THE ENDOCRINE SYSTEM

BCP II Physiology
6/26/14
Dr. Cominski
2013 Pearson Education, Inc.
Endocrine System: Overview
Acts with nervous system to coordinate
and integrate activity of body cells
Influences metabolic activities via
hormones transported in blood
Response slower but longer lasting than
nervous system
Endocrinology
Study of hormones and endocrine organs

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Endocrine System: Overview
Controls and integrates
Reproduction
Growth and development
Maintenance of electrolyte, water, and
nutrient balance of blood
Regulation of cellular metabolism and energy
balance
Mobilization of body defenses
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Endocrine System: Overview
Exocrine glands
Nonhormonal substances (sweat, saliva)
Have ducts to carry secretion to membrane
surface
Endocrine glands
Produce hormones
Lack ducts
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Endocrine System: Overview
Endocrine glands: pituitary, thyroid,
parathyroid, adrenal, and pineal glands
Hypothalamus is Neuroendocrine organ
Some have exocrine and endocrine
functions
Pancreas, gonads, placenta
Other tissues and organs that produce
hormones
Adipose cells, thymus, and cells in walls of
small intestine, stomach, kidneys, and heart
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Figure 16.1 Location of selected endocrine organs of the body.
Pineal gland
Hypothalamus
Pituitary gland
Thyroid gland
Parathyroid glands
(on dorsal aspect
of thyroid gland)
Thymus
Adrenal glands
Pancreas
Gonads
Testis (male)
Ovary (female)
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Chemical Messengers
Hormones: long-distance chemical
signals; travel in blood or lymph
Autocrines: chemicals that exert effects
on same cells that secrete them
Paracrines: locally acting chemicals that
affect cells other than those that secrete
them
Autocrines and paracrines are local
chemical messengers; not considered part
of endocrine system
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Chemistry of Hormones
Two main classes
Amino acid-based hormones
Amino acid derivatives, peptides, and proteins
Steroids
Synthesized from cholesterol
Gonadal and adrenocortical hormones

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Mechanisms of Hormone Action
Though hormones circulate systemically
only cells with receptors for that hormone
affected
Target cells
Tissues with receptors for specific hormone
Hormones alter target cell activity
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Mechanisms of Hormone Action
Hormone action on target cells may be to
Alter plasma membrane permeability and/or
membrane potential by opening or closing ion
channels
Stimulate synthesis of enzymes or other
proteins
Activate or deactivate enzymes
Induce secretory activity
Stimulate mitosis
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Mechanisms of Hormone Action
Hormones act at receptors in one of two
ways, depending on their chemical nature
and receptor location
1. Water-soluble hormones (all amino acid
based hormones except thyroid hormone)
Act on plasma membrane receptors
Act via G protein second messengers
Cannot enter cell
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Mechanisms of Hormone Action
2. Lipid-soluble hormones (steroid and thyroid
hormones)
Act on intracellular receptors that directly activate
genes
Can enter cell
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Plasma Membrane Receptors and Second-
messenger Systems
cAMP signaling mechanism:
1. Hormone (first messenger) binds to receptor
2. Receptor activates G protein
3. G protein activates adenylate cyclase
4. Adenylate cyclase converts ATP to cAMP
(second messenger)
5. cAMP activates protein kinases that
phosphorylate proteins
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Plasma Membrane Receptors and Second-
messenger Systems
cAMP signaling mechanism
Activated kinases phosphorylate various
proteins, activating some and inactivating
others
cAMP is rapidly degraded by enzyme
phosphodiesterase
Intracellular enzymatic cascades have huge
amplification effect
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Slide 1
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Adenylate cyclase
Extracellular fluid
G protein (G
s
)
GDP
Receptor
Hormone (1st messenger)
binds receptor.
Receptor
activates G
protein (G
s
).
G protein
activates
adenylate
cyclase.
Adenylate
cyclase converts
ATP to cAMP (2nd
messenger).
Inactive
protein
kinase
Triggers responses of
target cell (activates
enzymes, stimulates
cellular secretion,
opens ion channel, etc.)
Active
protein
kinase
cAMP activates
protein kinases.
Cytoplasm
cAMP
GTP
GTP
GTP
ATP
1
2 3 4
5
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Slide 2
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Hormone (1st messenger)
binds receptor.
1
Extracellular fluid
Receptor
Cytoplasm
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Slide 3
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Extracellular fluid
Hormone (1st messenger)
binds receptor.
1
G protein (G
s
)
GDP
Receptor
GTP
GTP
Receptor
activates G
protein (G
s
).
2
Cytoplasm
2013 Pearson Education, Inc.
Slide 4
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Adenylate cyclase
Extracellular fluid
G protein (G
s
)
GDP
Receptor
Hormone (1st messenger)
binds receptor.
Receptor
activates G
protein (G
s
).
G protein
activates
adenylate
cyclase.
Cytoplasm
GTP
GTP
GTP
1
2 3
2013 Pearson Education, Inc.
Slide 5
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Adenylate cyclase
Extracellular fluid
G protein (G
s
)
GDP
Receptor
Hormone (1st messenger)
binds receptor.
Receptor
activates G
protein (G
s
).
G protein
activates
adenylate
cyclase.
Adenylate
cyclase converts
ATP to cAMP (2nd
messenger).
Cytoplasm
cAMP
GTP
GTP
GTP
ATP
1
2 3 4
2013 Pearson Education, Inc.
Slide 6
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone
(1st messenger)
Receptor G protein Enzyme 2nd
messenger
Adenylate cyclase
Extracellular fluid
G protein (G
s
)
GDP
Receptor
Hormone (1st messenger)
binds receptor.
Receptor
activates G
protein (G
s
).
G protein
activates
adenylate
cyclase.
Adenylate
cyclase converts
ATP to cAMP (2nd
messenger).
Inactive
protein
kinase
Triggers responses of
target cell (activates
enzymes, stimulates
cellular secretion,
opens ion channel, etc.)
Active
protein
kinase
cAMP activates
protein kinases.
Cytoplasm
cAMP
GTP
GTP
GTP
ATP
1
2 3 4
5
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Plasma Membrane Receptors and Second-
messenger Systems
PIP
2
-calcium signaling mechanism
Involves G protein and membrane-bound
effector phospholipase C
Phospholipase C splits PIP
2
into two second
messengers diacylglycerol (DAG) and
inositol trisphosphate (IP
3
)
DAG activates protein kinase; IP
3
causes Ca
2+

