Testosterone
Also known as: androgen, dihydrotestosterone, DHT
The principal male sex steroid, secreted by testicular Leydig cells under LH control, which drives male sexual differentiation, puberty, spermatogenesis, muscle and bone growth, and libido; many actions require conversion to DHT or estradiol.
Overview
In men ≈95 % of testosterone comes from Leydig cells (≈6–7 mg/day); in women it derives from the ovaries and adrenals and from peripheral conversion of androstenedione. In plasma ≈98 % is bound — to sex hormone-binding globulin (SHBG) (tightly) and albumin (loosely) — with ≈2 % free. Very high intratesticular concentrations (≈50–100 × plasma), maintained by Sertoli-cell androgen-binding protein, are essential for spermatogenesis.
Testosterone acts on the nuclear androgen receptor directly or after conversion. 5α-reductase (type 2 in the prostate, genital skin and hair follicles) produces the more potent dihydrotestosterone (DHT); aromatase produces estradiol. Testosterone itself virilises the Wolffian (mesonephric) ducts into epididymis, ductus deferens and seminal vesicles in the fetus, increases muscle mass, stimulates spermatogenesis, erythropoiesis and libido, and deepens the voice. DHT masculinises the external genitalia and prostate in the fetus and drives prostate growth, facial/body hair, sebum and male-pattern baldness later. Estradiol derived from testosterone closes the epiphyses and maintains bone density and provides negative feedback to the hypothalamus.
- Location
Source: Leydig (interstitial) cells of the testis (also ovarian theca cells and adrenal precursors). Targets: reproductive tract, skeletal muscle, bone, skin, hair follicles, larynx, bone marrow, brain.
Function
- Fetal male differentiation (Wolffian ducts; with DHT, external genitalia and prostate).
- Pubertal virilisation: genital growth, voice change, sexual hair, muscle mass, growth spurt.
- Initiation and maintenance of spermatogenesis.
- Libido and erectile function; erythropoiesis; bone density.
- Negative feedback on GnRH and LH.
- Physiology
Class: C19 steroid. Receptor: nuclear androgen receptor. Binding: SHBG ≈45–65 %, albumin ≈30–50 %, free ≈2 %. Adult male morning total testosterone ≈10–35 nmol/L (≈300–1000 ng/dL); diurnal peak in the morning.
- Regulation
LH stimulates Leydig cells; testosterone (and its estradiol metabolite) inhibits GnRH and LH. FSH and inhibin B regulate the Sertoli side of the axis.
Clinical significance
Male hypogonadism
Primary (high LH/FSH): Klinefelter syndrome (47,XXY — small firm testes, gynaecomastia, tall stature, infertility), orchitis, torsion, chemotherapy. Secondary (low/normal LH): pituitary tumours, hyperprolactinaemia, Kallmann syndrome, opioids, obesity. Features: low libido, erectile dysfunction, fatigue, loss of body hair, reduced muscle and bone mass, anaemia.
Exogenous androgens
Anabolic steroid or testosterone use suppresses LH and FSH, causing testicular atrophy and azoospermia, plus polycythaemia, acne, gynaecomastia (aromatisation) and dyslipidaemia.
Disorders of androgen action
5α-reductase deficiency: 46,XY with ambiguous/female external genitalia at birth that virilise at puberty. Complete androgen insensitivity syndrome: 46,XY, testes, female external phenotype, blind-ending vagina, absent uterus (AMH acts normally) and scant pubic hair. 5α-reductase inhibitors (finasteride) treat BPH and male-pattern hair loss; androgen deprivation treats prostate cancer.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.