Androgens effect changes in hair distribution, skin texture, pitch of the voice, bone growth, and muscle development. Hair is classified by its sensitivity to androgens into nonsexual (eyebrows and extremities); ambisexual (axilla), which is responsive to low levels of androgens; and sexual (face, chest, upper pubic triangle), which is responsive only to high androgen levels. Hair follicles metabolize testosterone to DHT or androstenedione. Androgens stimulate the growth of facial, chest, and axillary hair; however, along with genetic factors, they also promote temporal hair recession and loss. Normal axillary and pubic hair growth in women is also under androgenic control, whereas excess androgen production in women causes the excessive growth of sexual hair (hirsutism).
The growth and secretory activity of the sebaceous glands on the face, upper back, and chest are stimulated by androgens, primarily DHT, and inhibited by estrogens. Increased sensitivity of target cells to androgenic action, especially during puberty, is the cause of acne vulgaris in both males and females. Skin derived from the urogenital ridge (e.g., the prepuce, scrotum, clitoris, and labia majora) remains sensitive to androgens throughout life and contains an active 5a-reductase. Growth of the larynx and thickening of the vocal cords are also androgen-dependent. Eunuchs maintain the high-pitched voice typical of prepuber-tal boys because they were castrated prior to puberty.
The growth spurt of adolescent males is influenced by a complex interplay between androgens, growth hormone (GH), nutrition, and genetic factors. The growth spurt includes growth of the vertebrae, long bones, and shoulders. The mechanism by which androgens (likely DHT) alter bone metabolism is unclear. Androgens accelerate closure of the epiphyses in the long bones, eventually limiting further growth. Because of the latter, precocious puberty is associated with a final short adult stature, whereas delayed puberty or eunuchoidism usually results in tall stature. An drogens have multiple effects on skeletal and cardiac muscle. Because 5a-reductase activity in muscle cells is low, the androgenic action is due to testosterone. Testosterone stimulates muscle hypertrophy, increasing muscle mass; however, it has minimal or no effect on muscle hyperplasia. Testosterone, in synergy with GH, causes a net increase in muscle protein.
Other nonreproductive organs and systems are affected, directly or indirectly, by androgens, including the liver, kidneys, adipose tissue, and hematopoietic and immune systems. The kidneys are larger in males, and some renal enzymes (e.g., ^-glucuronidase and ornithine decarboxy-lase) are induced by androgens. HDL levels are lower and triglyceride concentrations higher in men, compared to premenopausal women, a fact that may explain the higher prevalence of atherosclerosis in men. Androgens increase red blood cell mass (and, hence, hemoglobin levels) by stimulating erythropoietin production and by increasing stem cell proliferation in the bone marrow.
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