Puberty testosterone

At puberty, testosterone promotes sexual maturation of the male. 

B. Effects Testosterone is necessary for normal development of the male fetus and infant and is responsible for the major changes in the male at puberty (growth of penis, larynx, and skeleton development of facial, pubic, and axillary hair darkening of skin enlargement of muscle mass). After puberty, testosterone acts to maintain secondary sex characteristics, fertility and libido. It also acts upon hair cells to cause male-pattern baldness. 

Often, the enhancement is accomplished by the use of steroid compounds such as testosterone, the principal male sex hormone. Testosterone is responsible for the secondary sex changes that occur in males as they reach puberty. Testosterone is also produced by females, but only in amounts about 5% that of males. In both sexes, testosterone influences energy levels and protects the body from developing osteoporosis. 

Sex Hormones Testosterone and androsterone are the two most important male sex hormones, or androgens. Androgens are responsible for the development of male secondary sex characteristics during puberty and for promoting tissue and muscle growth. Both are synthesized in the testes from cholesterol. Androstenedione is another minor hormone that has received particular attention because of its use by prominent athletes. 

CYP17 is the 17 alpha-hydroxylase and 17-20 lyase, two different reactions catalyzed by one enzyme and required for production of testosterone and estrogen, respectively. Defects in this enzyme affect development at puberty. 

Evidence that BPH could be hormone related came from studies of a population of pseudohermaphrodites in the Dominican Republic. These individuals are genetically male, but do not display normal male genitalia until the onset of puberty. They are therefore raised as females until puberty. Studies revealed that these pseudohermaphrodites are deficient in an isoform of the enzyme steroid 5a-reductase, which is responsible for catalyzing the conversion of testosterone to dihydrotestosterone (DHT). In addition to the overt sexual manifestations of this condition, affected individuals show no incident of male pattern baldness, mild or no acne, and underdevelopment of the prostate. These observations led researchers to postulate that a selective inhibitor of steroid 5a-reductase would be an effective treatment for BPH. 

Methyl testosterone Hypogonadism, delayed puberty Oreton Methyl, Testred, Virilon... 

Molecular studies explained this apparent paradox when the temperature-sensitive G a Ala366Ser mutation of the G a protein was identified. At 32°C, the G a 366Ser mutation results in the constitutive cAMP accumulation that causes the testosterone secretion that is the hallmark of the testotoxicosis phenotype. At 37°C, however, the G a 366Ser mutation results in loss of adenylyl cyclase signaling, causing PHP-Ia. As a result, a single mutation that performs differently in different tissues causes precocious puberty and abnormalities of PTH and TSH (91). 

The explanation for this phenomenon is that in the prepubertal phase the amount of testosterone that is secreted is not sufficient to cause development of the male genitalia, which is normally stimulated by dihydrotestosterone. However, at puberty the secretion of testosterone increases. The increase is large in this syndrome, because lack of dihydrotestosterone decreases the extent of the feedback inhibition of the hormone secretions by the pituitary so that more gonadotrophins are released which stimulate, markedly, the rate of testosterone secretion and hence its concentration in the blood. At these high levels, testosterone has sufficient androgenic effects to stimulate development of the external genitalia. 

Replacement therapy - Replacement therapy in hypogonadism associated with a deficiency or absence of endogenous testosterone. Prior to puberty, androgen replacement therapy is needed for development of secondary sexual characteristics. Prolonged treatment is required to maintain sexual characteristics in these and other males who develop testosterone deficiency after puberty. Appropriate adrenal cortical and thyroid hormone replacement therapy are still necessary, however, and are of primary importance. 

Androgens produce both virilizing and protein anabolic actions (Table 63.1). The virilizing actions of testosterone include irreversible effects that occur during em-bryogenesis, that is, those that induce differentiation of the central nervous system and male reproductive tracts, and the excitatory actions at puberty that are... 

GnRH analogues (see Chapter 59) can induce chemical castration by suppressing the pulsatile release of LH and FSH, hence inhibiting testicular steroidogenesis. Administration of these compounds reduces circulating testosterone levels. These compounds are inhaled, injected subcutaneously, or implanted subcutaneously. They are used in males in the treatment of precocious puberty and carcinoma of the prostate. 

G. Other applications Limited data show some beneficial effects of leuprolide in the treatment of breast cancer. According to Micromedex, there is good documentation that leuprolide is effective for bowel pain and nausea associated with irritable bowel syndrome. Leuprolide has been used for controlled ovarian hyperstimulation to enhance the in vitro fertilization-embryo transfer procedure. In endometriosis, the goal of treatment is pain relief and reduction of endometriotic lesions. In children with central precocious puberty, stimulated and basal gonadotropins are reduced to prepubertal levels. Testosterone and estradiol are reduced to prepubertal levels in males and females, respectively. 

Sex hormones control tissue growth and reproduction. Male sex hormones are testosterone and Sa-dibydrotestosterone, also known as androgens, which are secreted by the testes. The primary male hormone, testosterone, is responsible for the development of secondary sex characteristics during puberty. They also promote muscle growth. The two most important female sex hormones are oestradiol and oestrone, also known as oestrogem estrogens). They are responsible for the development of female secondary sex characteristics. 

Other reported adverse effects of gonadotropin treatment are headache, depression, edema, precocious puberty, and (rarely) production of antibodies to hCG. In men treated with gonadotropins, the risk of gynecomastia is directly correlated with the level of testosterone produced in response to treatment. An association between ovarian cancer, infertility, and fertility drugs has been reported. However, it is not known which, if any, fertility drugs are causally related to cancer. 

In men, approximately 8 mg of testosterone is produced daily. About 95% is produced by the Leydig cells and only 5% by the adrenals. The testis also secretes small amounts of another potent androgen, dihydrotestosterone, as well as androstenedione and dehydroepiandrosterone, which are weak androgens. Pregnenolone and progesterone and their 17-hydroxylated derivatives are also released in small amounts. Plasma levels of testosterone in males are about 0.6 mcg/dL after puberty and appear to decline after age 50. Testosterone is also present in the plasma of women in concentrations of approximately 0.03 mcg/dL and is derived in approximately equal parts from the ovaries and adrenals and by the peripheral conversion of other hormones. 

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