In girls, mean levels of estradiol, secreted predominantly by the ovaries, increases steadily during puberty (19). Although, as noted, increases in estradiol first appear during the daytime hours, basal levels eventually increase during both the day and night. Estrone, which is secreted in part by the ovaries and arises in part from extraglandular conversion of estradiol and androstenedione, increases early in puberty but plateaus by midpuberty. Thus, the ratio of estrone to estradiol decreases throughout puberty, indicating that ovarian production of estradiol becomes increasingly important and peripheral conversion of androgens to estrone becomes less important during maturation.
In boys, most of the testosterone in the circulation arises from direct secretion by the Leydig cells of the testis. Testosterone induces development of a male body habitus and voice change, whereas dihydrotestosterone (DHT), produced following 5α reduction within target cells, induces enlargement of the penis and prostate gland, beard growth, and temporal hair recession during puberty. Mean plasma testosterone levels rise progressively during puberty, with the greatest increase occurring during Tanner stage 2 (24).
Growth hormone secretion increases along with increased gonadotropin secretion at the onset of puberty. It is believed that the increase in GH is mediated by estrogen, which in boys is dependent on aromatization of testosterone to estradiol and reﬂects increasing sex steroid production at puberty. Nonetheless, there are profound sex differences in GH secretion during puberty. Girls have higher basal levels of GH throughout puberty, reaching maximal levels around the time of menarche and decreasing thereafter. In contrast, basal concentrations of GH remain constant throughout puberty in boys. Growth hormone secretion is highly pulsatile, with most pulses occurring during sleep and with sex steroids increasing pulse amplitude rather than altering pulse frequency.
Growth hormone stimulates production of IGF-1 in all tissues, with concentrations found in the circulation spilling over from the liver. During puberty the negative feedback effect of IGF-1 on GH secretion must be reduced because both IGF-1 and GH levels are high. GH and IGF-1 play significant roles in the changes in body composition that occur at puberty because both hormones are potent anabolic agents.
In the final stages of puberty in both boys and girls, GH secretion begins to diminish, returning to prepubertal levels in adult life, despite continued exposure to high levels of gonadal steroids.
The mechanisms responsible for the numerous hormonal changes that occur during puberty are poorly understood, although it is recognized that a “central nervous system program” must be responsible for initiating puberty. It appears that the hypothalamic– pituitary–gonadal axis in girls develops in two distinct stages during puberty. First, sensitivity to the negative or inhibitory effects of the low levels of circulating sex steroids present in childhood decreases early in puberty. Second, late in puberty, there is maturation of the positive or stimulatory feedback response to estrogen, which is responsible for the ovulatory midcycle surge of LH.
Current evidence suggests that the central nervous system inhibits the onset of puberty until the appropriate time (25). Based on this theory, the neuroendocrine control of puberty is mediated by GnRH-secreting neurons in the medial basal hypothalamus, which together