HA101M Module 9 Endocrine System
HA101M Module 9 Endocrine System
LIPID-SOLUBLE HORMONES
1) STEROID HORMONES
• are derived from cholesterol
• Each steroid hormone is unique due to the presence of
different chemical groups attached at various sites on the
four rings at the core of its structure.
• These small differences allow for a large diversity of
functions.
WATER-SOLUBLE HORMONES
1) AMINE HORMONES
• Amine hormones are synthesized by decarboxylating
(removing a molecule of CO2) and otherwise modifying
certain amino acids.
• They are called amines because they retain an amino
group (–NH3+).
• The catecholamines—epinephrine, norepinephrine, and
dopamine—are synthesized by modifying the amino acid
tyrosine.
• Histamine is synthesized from the amino acid histidine
by mast cells and platelets.
• Serotonin and melatonin are derived from tryptophan.
• The receptors for lipid-soluble hormones à are located • The action of a typical water-soluble hormone occurs as
inside target cells. follows:
• The receptors for water-soluble hormones à are part 1. A water-soluble hormone (the first messenger)
of the plasma membrane of target cells. diffuses from the blood through interstitial fluid and
then binds to its receptor at the exterior surface of a
ACTION OF LIPID-SOLUBLE HORMONES target cell’s plasma membrane. The hormone–
• Lipid-soluble hormones, including steroid hormones and receptor complex activates a membrane protein
thyroid hormones, bind to receptors within target cells. called a G protein. The activated G protein in turn
• Their mechanism of action is as follows: activates adenylate cyclase.
1. A free lipid-soluble hormone molecule diffuses from 2. Adenylate cyclase converts ATP into cyclic AMP
the blood, through interstitial fluid, and through the (cAMP). Because the enzyme’s active site is on the
lipid bilayer of the plasma membrane into a cell. inner surface of the plasma membrane, this reaction
occurs in the cytosol of the cell.
2. If the cell is a target cell, the hormone binds to and
activates receptors located within the cytosol or 3. Cyclic AMP (the second messenger) activates one
nucleus. The activated receptor–hormone complex or more protein kinases, which may be free in the
then alters gene expression: It turns specific genes cytosol or bound to the plasma membrane. A protein
of the nuclear DNA on or off. kinase is an enzyme that phosphorylates (adds a
phosphate group to) other cellular proteins (such as
3. As the DNA is transcribed, new messenger RNA enzymes). The donor of the phosphate group is ATP,
(mRNA) forms, leaves the nucleus, and enters the which is converted to ADP.
cytosol. There, it directs synthesis of a new protein,
often an enzyme, on the ribosomes. 4. Activated protein kinases phosphorylate one or more
cellular proteins. Phosphorylation activates some
4. The new proteins alter the cell’s activity and cause of these proteins and inactivates others, rather like
the responses typical of that hormone. turning a switch on or off.
5. Phosphorylated proteins in turn cause reactions that
produce physiological responses. Different protein
kinases exist within different target cells and within
different organelles of the same target cell. Thus, one
protein kinase might trig- ger glycogen synthesis, a
second might cause the break- down of triglyceride,
a third may promote protein synthesis, and so forth.
As noted in step 4, phosphorylation by a protein
kinase can also inhibit certain proteins. For example,
some of the kinases unleashed when epinephrine
binds to liver cells inactivate an enzyme needed for
glycogen synthesis.
6. After a brief period, an enzyme called
phosphodiesterase inactivates cAMP. Thus, the
cell’s response is turned off unless new hormone
molecules continue to bind to their receptors in the
plasma membrane.
HYPOTHALAMUS
• The hypothalamus is also known as “the master
endocrine gland”
• It is the major link between the nervous and endocrine
systems
• It is a small region in the brain below the thalamus
• Cells in the hypothalamus synthesizes at least 9 different
hormones and the pituitary gland secretes seven.
• Together, these hormones play important roles in the
regulation of virtually all aspects of growth, development,
metabolism, and homeostasis.
3) GONADOTROPHS
• Secrete two gonadotropins:
o follicle-stimulating hormone (FSH)
o luteinizing hormone (LH).
• FSH and LH both act on the gonads.
• They stimulate secretion of estrogens and
progesterone and the maturation of oocytes in the
• NEUROSECRETORY CELLS ovaries.
o Near the median eminence and above the optic • They also stimulate sperm production and secretion of
chiasm are clusters of specialized neurons, called testosterone in the testes.
neurosecretory cells.
