| Testosterone, (17ß-Hydroxy-4-androstene-3-one), a C19 steroid, is one of the most potent naturally secreted androgens [1]. In postpubertal males, testosterone is secreted primarily by the testes with only a small amount derived from peripheral conversion of androstenedione [2]. In adult women, it has been estimated that over 50% of serum testosterone is derived from peripheral conversion of androstenedione secreted by the adrenal and ovary, with the remainder from direct secretion of testosterone by these glands [2,3]. The majority of circulating testosterone is bound by SHBG and a smaller portion is bound by albumin. Only 1-2% exists in circulation as unbound or free testosterone [4].
In males, testosterone, either directly or after conversion to DHT, normally functions in fetal Wolffian duct differentiation, development of male external genetalia, stimulation of spermatogenesis, stimulation of anabolic activity in a variety of tissues and, possibly, behavioral and psychological effects [5,6]. In both sexes, testosterone contributes to the development of secondary sexual hair, acne, and scalp hair patterns. In prepubertal males, elevated testosterone levels are found in precocious puberty [7] and in androgen receptor defects [5]. In adult males, low testosterone levels are associated with various pathological conditions, including primary hypogonadism. In females of all ages, elevated testosterone levels can be associated with a variety of virilizing conditions, including adrenal tumors and polycystic ovarian disease [3].
- Dorfman RI & Shipley RA. Androgens. JohnWiley and Sons, Inc., New York, 1956, pp. 116-128.
- Horton E & Tait JF. J clin Invest 45:301-313, 1966.
- Pang S & Riddick L. Hirsutism. IN Lifshitz F (ed). Pediatric Endocronology, A Clinical Guide, second edition. Marcel Dekker, Inc., New York, 1990, pp. 259-291.
- Cumming DC & Wall SR. J. Cin Endocrinol Metab 61: 873-876, 1985.
- Griffin JE & Wilson JD, The androgen resistance syndroms: 5alpha-reductase deficiency, testicular feminization, and related syndromes. IN: Scriver CR, et al. (eds.): The Metabolic Basis of Inherited Disease, 6th ed. McGraw-Hill, New York, 1989, pp. 1919-1944
- Wilson JD. Endocrin Rev 9:181-199,1988.
- Holland FJ. Endocrinol Metab Clin North Am 64: 191-210, 1991
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