release
Calcium ions act as second messenger

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Plasma Membrane Receptors and Second-
messenger Systems
Ca
2+
alters enzyme activity and channels, or
binds to regulatory protein calmodulin
Calcium-bound calmodulin activates enzymes
that amplify cellular response
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Other Signaling Mechanisms
Cyclic guanosine monophosphate (cGMP)
is second messenger for some hormones
Some work without second messengers
E.g., insulin receptor is tyrosine kinase
enzyme that autophosphorylates upon insulin
binding docking for relay proteins that
trigger cell responses

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Intracellular Receptors and Direct Gene
Activation
Steroid hormones and thyroid hormone
1. Diffuse into target cells and bind with
intracellular receptors
2. Receptor-hormone complex enters nucleus;
binds to specific region of DNA
3. Prompts DNA transcription to produce
mRNA
4. mRNA directs protein synthesis
5. Promote metabolic activities, or promote
synthesis of structural proteins or proteins
for export from cell
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Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Slide 1
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
5
The receptor-
hormone complex enters the
nucleus.
The receptor- hormone
complex binds a specific DNA
region.
Binding initiates
transcription of the gene to
mRNA.
The mRNA directs protein
synthesis.
New protein
Nucleus
mRNA
DNA
Receptor
Binding region
Receptor-
hormone
complex
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
2
3
4
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Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Slide 2
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
Nucleus
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
Receptor-
hormone
complex
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Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Slide 3
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
The receptor-
hormone complex enters the
nucleus.
Nucleus
Receptor-
hormone
complex
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
2
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Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Slide 4
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
The receptor-
hormone complex enters the
nucleus.
The receptor- hormone
complex binds a specific DNA
region.
Nucleus
DNA
Receptor
Binding region
Receptor-
hormone
complex
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
2
3
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Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Slide 5
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
The receptor-
hormone complex enters the
nucleus.
The receptor- hormone
complex binds a specific DNA
region.
Binding initiates
transcription of the gene to
mRNA.
Nucleus
mRNA
DNA
Receptor
Binding region
Receptor-
hormone
complex
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
2
3
4
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Slide 6
Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
1
5
The receptor-
hormone complex enters the
nucleus.
The receptor- hormone
complex binds a specific DNA
region.
Binding initiates
transcription of the gene to
mRNA.
The mRNA directs protein
synthesis.
New protein
Nucleus
mRNA
DNA
Receptor
Binding region
Receptor-
hormone
complex
Receptor
protein
Steroid
hormone
Plasma
membrane
Extracellular
fluid
Cytoplasm
2
3
4
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Target Cell Specificity
Target cells must have specific receptors
to which hormone binds, for example
ACTH receptors found only on certain cells of
adrenal cortex
Thyroxin receptors are found on nearly all
cells of body
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Target Cell Activation
Target cell activation depends on three
factors
Blood levels of hormone
Relative number of receptors on or in target
cell
Affinity of binding between receptor and
hormone
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Target Cell Activation
Hormones influence number of their
receptors
Up-regulationtarget cells form more
receptors in response to low hormone levels
Down-regulationtarget cells lose receptors
in response to high hormone levels
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Control of Hormone Release
Blood levels of hormones
Controlled by negative feedback systems
Vary only within narrow, desirable range
Endocrine gland stimulated to synthesize
and release hormones in response to
Humoral stimuli
Neural stimuli
Hormonal stimuli
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Humoral Stimuli
Changing blood levels of ions and
nutrients directly stimulate secretion of
hormones
Example: Ca
2+
in blood
Declining blood Ca
2+
concentration stimulates
parathyroid glands to secrete PTH
(parathyroid hormone)
PTH causes Ca
2+
concentrations to rise and
stimulus is removed
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Figure 16.4a Three types of endocrine gland stimuli.
Slide 1
Humoral Stimulus
Hormone release caused by altered
levels of certain critical ions or
nutrients.
Stimulus: Low concentration of Ca
2+
in
capillary blood.
Parathyroid
glands
Parathyroid
glands
Capillary (low Ca
2+

