Testicular steroidogenesis and its regulation in the primate fetus and newborn

The regulation of steroidogenesis of human fetal, rhesus monkey fetal and newborn testes was studied in vitro and in vivo. Human fetal testes (first half of gestation) bound specifically radioiodinated human chorionic gonadotropin (hCG) and responded with an increase of testosterone (T) production to physiologic levels (5 to 50 ng/mi) of hCG in incubations. Furthermore, placental effusate stimulated T release from fetal testicular minces in perifusion. In male monkeys chronically catheterized in utero (last third of gestation), intravenous administration of hCG or 100 >gjkg gonadotropin releasing hormone (GnRH) stimulated an increase in circulating T. Between two weeks and three months of postnatal age, this response clearly increased in both sensitivity and magnitude : doses as low as 10 to 20 >gjkg stimulated T responses 3-5 times higher than those seen in utero. Basal T levels also reached maximum concentrations during this period. Between three months and one year, the pituitary-testicular response to GnRH stimulation was gradually lost, and virtually no T response was seen by 1 year of age. Our observations confirmed the role of hCG as a tropic stimulus of human fetal testicular steroidogenesis during the first half of gestation. The monkey studies demonstrated that, during the second half of gestation, the pituitary-testicular axis was responsive to hypothalamic stimulation. This axis was less sensitive to GnRH in utero than immediately after birth. Postnatally, the response increased temporarily for 2-3 months, and was gradually lost thereafter. Accordingly, the loss of pituitary response to hypothalamic stimulation might be a major factor leading to low activity of prepubertal gonads.