4) LACTOTROPHS
• Secrete: prolactin (PRL) HORMONES SECRETED BY THE PITUITARY
o which initiates milk production in the mammary GLAND
glands.
HUMAN GROWTH HORMONE AND INSULIN-LIKE
GROWTH FACTORS
• Human Growth Hormone (hGH) are produced by
somatotrophs
• The most numerous cells in anterior pituitary
• The most plentiful anterior pituitary hormone in the
anterior pituitary gland
• Main function: promote synthesis and secretion of small
protein hormones called insulin-like growth factors
(IGFs) or somatomedins.
1. Hypoglycemia, an abnormally low blood glucose • Release of TRH in turn depends on blood levels of T3 and
concentration, stimulates the hypothalamus to T4; high levels of T3 and T4 inhibit secretion of TRH via
secrete GHRH, which flows toward the anterior negative feedback.
pituitary in the hypophyseal portal veins. • There is no thyrotropin-inhibiting hormone.
2. Upon reaching the anterior pituitary, GHRH
stimulates somatotrophs to release human growth FOLLICLE-STIMULATING HORMONE
hormone. • In females, the ovaries are the targets for follicle-
3. Human growth hormone stimulates secretion of stimulating hormone (FSH).
insulin-like growth factors, which speed up • Each month FSH initiates the development of several
breakdown of liver glycogen into glucose, causing ovarian follicles àsaclike arrangements of secretory
glucose to enter the blood more rapidly. cells that surround a developing oocyte.
4. As a result, blood glucose rises to the normal level • FSH also stimulates follicular cells to secrete estrogens
(about 90 mg/100 mL of blood plasma). (female sex hormones).
5. An increase in blood glucose above the normal level
• In males, FSH stimulates sperm production in the
inhibits release of GHRH.
testes.
6. Hyperglycemia, an abnormally high blood glucose
• Gonadotropin-releasing hormone (GnRH) from the
concentration, stimulates the hypothalamus to
hypothalamus stimulates FSH release.
secrete GHIH (while inhibiting the secretion of
GHRH). • Release of GnRH and FSH is suppressed by estrogens
7. Upon reaching the anterior pituitary in portal blood, in females and by testosterone (the principal male sex
hormone) in males through negative feedback systems.
GHIH inhibits secretion of human growth hormone by
somatotrophs. • Through a negative feedback mechanism, if there are
8. A low level of human growth hormone and IGFs high levels of estrogen and testosterone, there will be a
slows breakdown of glycogen in the liver, and decrease in your GnRH and FSH.
glucose is released into the blood more slowly. • If there is a decrease in the levels of estrogen and
9. Blood glucose falls to the normal level. testosterone, the opposite will be true. There will be
10. A decrease in blood glucose below the normal level increased levels of GnRH and FSH.
(hypoglycemia) inhibits release of GHIH. • There is no gonadotropin-inhibiting hormone.
LUTEINIZING HORMONE
• In females, luteinizing hormone (LH) triggers ovulation
à the release of a secondary oocyte (future ovum) by an
ovary.
• LH stimulates formation of the corpus luteum (structure
formed after ovulation) in the ovary and the secretion of
progesterone (another female sex hormone) by the
corpus luteum.
• Together, FSH and LH also stimulate secretion of
estrogens by ovarian cells.
• Estrogens and progesterone prepare the uterus for
implantation of a fertilized ovum and help prepare the
mammary glands for milk secretion.
• In males, LH stimulates cells in the testes to secrete
testosterone.
• Secretion of LH, like that of FSH, is controlled by
gonadotropin-releasing hormone (GnRH).
PROLACTIN
• Prolactin (PRL) initiates and maintains milk secretion by
the mammary glands.
• By itself, prolactin has only a weak effect.
• Only after the mammary glands have been primed by
estrogens, progesterone, glucocorticoids, human growth
hormone, thyroxine, and insulin, which exert permissive
effects, does PRL bring about milk secretion.
• Ejection of milk from the mammary glands depends on
the hormone oxytocin, which is released from the
posterior pituitary.
• Milk secretion and ejection = constitute lactation.
• The hypothalamus secretes both inhibitory and excitatory
hormones that regulate prolactin secretion.
