Chapter 16
The Endocrine System
609
16
dopamine, and rising levels of glucocorticoids. Excessively high
blood iodide concentrations also inhibit TH release.
Homeostatic Imbalance
16.4
Both overactivity and underactivity of the thyroid gland can cause
severe metabolic disturbances. Hypothyroid disorders may result
from some thyroid gland defects or secondarily from inadequate
TSH or TRH release. ±ey also occur when the thyroid gland is
removed surgically and when dietary iodine is inadequate.
In adults, the full-blown hypothyroid syndrome is called
myxedema
(mik
0
sĕ-de
9
mah; “mucous swelling”). Symptoms
include a low metabolic rate; feeling chilled; constipation; thick,
dry skin and puffy eyes; edema; lethargy; and mental sluggish-
ness (but not mental retardation). A
goiter
(an enlarged pro-
truding thyroid gland) occurs if myxedema results from lack of
iodine
(Figure 16.11a)
. ±e follicular cells produce colloid but
cannot iodinate it and make functional hormones. ±e pituitary
gland secretes increasing amounts of TSH in a futile attempt to
stimulate the thyroid to produce TH, but the only result is that
the follicles accumulate more and more
unusable
colloid. De-
pending on the cause, iodine supplements or hormone replace-
ment therapy can reverse myxedema.
Before iodized salt became available, the midwestern United
States was called the “goiter belt.” Goiters were common there
because this area had iodine-poor soil and no access to iodine-
rich seafood. In places where goiters are especially common,
these goiters are called
endemic goiters
.
Like many other hormones, the important effects of TH
depend on a person’s age and development. Severe hypothy-
roidism in infants is called
cretinism
(kre
9
tĭ-nizm). ±e child
is mentally retarded and has a short, disproportionately sized
body and a thick tongue and neck. Cretinism may reflect a ge-
netic deficiency of the fetal thyroid gland or maternal factors,
such as lack of dietary iodine. ±yroid hormone replacement
therapy can prevent cretinism if diagnosed early enough, but
cell and the colloid. Attachment of one iodine to a tyrosine
produces
monoiodotyrosine
(
MIT
), and attachment of
two iodines produces
diiodotyrosine
(
DIT
).
5
Iodinated tyrosines are linked together to form T
3
and T
4
.
Enzymes in the colloid link MIT and DIT together. Two
linked DITs result in T
4
, and coupling of MIT and DIT pro-
duces T
3
. At this point, the hormones are still part of the
thyroglobulin colloid.
6
Thyroglobulin colloid is endocytosed.
To secrete the hor-
mones, the follicular cells must reclaim iodinated thyroglob-
ulin by endocytosis and combine the vesicles with lysosomes.
7
Lysosomal enzymes cleave T
4
and T
3
from thyroglobulin
and the hormones diffuse from the follicular cell into the
bloodstream.
±e main hormonal product secreted is T
4
.
Some T
4
is converted to T
3
before secretion, but most T
3
is
generated in the peripheral tissues.
Transport and Regulation
Most released T
4
and T
3
immediately binds to
thyroxine-binding
globulins
(
TBGs
) and other transport proteins produced by the
liver. Both T
4
and T
3
bind to target tissue receptors, but T
3
binds
more avidly and is about 10 times more active. Most peripheral
tissues have the enzymes needed to convert T
4
to T
3
by remov-
ing one iodine atom.
Figure 16.8 shows the negative feedback loop that regulates
blood levels of TH. Falling TH blood levels trigger release of
thyroid-stimulating hormone
(
TSH
), and ultimately of more
TH. Rising TH levels feed back to inhibit the hypothalamic–
anterior pituitary axis, temporarily shutting off the stimulus for
TSH release.
In infants, exposure to cold stimulates the hypothalamus to
secrete
thyrotropin-releasing hormone
(
TRH
), which triggers
TSH release. ±e thyroid gland then releases larger amounts
of thyroid hormones, enhancing body metabolism and heat
production. Factors that inhibit TSH release include GHIH,
(a)
(b)
Figure 16.11
Thyroid disorders.
(a)
An enlarged thyroid (goiter) of a Bangladeshi boy.
(b)
Bulging eyes (exophthalmos) of Graves' disease.
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