Regulation of Organic Metabolism and Energy Balance
577
Summary of Hormonal Controls
To a great extent, insulin may be viewed as the “hormone of
plenty.” Its secretion and plasma concentration are increased
during the absorptive period and decreased during postab-
sorption. These changes are adequate to cause most of the
metabolic changes associated with these periods. In addition,
opposed in various ways to insulin’s effects are the actions
of the major glucose-counterregulatory controls—glucagon,
epinephrine and the sympathetic nerves to the liver and adi-
pose tissue, cortisol, and growth hormone (
Table 16–4
).
Glucagon and the sympathetic nervous system defi nitely play
roles in preventing hypoglycemia. The rates of secretion of
cortisol and growth hormone are not usually coupled to
the absorptive-postabsorptive pattern. Nevertheless, their
presence in the blood at basal concentrations is necessary
for normal adjustment of lipid and carbohydrate metabo-
lism to the postabsorptive period, and excessive amounts of
either hormone cause abnormally elevated plasma glucose
concentrations.
Energy Homeostasis
in Exercise and Stress
During exercise, large quantities of fuels must be mobilized
to provide the energy required for muscle contraction. These
include plasma glucose and fatty acids as well as the muscle’s
own glycogen.
The plasma glucose used during exercise is supplied by
the liver, both by breakdown of its glycogen stores and by
gluconeogenesis. Glycerol is made available to the liver by a
marked increase in adipose tissue lipolysis, with a resultant
release of glycerol and fatty acids into the blood, the fatty
acids serving as a fuel source for the exercising muscle.
What happens to plasma glucose concentration during
exercise? It changes very little in short-term, mild-to-moderate
exercise and may even increase slightly with strenuous, short-
term activity. However, during prolonged exercise (
Figure
16–11
)—more than about 90 min—plasma glucose concentra-
tion does decrease, but usually by less than 25 percent. Clearly,
glucose output by the liver increases approximately in propor-
tion to increased glucose utilization during exercise, at least
until the later stages of prolonged exercise when it begins to lag
somewhat.
The metabolic profi le seen in an exercising person—
increases in hepatic glucose production, triglyceride break-
down, and fatty acid utilization—is similar to that seen in a
fasting person, and the endocrine controls are also the same.
Exercise is characterized by a decrease in insulin secretion and
an increase in glucagon secretion (see Figure 16–11), and the
changes in the plasma concentrations of these two hormones
are the major controls during exercise. In addition, activity of
the sympathetic nervous system increases (including secretion
of epinephrine), and cortisol and growth hormone secretion
both increase as well.
What triggers increased glucagon secretion and decreased
insulin secretion during exercise? One signal, at least during
pro-
longed
exercise, is the modest decrease in plasma glucose that
occurs (see Figure 16–11). This is the same signal that controls
Table 16–3
Effects of Cortisol on Organic
Metabolism
1.
Basal concentrations are permissive for stimulation of
gluconeogenesis and lipolysis in the postabsorptive state.
2.
Increased plasma concentrations cause:
a. Increased protein catabolism
b. Increased gluconeogenesis
c. Decreased glucose uptake by muscle cells and adipose
tissue cells
d. Increased triglyceride breakdown
Net result:
Increased plasma concentrations of amino acids,
glucose, and free fatty acids
Table 16–4
Summary of Glucose-Counterregulatory Controls*
Glucagon
Epinephrine
Cortisol
Growth Hormone
Glycogenolysis
✓✓
Gluconeogenesis
✓✓✓✓
Lipolysis
✓✓✓
Inhibition of
glucose uptake by
muscle cells and
adipose tissue cells
✓✓
*A
indicates that the hormone stimulates the process; no
indicates that the hormone has no major physiological effect on the process. Epinephrine stimulates glycogenolysis in both liver and skeletal
muscle, whereas glucagon does so only in liver.
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