The Endocrine System
351
SECTION E SUMMARY
Bone Growth
I. A bone lengthens as osteoblasts at the shaft edge of the
epiphyseal growth plates convert cartilage to bone while new
cartilage is being laid down in the plates.
II. Growth ceases when the plates are completely converted to
bone.
Environmental Factors Infl
uencing Growth
I. The major environmental factors infl uencing growth are
nutrition and disease.
II. Maternal malnutrition during pregnancy may produce
irreversible growth stunting and mental defi
ciency in
offspring.
Hormonal Infl
uences on Growth
I. Growth hormone is the major stimulus of postnatal growth.
a. It stimulates the release of IGF-1 from the liver and many
other cells, and IGF-1 then acts locally (and perhaps also as
a hormone) to stimulate cell division.
(a)
(b)
(c)
Figure 11–29
Gigantism and acromegaly in one individual of a pair of identical twins. Note the increased height and facial bone thickening (a), as well as the
bone thickening of hands (b) and feet (c).
Figure 11–29
physiological
inquiry
Did the individual in (a) develop excess growth hormone production before or after puberty?
Answer can be found at end of chapter.
blood fatty acid levels, and decrease target cell sensitivity
to insulin. Not surprisingly, therefore, one of the stimuli
that increases GH levels in the normal adult is a lowering of
blood sugar or fatty acids. The secretion of GH during these
metabolic crises, however, is transient; once plasma glucose
or fatty acid concentrations are restored to normal, GH levels
decrease to baseline. In acromegaly, however, GH levels are
always elevated. Thus, acromegaly is associated with elevated
plasma levels of glucose and fatty acids, similar to the levels in
diabetes. As in Cushing’s Syndrome (Section D), therefore,
the presence of chronically elevated levels of GH may result in
diabetic-like symptoms.
Treatment of gigantism and acromegaly usually
requires surgical removal of the pituitary tumor. The
residual normal pituitary tissue is then suffi
cient to
maintain baseline GH levels. If this treatment is impossible
or not successful, treatment with long-acting analogs of
somatostatin is sometimes necessary. (Recall that somatostatin
is the hypothalamic hormone that normally inhibits GH
secretion.)
b. Growth hormone also acts directly on cells to stimulate
protein synthesis.
c. Growth hormone secretion is highest during adolescence.
II. Because thyroid hormones are required for growth hormone
synthesis and the growth-promoting effects of this hormone,
they are essential for normal growth during childhood and
adolescence. They are also permissive for brain development
during infancy.
III. Insulin stimulates growth mainly during fetal life.
IV. Mainly by stimulating growth hormone secretion, testosterone
and estrogen promote bone growth during adolescence, but
these hormones also cause epiphyseal closure. Testosterone also
stimulates protein synthesis.
V. High concentrations of cortisol inhibit growth and stimulate
protein catabolism.
Additional Clinical Examples
I. Gigantism occurs when excess growth hormone is secreted
during the prepubertal period. If excess growth hormone
secretion occurs after linear growth has stopped, the
condition—known as acromegaly—results in bone thickening
and metabolic derangements.
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