Pituitary-gonadal relations in male children and adolescents.

Abstract

Extract: Data are provided on levels of circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in healthy male children and adolescents, and these levels are correlated with the stage of sexual maturation, bone maturation, whole body 40K content, and the 24-hr excretion of creatinine, estrogens, 17-hydroxy-corticosteroids, total 17-ketosteroids, and fractionated ll-deoxy-17-ketosteroids (see Tables I and II). Before age 6 there was no significant change with age in testis size or hormone concentrations. From age 6–10 years there was a gradual rise in testis size (Fig. 1), serum FSH (Fig. 4) and serum LH (Fig. 3), but no change in plasma testosterone (Fig. 2), which remained below 40 ng/100 ml. From age 11–17 years there was a doubling of mean testis length, continued rise in serum FSH, and a steeper rise in LH; these changes were accompanied by a 20-fold increase in plasma testosterone concentration, the appearance of male secondary sexual characteristics (Figure 5), more rapid bone maturation and whole body 40K accretion, and enhanced excretion of estrogens and ll-deoxy-17-ketosteroids. Mean levels of FSH in the adult range (> 10 μUg/100 ml) were achieved by age 8, and levels reached a plateau by age 15 (Fig. 6). Adult LH levels (> 2.5 μUg/100 ml) were reached by age 13 and a plateau was observed after 17 years. Plasma testosterone also ceased to rise after age 17. The data suggest that the testis may undergo progressive gonadotropin-mediated maturation in late childhood. Testosterone secretion by the Leydig cells at puberty may result from a further rise in LH levels. Speculation: Pituitary secretion of gonadotropins, particularly FSH, in male children is a gradual phenomenon, antedeating by several years the release of testosterone by the testis. This gradual rise may represent a progressive reduction in hypothalamic sensitivity to feedback by testicular steroids other than testosterone. In late childhood, rising FSH and LH levels may induce increased activity of the enzymes responsible for both synthesis and catabolism of tesoterone. At puberty, an LH-mediated reduction in reductase activity might then result in testosterone accumulation and secretion.