Human Physiology, 14th edition (2016)

686 Chapter 19

adipose tissue (there appears to be few b 3 receptors in the ordi-

nary, white fat of humans, and none in other tissues). As may

be recalled from earlier in this chapter, brown fat is a special-

ized tissue that contains an uncoupling protein that dissoci-

ates electron transport from the production of ATP. As a result,

brown fat can have a very high rate of energy expenditure

(unchecked by negative feedback from ATP) that is stimulated

by epinephrine.

Metabolic Effects of Glucocorticoids

Hydrocortisone (cortisol) and other glucocorticoids are secreted

by the adrenal cortex in response to ACTH stimulation. The

secretion of ACTH from the anterior pituitary occurs as part of

the general adaptation syndrome in response to stress (chap-

ter 11; section 11.4). Because prolonged fasting or prolonged

exercise certainly qualify as stressors, ACTH—and thus gluco-

corticoid secretion—is stimulated under these conditions. The

increased secretion of glucocorticoids during prolonged fast-

ing or exercise supports the effects of increased glucagon and

decreased insulin secretion from the pancreatic islets.

Like glucagon, hydrocortisone promotes lipolysis and

ketogenesis; it also stimulates the synthesis of hepatic enzymes

that promote gluconeogenesis. Although hydrocortisone stim-

ulates enzyme (protein) synthesis in the liver, it promotes pro-

tein breakdown in the muscles. Breakdown of muscle proteins

increases the blood levels of amino acids, providing the sub-

strates needed for gluconeogenesis by the liver. The release

of circulating energy substrates—amino acids, glucose, fatty

acids, and ketone bodies—into the blood in response to hydro-

cortisone ( fig. 19.15 ) helps compensate for a state of prolonged

fasting or exercise.

Thyroxine

The thyroid follicles secrete thyroxine, also called tetraiodo-

thyronine ( T 4 ), in response to stimulation by thyroid-stimulating

hormone (TSH) from the anterior pituitary. The thyroid also

secretes smaller amounts of triiodothyronine ( T 3 ) in response

to stimulation by TSH. Almost all organs in the body are targets

of thyroxine action. Thyroxine itself, however, is not the active

form of the hormone within the target cells; thyroxine is a pre-

hormone that must first be converted to triiodothyronine (T 3 )

within the target cells to be active (chapter 11; see fig. 11.6).

Acting via its conversion to T 3 , thyroxine (1) regulates the rate

of cell respiration and (2) contributes to proper growth and

development, particularly during early childhood.

Thyroxine (via its conversion to T 3 ) stimulates the rate of cell

respiration in almost all cells in the body—an effect believed to

be due to a lowering of cellular ATP concentrations. This effect is

produced by the production of uncoupling proteins (as in brown

fat, discussed previously). ATP exerts an end-product inhibition

(chapter 4, section 4.2) of cell respiration, so that when ATP con-

centrations decrease, the rate of cell respiration increases.

Much of the energy liberated during cell respiration escapes

as heat, and uncoupling proteins increase the proportion of

19.5 METABOLIC REGULATION

BY ADRENAL HORMONES,

THYROXINE, AND GROWTH

HORMONE

Epinephrine, cortisol, thyroxine, and growth hormone stim-

ulate the catabolism of carbohydrates and lipids. Thyrox-

ine and growth hormone promote protein synthesis, body

growth, and proper development of the central nervous

system.

LEARNING OUTCOMES

After studying this section, you should be able to:

12. Explain how catecholamines, glucocorticoids, and
    thyroid hormones regulate metabolism.


13. Explain how growth hormone regulates metabolism.

The anabolic effects of insulin are antagonized by glucagon, as
previously described, and by the actions of a variety of other
hormones. The hormones of the adrenals, thyroid, and anterior
pituitary (specifically growth hormone) antagonize the action
of insulin on carbohydrate and lipid metabolism. The actions
of insulin, thyroxine, and growth hormone, however, can act
synergistically in the stimulation of protein synthesis.

Adrenal Hormones

The adrenal gland consists of two parts that function as separate
glands, secreting different hormones and regulated by different
control systems (chapter 11, section 11.4). The adrenal medulla
secretes catecholamine hormones—epinephrine and lesser amounts
of norepinephrine—in response to sympathetic nerve stimulation.
The adrenal cortex secretes corticosteroid hormones. These are
grouped into two functional categories: mineralocorticoids, such
as aldosterone, which act on the kidneys to regulate Na^1 and K^1
balance (chapter 17, section 17.5), and glucocorticoids, such as
hydrocortisone (cortisol), which participate in metabolic regulation.

Metabolic Effects of Catecholamines

The metabolic effects of catecholamines (epinephrine and nor-
epinephrine) are similar to those of glucagon. They stimulate
glycogenolysis and the release of glucose from the liver, as
well as lipolysis and the release of fatty acids from adipose
tissue. These actions occur in response to glucagon during fast-
ing, when low blood glucose stimulates glucagon secretion,
and in response to catecholamines during the fight-or-flight
reaction to stress. The latter effect provides circulating energy
substrates in anticipation of the need for intense physical activ-
ity. Glucagon and epinephrine have similar mechanisms of
action, where both are mediated by cyclic AMP ( fig. 19.14 ).
Sympathetic nerves, acting through the release of norepi-
nephrine, can stimulate b 3 -adrenergic receptors in brown