Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 25

The Gonads: Development & Function of the Reproductive System 399

from birth to puberty, a neural mechanism is operating to pre-
vent 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

The major causes of precocious sexual development in hu-
mans are listed in Table 25–2. Early development of secondary
sexual characteristics without gametogenesis is caused by ab-
normal exposure of immature males to androgen or females to
estrogen. This syndrome should be called
precocious pseudo-
puberty
to distinguish it from
true precocious puberty
due to
an early but otherwise normal pubertal pattern of gonadotro-
pin secretion from the pituitary.

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 endo-

crine symptom of hypothalamic disease. In experimental

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 be-
ginning 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.)

3.0

2.0

1.0

0.5

6

4

2

FSH

LH

(ng/mL)

1

7.7 12 13.7 15.7 Bone age

23

Stage of puberty

4–5 Adult

Testosterone

(ng/mL)

3.0

2.0

1.0

0.5

60

40

20

FSH

LH

(ng/mL)

1

7.0 10.5 11.6 13.0 14.0 Bone age

23

Stage of puberty

45

17 β-

Estradiol

(pg/mL)

FSH

LH

FSH

LH

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 an-

orexia nervosa. If these girls start to eat and gain weight,

they menstruate again, that is, they “go back through pu-

berty.” 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 in-

jections 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.

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