Regulation of Metabolism 687
normal, while a person who is hyperthyroid may have a basal O 2
consumption up to 50% higher than normal.
A normal level of thyroxine secretion is required for
growth and proper development of the central nervous system
in children. This is why hypothyroidism in children can cause
cretinism. The symptoms of hypothyroidism and hyperthyroid-
ism in adults are compared in chapter 11, table 11.8.
A normal level of thyroxine secretion is required in order
to maintain a balance of anabolism and catabolism. For reasons
that are incompletely understood, both hypothyroidism and
hyperthyroidism cause protein breakdown and muscle wasting.
Growth Hormone
The anterior pituitary secretes growth hormone, also called
somatotropin, in larger amounts than any other of its hormones.
As its name implies, growth hormone stimulates growth in chil-
dren and adolescents. The continued high secretion of growth
food energy that escapes as heat. Because thyroxine stimulates
the production of uncoupling proteins and the rate of cell respi-
ration, the actions of thyroxine increase the production of met-
abolic heat. The heat-producing, or calorigenic ( calor 5 heat),
effects of thyroxine are required for cold adaptation. Recent
evidence suggests that thyroxine has a permissive effect on the
ability of brown adipose tissue to generate heat in response to
sympathetic nerve stimulation. Through this permissive effect,
thyroxine contributes to adaptive thermogenesis as well as to
the basal metabolic rate.
The basal metabolic rate (BMR) has two components—one
that is independent of thyroxine action and one that is regulated
by thyroxine. In this way, thyroxine acts to “set” the BMR. The
BMR can thus be used as an index of thyroid function. Indeed,
such measurements were used clinically to evaluate the condi-
tion of the thyroid prior to the development of direct chemical
determinations of T 4 and T 3 in the blood. A person who is hypo-
thyroid may have a basal O 2 consumption about 30% lower than
Figure 19.14 How epinephrine and glucagon affect metabolism. (1) The hormone binds to its receptor, causing
G-proteins to dissociate. The alpha subunit diffuses through the membrane to activate adenylate cyclase, which catalyzes the
production of cAMP as a second messenger. (3) The cAMP binds to and removes the regulatory subunit of protein kinase, activating
this enzyme. (4) The activation and inactivation of different enzymes by protein kinase promotes glycogenolysis in the liver and lipolysis
in adipose tissue.
α α
α
G-proteins
Cell
membrane
Epinephrine
or glucagon
receptor
Epinephrine
or glucagon Adenylate
cyclase
ATP
Protein kinase
(active)
cAMP + PP
Protein kinase
(inactive)
Regulatory subunit Regulatory subunit
cAMP
Phosphorylation
of enzymes
Glycogenolysis
(liver)
Lipolysis
(adipose tissue)
Activation of
specific enzymes
Inactivation of
specific enzymes
2
1
3
4
β
γ