• In females: prolactin-inhibiting hormone (PIH), which
is DOPAMINE, inhibits the release of prolactin from the
anterior pituitary most of the time.
o Each month, just before menstruation begins, the
THYROID-STIMULATING HORMONE secretion of PIH diminishes and the blood level of
• Thyroid-stimulating hormone (TSH) stimulates the prolactin rises, but not enough to stimulate milk
production.
synthesis and secretion of the two thyroid hormones:
o triiodothyronine (T3) o Breast tenderness just before menstruation may be
caused by elevated prolactin.
o thyroxine (T4)
(both produced by the thyroid gland) o As the menstrual cycle begins anew, PIH is again
secreted and the prolactin level drops.
• Thyrotropin-releasing hormone (TRH) from the
hypothalamus controls TSH secretion.
o During pregnancy, the prolactin level rises, • The paraventricular nucleus à synthesizes the
stimulated by prolactin-releasing hormone (PRH) hormone oxytocin.
from the hypothalamus. • The supraoptic nucleus à produces antidiuretic
o The sucking action of a nursing infant causes a hormone, also called vasopressin.
reduction in hypothalamic secretion of PIH. • The axon terminals in the posterior pituitary are
• The function of prolactin is not known in males, but its associated with specialized neuroglia called pituicytes.
hypersecretion causes erectile dysfunction (impotence, o These cells have a supporting role similar to that of
the inability to have an erection of the penis). astrocytes.
• In females, hypersecretion of prolactin causes • After their production in the cell bodies of neurosecretory
galactorrhea (inappropriate lactation) and amenorrhea cells, oxytocin and antidiuretic hormone are packaged
(absence of menstrual cycles). into secretory vesicles, which move by fast axonal
transport to the axon terminals in the posterior pituitary,
ADRENOCORTICOTROPIC HORMONE where they are stored until nerve impulses trigger
• Corticotrophs secrete mainly adrenocorticotropic exocytosis and release of the hormone.
hormone (ACTH).
• ACTH controls the production and secretion of cortisol
and other glucocorticoids by the cortex (outer portion) of
the adrenal glands.
• Corticotropin-releasing hormone (CRH) from the
hypothalamus stimulates secretion of ACTH by
corticotrophs.
• Stress-related stimuli, such as low blood glucose or
physical trauma, and interleukin-1, a substance produced
by macrophages, also stimulate release of ACTH.
• Glucocorticoids inhibit CRH and ACTH release via
negative feedback.
OXYTOCIN
• During and after delivery of a baby, oxytocin affects two
target tissues:
o the mother’s uterus and breasts
• During delivery, oxytocin enhances contraction of
smooth muscle cells in the wall of the uterus;
• After delivery, it stimulates milk ejection (“letdown”) from
the mammary glands in response to the mechanical
stimulus provided by a suckling infant.
• The function of oxytocin in males and in nonpregnant
females is not clear.
• Experiments with animals have suggested that it has
actions within the brain that foster parental caretaking
behavior toward young offspring.
• It may also be responsible, in part, for the feelings of
sexual pleasure during and after intercourse.
• This hormone’s other name, vasopressin, reflects this 5. Low osmotic pressure of blood (or increased blood
effect on blood pressure. volume) inhibits the osmoreceptors.
• The amount of ADH secreted varies with blood osmotic
pressure and blood volume. 6. Inhibition of osmoreceptors reduces or stops ADH
secretion. The kidneys then retain less water by
forming a larger volume of urine, secretory activity of
sweat glands increases, and arterioles dilate. The
blood volume and osmotic pressure of body fluids
return to normal.
THYROID GLAND
• Butterfly-shaped
• Located just inferior to the larynx (voice box).
• Composed of:
o Lateral lobes (right and left)
o Isthmus
• Pyramidal-shaped lobe (sometimes extends upward from
the isthmus)
• Wt: 30 g (1 oz).
• Highly vascularized - receives 80–120 mL of blood per • The thyroid gland is the only endocrine gland that stores
minute its secretory product in large quantities—normally about
a 100-day supply. Synthesis and secretion of T3 and T4
MICROSCOPIC FEATURES: occurs as follows:
• Thyroid follicles - spherical sacs; make up most of the
thyroid gland (1) IODINE TRAPPING
o Follicular cells – cells that line the wall of each • Thyroid follicular cells trap iodide ions (I) by actively
follicle; most of which extend to the lumen (internal transporting them from the blood into the cytosol.
space) of the follicle.
