Figure 1.

The hypothalamic–pituitary–gonadal axis in men and the impact of testosterone therapy and estradiol on spermatogenesis. In obese patients, increased aromatase activity is thought to result in increased estradiol production. The increased estradiol level inhibits FSH and LH secretion from the pituitary, which results in reduced FSH and LH stimulation of the Sertoli and Leydig cells in the testes and a reduction in testosterone synthesis and sperm production. Administration of exogenous testosterone effectively raises serum testosterone levels. If fertility is desired administration of testosterone is, however, counterproductive because it provides negative feedback to the pituitary and causes inhibition of LH and FSH secretion. Decreased LH and FSH stimulation of the testes further inhibits spermatogenesis. Abbreviations: DHT, dihydrotestosterone; FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone.