Human Physiology, 14th edition (2016)

338 Chapter 11

Exogenous glucocorticoids (taken as pills, injections,

sprays, and topical creams) are used medically to suppress

the immune response and inhibit inflammation. Thus, these

drugs are very useful in treating inflammatory diseases such as

asthma and rheumatoid arthritis. As might be predicted based

on their metabolic actions, the side effects of glucocorticoids

include hyperglycemia and decreased glucose tolerance. Other

negative side effects include decreased synthesis of collagen

and other extracellular matrix proteins and increased bone

resorption, leading to osteoporosis (chapter 19, section 19.6).

of cortisol is stimulated by ACTH from the anterior pituitary
( fig.  11.20 ). Cortisol and other glucocorticoids have many
effects on metabolism. These effects include: (1) stimulation
of protein degradation; (2) stimulation of gluconeogenesis
(production of glucose from amino acids and other noncarbo-
hydrate molecules) and inhibition of glucose utilization, which
help to raise the blood glucose concentration; and (3) stimula-
tion of lipolysis (breakdown of fat) and the consequent release
of free fatty acids into the blood. These effects provide more
energy molecules of glucose and fatty acids in the blood, as
described in chapter 19.

Adrenal gland

Adrenal

cortex

Adrenal

cortex

Zona glomerulosa

Zona fasciculata

Zona reticularis

Adrenal

medulla

Adrenal

medulla

Kidney

Conective

tissue

capsule

Figure 11.18 The structure of the adrenal gland,
showing the three zones of the adrenal cortex. The
zona glomerulosa secretes the mineralocorticoids (including
aldosterone), whereas the other two zones secrete the
glucocorticoids (including cortisol).

CLINICAL APPLICATION

Cushing’s syndrome, resulting from chronically high levels

of glucocorticoids, can produce a “buffalo hump” (a fatty

deposit behind between the shoulders and the back of the

neck), a “moon” (round) face, and other symptoms. It most

commonly occurs when a person takes sustained high

doses of glucocorticoid medicines (prednisone, predniso-

lone, and dexamethasone), but it can be produced by either

(1) a pituitary tumor that secretes excessive ACTH, or (2) a

benign tumor of the adrenal that secretes excessive cortisol

without requiring ACTH stimulation.

Addison’s disease (or adrenal insufficiency ) is caused

by inadequate secretion of corticosteroids. Inadequate

cortisol produces hypoglycemia (low blood glucose); inad-

equate aldosterone produces sodium and potassium imbal-

ances, dehydration, and dangerously low blood pressure.

Primary adrenal insufficiency results from autoimmune

destruction of the adrenal cortex. This produces minimal

corticosteroid secretion and—because of the absence of

negative feedback—very high ACTH secretion. High levels

of ACTH stimulate the melanocytes, causing a darkening

of the skin. Primary adrenal insufficiency can be fatal if not

treated by hormone replacement. President John F. Ken-

nedy had Addison’s disease, but few knew of it because

it was well treated. Secondary adrenal insufficiency, by

contrast, is caused by inadequate ACTH secretion from the

anterior pituitary, perhaps because of a tumor. However,

more often this occurs when a patient takes exogenous cor-

ticosteroids, which inhibit the pituitary secretion of ACTH,

and then abruptly stops taking them.

Clinical Investigation CLUES

Rachel abruptly stopped taking prednisolone and mea-

sured a low blood glucose level.

• What happened to her ACTH secretion while she
  was taking prednisolone, and how does taking
  prednisolone relate to her puffy appearance?


• What condition did she acquire when she abruptly
  stopped taking prednisolone?