The Male Life Span

Physiological studies have clarified in great detail the role of gonadotropins in the development and mature functions of male reproduction. In the fetal period, placental hCG, a superagonist of pituitary LH, is responsible for the stimulation of testosterone production by fetal Leydig cells, which is essential for masculinization of the male reproductive organs (15). This occurs in collaboration with the Sertoli cell product, anti-Mullerian hormone (or Mullerian-inhibiting substance), and another Leydig cell product, insulin-like factor-3 (INSL-3) that regulate the transabdominal phase of testicular descent (16,17). Although FSH secretion begins in the fetus and fetal testes express FSH-R (18), FSH's role in the fetal period is uncertain. Data from animal models indicate that its first role is the stimulation of Sertoli cell proliferation in the prepubertal testis (19). Fetal pituitary gonadotropin secretion begins at the end of the first trimester, with high levels in midpregnancy, followed by a decline toward the end of gestation, apparently resulting from development of feedback regulation (20). A secondary increase occurs during the first 4-6 mo of postnatal life, which is accompanied by a similar peak in testosterone production (21). No function has been demonstrated for this period of activation, and it may represent an adaptation to extrauterine life and the hormonal milieu in the absence of placental hormones.

The prepubertal phase of male development is typified by low circulating gonadotropin levels, but they are not absent, and ultrasensitive assays can detect pulsatile LH secretion especially during the night (22). Prepubertal testes also have receptors for both gonadotropins, as shown indirectly by their functional responses to stimulation by hCG or FSH (23).

Puberty is the period of reawakening of gonadotropin secretion (see Chapter 4). At this time, both hormones reach adult levels and the pulsatile pattern of secretion. LH activates Leydig cell growth, proliferation, and steroid production, and FSH stimulates Sertoli cell proliferation and the metabolic functions that are needed for the maintenance of spermatogenesis. Whether FSH is mandatory for the pubertal initiation and adult maintenance of spermatogenesis is controversial, but it is clear that qualitatively and quantitatively normal spermatogenesis is possible only in the presence of all endocrine and paracrine factors, including FSH, that are functioning in the pituitary-gonadal axis (24).

Human testicular function is maintained through old age. However, mean testosterone levels and spermatogenesis decline with aging (25). This phenomenon of "andropause" and the effect of testosterone replacement therapy, have recently received a great deal of attention (see Chapter 14).

When considering the influence of gonadotropin or gonadotropin receptor mutations on male reproductive functions, specific phenotypic effects can be identified during all stages of the male life span.

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