter takes places in the Leydig cells The daily production of T in adulthood is about 5 7 mg T diffuses passively into cells of the target organs of androgens To exert its biologic action, it must bind to the androgen receptor, though there are also a number of biologic actions of T that do not require receptor activation For some of its biologic actions T is a prohormone After diffusion into the cell, T may be converted to 5 -dihydrotestosterone (DHT) or estradiol There are two types of 5 reductase enzymes that convert T to DHT 5 reductase type 1 is predominantly located in skin, liver, and brain whereas 5 reductase type 2 is almost exclusively distributed in the classical androgendependent organs such as prostate,seminal vesicles, and testicles DHT and T bind to the same androgen receptor, although DHT has an approximately tenfold greater af nity for the receptor and its dissociation is slower, resulting in a considerably higher biopotency than T The conversion of T to DHT can be viewed as an androgen ampli cation mechanism in organs that require a strong androgen action, such as
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Testosterone is a lipophilic molecule and its solubility in blood is limited Only 2% of circulating T is free, non-bound to transport proteins, able to diffuse into cells, and immediately available for biologic action Approximately 60% of circulating T is bound with high af nity to sex hormone binding globulin (SHBG), and 38% is loosely bound and transported by albumin The free fraction of T (FT, 2%) and the albumin-bound fraction ( 38%) have been termed bioavailable testosterone (BT), since these two fractions are readily available for biologic action Testosterone has a high af nity with SHBG and changes in concentrations of circulating SHBG impact on the bioavailability of T SHBG is produced by the liver and a number of conditions and hormones in uence its production Androgens and growth hormone decrease circulating SHBG, which increases BT, and ampli es the action of T along with the combined anabolic effects of growth hormone (GH) and T Andro-
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Hormones, Metabolism, Aging, and Men s Health
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CNS stimulation
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Hypothalamus
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GnRH
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Hypothalamic pituitary portal system
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Posterior pituitary
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Anterior pituitary
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LH Sertoli cells Leydig cells Testosterone
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Fig 181 Production and regulation of
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testosterone CNS, central nervous system; FSH, follicle stimulating hormone; GnRH, gonadotropinreleasing hormone; LH, luteinizing hormone
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Testis Sperm inhibin
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gen de ciency, estrogens, hyperthyroidism, and liver disease increase circulating SHBG, and consequently limit its biologic action SHBG also binds estradiol but with lower af nity than T, such that certain conditions may be associated with signs of estrogen excess such as gynecomastia Overweightness with its associated hyperinsulinism, corticosteroids, and hypothyroidism reduce circulating SHBG and result in low total plasma concentrations
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Secretion
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T secretion follows a daily rhythm with highest T levels in the early morning hours, gradually declining to reach the lowest levels in the early evening The biologic signi cance of this diurnal rhythm has not been established, and dissipates with aging It is usually recommended to measure T in the early morning hours to avoid an erroneous diagnosis of hypogonadism, on the basis of the physiologically lower T levels in the afternoon Two recent papers questioned this recommendation because they did not nd any signi cant diurnal variation in men over 40 [6,7], contrary to younger healthy men in whom this variation was marked [7] The secretion of T from the Leydig cell is stimulated by the pituitary hormone, luteinizing hormone (LH) (Fig 181) Human chorionic gonadotropin (hCG) is
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chemically largely identical with LH and is capable of stimulating T production Follicle stimulating hormone (FSH) binds to the Sertoli cells and promotes spermatogenesis The pituitary production of LH and FSH, in turn, is regulated by the hormone, luteinizing hormone releasing hormone (LHRH), also called gonadotropin-releasing hormone (GnRH), produced in the arcuate nucleus and the preoptic area of the hypothalamus under the stimulating and inhibitory in uence of local neurotransmitters LHRH is secreted in regular pulses, with peaks in adulthood every 90 120 minutes, due to the intrinsic capacity of LHRH neurons to secrete episodically The pulsatility of LHRH is essential to its gonadotropin-releasing effect Continuous stimulation of the pituitary by LHRH leads to desensitization and to a cessation of LH and FSH release The hypothalamus is connected with the anterior pituitary through a portal system through which LHRH reaches the pituitary Due to this anatomic situation the concentration of LHRH in peripheral blood is immeasurably low
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