• As a result, the thyroid gland normally contains most of
§ INACTIVE = their shape is low cuboidal to
the iodide in the body.
squamous
§ ACTIVE (under TSH influence) = cuboidal to low
columnar
(2) SYNTHESIS OF THYROGLOBULIN
o Basement membrane - surrounds each follicle • While the follicular cells are trapping I, they are also
• The follicular cells produce two hormones: synthesizing thyroglobulin (TGB), a large glycoprotein
o Tetraiodothyronine or T4 (aka Thyroxine) packaged into secretory vesicles n that is produced in the
§ contains four atoms of iodine rough endoplasmic reticulum, modified in the Golgi
o Triiodothyronine or T3 complex, and packaged into secretory vesicles.
§ contains three atoms of iodine • The vesicles then undergo exocytosis, which releases
• T3 and T4 together are also known as thyroid hormones. TGB into the lumen of the follicle.
• Parafollicular cells or C cells lie between follicles. (3) OXIDATION OF IODIDE
Produces: • Some of the amino acids in TGB are tyrosines that will
o Calcitonin - helps regulate calcium homeostasis. become iodinated.
• Negatively charged iodide ions cannot bind to tyrosine
(an amino acid) until they undergo oxidation (removal of
electrons) to iodine: 2 I- à I2
• As the iodide ions are being oxidized, they pass through
the membrane into the lumen of the follicle.
• TGB with attached iodine atoms, a sticky material that 3. Stimulate protein synthesis and increase the use of
accumulates and is stored in the lumen of the thyroid glucose and fatty acids for ATP production. They also
follicle, is termed colloid. increase lipolysis and enhance cholesterol excretion.
3. TSH stimulates virtually all aspects of thyroid • PTH also acts on the kidneys.
follicular cell activity, including iodide trapping, • First, it slows the rate at which Ca2+ and Mg2+ are lost from
hormone synthesis and secretion, and growth of the blood into the urine.
follicular cells. • Second, it increases loss of HPO42- from blood into the
4. The thyroid follicular cells release T3 and T4 into the urine.
blood until the metabolic rate returns to normal. • Because more HPO42- is lost in the urine than is gained
5. An elevated level of T3 inhibits release of TRH and from the bones, PTH decreases blood HPO42- level and
TSH (negative feedback inhibition). increases blood Ca2+ and Mg2+ levels.
• A third effect of PTH on the kidneys is to promote
• Conditions that increase ATP demand—a cold formation of the hormone calcitriol, the active form of
environment, hypoglycemia, high altitude, and vitamin D.
pregnancy—also increase the secretion of the thyroid • Calcitriol, also known as 1, 25-dihydroxy vitamin D3,
hormones. increases the rate of Ca2+, Mg2+ , and HPO42- absorption
CALCITONIN from the gastrointestinal tract into the blood.
• Produced by the parafollicular cells of the thyroid gland • The blood calcium level directly controls the secretion of
• CT can decrease the level of calcium in the blood by both calcitonin and parathyroid hormone via negative
inhibiting the action of osteoclasts, the cells that break feedback loops that do not involve the pituitary gland.
down bone extra-cellular matrix.
• The secretion of CT is controlled by a negative feedback
system.
• When blood level is high:
o Calcitonin lowers the amount of blood calcium and
phosphates by inhibiting bone resorption (breakdown
of bone extracellular matrix) by osteoclasts and by
accelerating uptake of calcium and phosphates into
bone extracellular matrix.
• Calcitonin promotes calcium deposition in your bones.
PARATHYROID GLANDS
• In adults:
o 3–5 cm in height
o 2–3 cm in width
PARATHYROID HORMONE o less than 1 cm thick
• Parathyroid hormone is the major regulator of the levels o mass of 3.5–5 g
of calcium (Ca2+), magnesium (Mg2+), and phosphate • Only half its size at birth.
(HPO42-) ions in the blood. • During embryonic development, the adrenal glands
• The specific action of PTH is to increase the number and differentiate into TWO STRUCTURALLY AND
activity of osteoclasts. (somehow opposite to the calcitonin) FUNCTIONALLY DISTINCT REGIONS:
• The result is elevated bone resorption, which releases o Adrenal cortex
ionic calcium (Ca2+), and phosphates (HPO42-) into the § large, peripherally located;
blood. § 80– 90% of the gland
o CRH (together with a low level of cortisol) promotes § For this reason, glucocorticoids are prescribed for
the release of ACTH from the anterior pituitary. organ transplant recipients to retard tissue
o ACTH flows in the blood to the adrenal cortex, where rejection by the immune system.
it stimulates glucocorticoid secretion.
