Ganong's Review of Medical Physiology, 23rd Edition

FSH
3.0
2.0
LH
(ng/mL)
1.0
0.5
FSH
3.0
2.0
LH
(ng/mL)
1.0
0.5
FIGURE 25–9 Changes in plasma hormone concentrations
during puberty in boys (top) and girls (bottom). Stage 1 of puberty
is preadolescence in both sexes. In boys, stage 2 is characterized by beginning
enlargement of the testes, stage 3 by penile enlargement,
stage 4 by growth of the glans penis, and stage 5 by adult genitalia. In
girls, stage 2 is characterized by breast buds, stage 3 by elevation and
enlargement of the breasts, stage 4 by projection of the areolas, and
stage 5 by adult breasts. (Modified and reproduced with permission from
Berenberg SR [editor]: Puberty: Biologic and Psychosocial Components. HE Stenfoert
Kroese BV, 1975.)
from birth to puberty, a neural mechanism is operating to prevent
the normal pulsatile release of GnRH. The nature of the
mechanism inhibiting the GnRH pulse generator is unknown.
However, one or more genes produce products that stimulate
secretion of GnRH, and inhibition of these genes before puberty
is an interesting possibility (see Clinical Box 25–2).
PRECOCIOUS & DELAYED PUBERTY
Sexual Precocity
FSH
The major causes of precocious sexual development in humans
are listed in Table 25–2. Early development of secondary
sexual characteristics without gametogenesis is caused by abnormal
exposure of immature males to androgen or females to
estrogen. This syndrome should be called precocious pseudopuberty
to distinguish it from true precocious puberty due to
an early but otherwise normal pubertal pattern of gonadotropin
secretion from the pituitary.
CHAPTER 25 The Gonads: Development & Function of the Reproductive System 399
6
4
Testosterone
(ng/mL)
2
1 2 3 4–5 Adult
Stage of puberty
7.7 12 13.7 15.7 Bone age
FSH
LH
LH
60
40
20
17β-
Estradiol
(pg/mL)
1 2 3 4 5
Stage of puberty
7.0 10.5 11.6 13.0 14.0 Bone age
CLINICAL BOX 25–2
Leptin
It has been argued for some time that a critical body weight
must normally be reached for puberty to occur. Thus, for
example, young women who engage in strenuous athletics
lose weight and stop menstruating, as do girls with anorexia
nervosa. If these girls start to eat and gain weight,
they menstruate again, that is, they “go back through puberty.”
It now appears that leptin, the satiety-producing
hormone secreted by fat cells, may be the link between
body weight and puberty. Obese ob/ob mice that cannot
make leptin are infertile, and their fertility is restored by injections
of leptin. Leptin treatment also induces precocious
puberty in immature female mice. However, the way that
leptin fits into the overall control of puberty remains to be
determined.
Constitutional precocious puberty; that is, precocious puberty
in which no cause can be determined, is more common in girls
than in boys. In both sexes, tumors or infections involving the
hypothalamus cause precocious puberty. Indeed, in one large
series of cases, precocious puberty was the most common endocrine
symptom of hypothalamic disease. In experimental
TABLE 25–2 Classification of the causes
of precocious sexual development in humans.
True precocious puberty
Constitutional
Cerebral: Disorders involving posterior hypothalamus
Tumors
Infections
Developmental abnormalities
Gonadotropin-independent precocity
Precocious pseudopuberty (no spermatogenesis or ovarian
development)
Adrenal
Congenital virilizing adrenal hyperplasia
Androgen-secreting tumors (in males)
Estrogen-secreting tumors (in females)
Gonadal
Leydig cell tumors of testis
Granulosa cell tumors of ovary
Miscellaneous