Current trends in the timing of puberty have been reported recently in both sexes. In North American boys, recent data indicate earlier genital growth (3). However, that study has elicited significant criticism, because the boys were not investigated thoroughly, although strong conclusions were drawn from the data. European studies do not support the American experience of strikingly earlier onset of puberty, e.g., in the Netherlands, a halt in the trend toward earlier puberty has been found during the last decades (4). Therefore, further studies are needed to confirm the earlier onset of puberty in male and female American adolescents.
A subgroup of children having exceptionally early puberty are those adopted from developing countries. These children are often malnourished on arrival in their new home country. Early or even precocious puberty can result in a final height much lower than expected, but this height may not be much different from that of peers living in the country of origin. One speculation is that the intensive growth period after adaptation is "corrected" by an earlier onset of puberty, which results in a final height that is consistent with the original genetic growth potential.
Endocrine Changes During Puberty Gonadotropin-Releasing Hormone and Gonadotropins
The hypothalamus-pituitary-gonadal axis is already mature in the fetal period. Gonadotropin-releasing hormone (GnRH) is produced by hypothalamic neurons that originate from the medial olfactory placode of the nose. These neurons migrate during central nervous system (CNS) development and are finally located in the arcuate nucleus, in the preoptic area and in the medial basal hypothalamus. During gestation, there is an increase in GnRH content, which reaches its peak at 34-38 wk in the male fetus (5). The secondary plexus of the portal capillary network is completed by weeks 19-21, coinciding with a striking rise of circulating gonadotropin levels at midgesta-tion in both male and female fetuses. After midgestation, high circulating gonadotropin levels decrease to low levels at birth. This change in gonadotropin secretion results from the development of negative feedback system to sex steroids, as well as from the development of inhibiting influences from the CNS to the GnRH neurons (vide infra).
Luteinizing hormone (LH) and follicle-stimulating hormone secretion rise during the first month after birth, probably because the negative feedback effect of placental estrogens are withdrawn (see Figs. 1 and 2). LH is secreted in pulses during this postnatal period (6). By the age of 6 to 12 mo, the GnRH pulse generator becomes quiescent, and gonadotropin levels decrease. However, LH pulses can be detected throughout childhood, with highly sensitive immunofluorometric methods (7,8).
With the onset of puberty, LH secretion is augmented, first only during the night (see Fig. 2). In boys, this increase in LH is associated with an increase in plasma testosterone levels during the morning hours. With progression of puberty, LH secretion increases through an increase in both LH pulse frequency and amplitude. The day-night rhythm of gonadotropin secretion is evident during puberty, but it disappears in adulthood (7,8).
LH controls sex steroid production by upregulating expression of the steroidogenic enzymes (see Chapter 2) and by controlling metabolic activity of the steroid-producing
neonate prepuberty puberty neonate prepuberty
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