ADRENAL CORTEX: ANDROGENS
• The adrenal cortex secretes small amounts of weak
androgens in both males and females.
• Major androgen: Dehydroepiandrosterone (DHEA)
o MALES
§ Amount of androgens secreted by the adrenal
gland are usually so low and effects are
insignificant in MALES after puberty due to greater
quantity of TESTOSTERONE release by the
testes
o FEMALES
§ In FEMALES à promote libido (sex drive) and are
converted into ESTROGENS (feminizing sex
steroids) by other body tissues.
§ After menopause, when ovarian secretion of
estrogens ceases, all female estrogens come
from conversion of adrenal androgens.
• Also stimulate growth of axillary and pubic hair in boys
and girls and contribute to the prepubertal growth spurt.
• Although control of adrenal androgen secretion is not fully
understood, the main hormone that stimulates its
secretion is ACTH.
• GLUCOCORTICOID EFFECTS:
1. Protein breakdown. ADRENAL MEDULLA
à increase rate of protein breakdown • The inner region of the adrenal gland
(mainly in muscle fibers) à increase amino is a modified sympathetic ganglion of
acids into the bloodstream à amino acids the autonomic nervous system (ANS)
may be used by body cells for synthesis of • It develops from the same embryonic
new proteins or for ATP production. tissue as all other sympathetic
2. Glucose formation. ganglia, but its cells, which lack
à liver cells convert certain amino acids or axons, form clusters around large
lactic acid to glucose à (neurons and other blood vessels.
cells can use for…) ATP production à • Rather than releasing a
gluconeogenesis (derivation of glucose neurotransmitter, the cells of the
from other substance other that glycogen) adrenal medulla secrete hormones.
(conversion of a substance other than • Its hormone-producing cells are called chromaffin cells
glycogen or another monosaccharide into o Are innervated by sympathetic preganglionic neurons
glucose) of the ANS.
3. Lipolysis. o Because the ANS exerts direct control over the
à breakdown of triglycerides and release chromaffin cells, hormone release can occur very
of fatty acids from adipose tissue into the quickly.
blood.
4. Resistance to stress. • Two major hormones synthesized are:
§ Glucocorticoids work in many ways to provide o Epinephrine (Adrenaline) – secreted 80%
resistance to stress. o Norepinephrine (Noradrenalin) – 20%
• Unlike the hormones of the adrenal cortex, the hormones
à Additional glucose supplied by the liver cells of the adrenal medulla are not essential for life since they
provides tissues with a ready source of ATP to only intensify sympathetic responses in other parts of the
combat a range of stresses (exercise, fasting, body.
fright, temperature extremes, high altitude,
bleeding, infection, surgery, trauma, and disease). • In stressful situations (e.g. exercise) à impulses from the
à (Glucocorticoids make blood vessels more hypothalamus stimulate sympathetic preganglionic
sensitive to other hormones that…) cause neurons à stimulate the chromaffin cells to secrete
vasoconstriction à raise blood pressure epinephrine and norepinephrine à two hormones greatly
§ This effect would be an advantage in cases of augment the fight-or-flight response
severe blood loss, which causes blood pressure o Increasing heart rate and force of contraction à
to drop. increase the output of the heart à increases blood
pressure.
5. Anti-inflammatory effects. o They also increase blood flow to the heart, liver,
àThey inhibit white blood cells that skeletal muscles, and adipose tissue
participate in inflammatory responses à o Dilate airways to the lungs
also retard tissue repair à slow wound o Increase blood levels of glucose and fatty acids.
healing
§ Although high doses can cause severe mental
disturbances, glucocorticoids are very useful in
the treatment of chronic inflammatory disorders
such as rheumatoid arthritis.
6. Depression of immune responses.
à High doses depress immune responses.
EATIC ISLETS:
YPES
hormone-
s: A cells
A cells – secrete
(increases B cells
D cells F cell
cells – secrete
owers glucose)
D cells – secrete
atin (inhibits both PANANGHID SA DAAN SA GAHIMO ^-^ | 1D-MT 16
TRANS: Endocrine System
• The responses to stressors may be pleasant or • A third hypothalamic releasing hormone, TRH, stimulates
unpleasant, and they vary among people and even within the anterior pituitary to secrete thyroid-stimulating
the same person at different times. hormone (TSH).
• TSH promotes secretion of thyroid hormones, which
• The body’s homeostatic mechanisms normally attempt to stimulate the increased use of glucose for ATP
COUNTERACT STRESS. production.
• When they are successful, the internal environment • The combined actions of hGH and TSH supply additional
remains within normal physiological limits. ATP for metabolically active cells throughout the body.
• If stress is extreme, unusual, or long lasting, the normal
mechanisms may not be enough. • The resistance stage helps the body continue fighting a
stressor long after the fight-or-flight response dissipates.
• The stress response or general adaptation syndrome • This is why your heart continues to pound for several
(GAS) minutes even after the stressor is removed.
o controlled mainly by the hypothalamus. • Generally, it is successful in seeing us through a stressful
o are a variety of stressful conditions or noxious agents episode, and our bodies then return to normal.
that elicit a similar sequence of bodily changes • Occasionally, however, the resistance stage fails to
o occurs in three stages: combat the stressor, and the body moves into the state of
(1) an initial fight-or-flight response exhaustion.
(2) a slower resistance reaction
(3) exhaustion EXHAUSTION
• The resources of the body may eventually become so
FIGHT-OR-FLIGHT RESPONSE depleted that they cannot sustain the resistance stage,
• The fight-or-flight response, initiated by nerve impulses and exhaustion ensues.
from the hypothalamus to the sympathetic division of the • Prolonged exposure to high levels of cortisol and other
autonomic nervous system (ANS), including the adrenal hormones involved in the resistance reaction causes
medulla, quickly mobilizes the body’s resources for wasting of muscle, suppression of the immune system,
immediate physical activity. ulceration of the gastrointestinal tract, and failure of
• It brings huge amounts of glucose and oxygen to the pancreatic beta cells.
organs that are most active in warding off danger: • In addition, pathological changes may occur because
o the brain, which must become highly alert; resistance reactions persist after the stressor has been
o the skeletal muscles, which may have to fight off an removed.
attacker or flee;
o and the heart, which must work vigorously to pump STRESS AND DISEASE
enough blood to the brain and muscles. • Although the exact role of stress in human diseases is not
• During the fight-or-flight response, nonessential body known, it is clear that stress can lead to particular
functions such as digestive, urinary, and reproductive diseases by temporarily inhibiting certain components of
activities are inhibited. the immune system.
• Reduction of blood flow to the kidneys promotes release • Stress-related disorders include gastritis, ulcerative
of renin, which sets into motion the renin–angiotensin– colitis, irritable bowel syndrome, hypertension, asthma,
aldosterone pathway. rheumatoid arthritis (RA), migraine headaches, anxiety,
• Aldosterone causes the kidneys to retain Na+, which and depression.
leads to water retention and elevated blood pressure. • People under stress are at a greater risk of developing
• Water retention also helps preserve body fluid volume in chronic disease or dying prematurely. Interleukin-1, a
the case of severe bleeding. substance secreted by macrophages of the immune
system, is an important link between stress and immunity.
THE RESISTANCE REACTION
• One action of interleukin-1 is to stimulate secretion of
• The second stage in the stress response is the resistance ACTH, which in turn stimulates the production of cortisol.
reaction.
• Not only does cortisol provide resistance to stress and
• Unlike the short-lived fight-or-flight response, which is inflammation, but it also suppresses further production of
initiated by nerve impulses from the hypothalamus, the interleukin-1.
resistance reaction is initiated in large part by • Thus, the immune system turns on the stress response,
hypothalamic releasing hormones and is a longer-lasting
and the resulting cortisol then turns off one immune
response.
system mediator.
• The hormones involved are: • This negative feedback system keeps the immune
o corticotropin-releasing hormone (CRH), response in check once it has accomplished its goal.
o growth hormone–releasing hormone (GHRH), and
• Because of this activity, cortisol and other glucocorticoids
o thyrotropin-releasing hormone (TRH).
are used as immunosuppressive drugs for organ
• CRH stimulates the anterior pituitary to secrete ACTH, transplant recipients.
which in turn stimulates the adrenal cortex to increase
release of cortisol.
• Cortisol then stimulates gluconeogenesis by liver cells,
breakdown of triglycerides into fatty acids (lipolysis), and REFERENCE
catabolism of proteins into amino acids.
• Tissues throughout the body can use the resulting Tortora – Principles of Anatomy and Physiology, 12th
glucose, fatty acids, and amino acids to produce ATP or edition Chapter 18 pp. 642 - 688
to repair damaged cells.
• Cortisol also reduces inflammation. Lecture and PPT of Danilo Gallardo Jr., MD, FM, FMCP