in blood)
Thyroid gland
(posterior view)
PTH
Response: Parathyroid glands secrete
parathyroid hormone (PTH), which
increases blood Ca
2+
.
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Neural Stimuli
Nerve fibers stimulate hormone release
Sympathetic nervous system fibers stimulate
adrenal medulla to secrete catecholamines
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Figure 16.4b Three types of endocrine gland stimuli.
Slide 1
Neural Stimulus
Hormone release caused
by neural input.
Stimulus: Action potentials in preganglionic
sympathetic fibers to adrenal medulla.
CNS (spinal cord)
Preganglionic
sympathetic
fibers
Medulla of
adrenal gland
Capillary
Response: Adrenal medulla cells secrete
epinephrine and norepinephrine.
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Hormonal Stimuli
Hormones stimulate other endocrine
organs to release their hormones
Hypothalamic hormones stimulate release of
most anterior pituitary hormones
Anterior pituitary hormones stimulate targets
to secrete still more hormones
Hypothalamic-pituitary-target endocrine organ
feedback loop: hormones from final target
organs inhibit release of anterior pituitary
hormones
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Figure 16.4c Three types of endocrine gland stimuli.
Slide 1
Hormonal Stimulus
Hormone release caused by another
hormone (a tropic hormone).
Stimulus: Hormones from hypothalamus.
Anterior
pituitary
gland
Thyroid
gland
Adrenal
cortex
Gonad
(Testis)
Hypothalamus
Response: Anterior pituitary gland secretes
hormones that stimulate other endocrine
glands to secrete hormones.
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Nervous System Modulation
Nervous system modifies stimulation of
endocrine glands and their negative
feedback mechanisms
Example: under severe stress, hypothalamus
and sympathetic nervous system activated
body glucose levels rise
Nervous system can override normal
endocrine controls
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Hormones in the Blood
Hormones circulate in blood either free or
bound
Steroids and thyroid hormone are attached to
plasma proteins
All others circulate without carriers
Concentration of circulating hormone
reflects
Rate of release
Speed of inactivation and removal from body
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Hormones in the Blood
Hormones removed from blood by
Degrading enzymes
Kidneys
Liver
Half-lifetime required for hormone's blood level
to decrease by half
Varies from fraction of minute to a week
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Onset of Hormone Activity
Some responses ~ immediate
Some, especially steroid, hours to days
Some must be activated in target cells
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Duration of Hormone Activity
Limited
Ranges from 10 seconds to several hours
Effects may disappear as blood levels drop
Some persist at low blood levels
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Interaction of Hormones at Target Cells
Multiple hormones may act on same target
at same time
Permissiveness: one hormone cannot exert
its effects without another hormone being
present
Synergism: more than one hormone
produces same effects on target cell
amplification
Antagonism: one or more hormones
oppose(s) action of another hormone
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The Pituitary Gland and Hypothalamus
Pituitary gland (hypophysis) has two
major lobes
Posterior pituitary (lobe)
Neural tissue
Anterior pituitary (lobe)
(adenohypophysis)
Glandular tissue
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Pituitary-hypothalamic Relationships
Posterior pituitary (lobe)
Downgrowth of hypothalamic neural tissue
Neural connection to hypothalamus
(hypothalamic-hypophyseal tract)
Nuclei of hypothalamus synthesize
neurohormones oxytocin and antidiuretic
hormone (ADH)
Neurohormones are transported to and stored
in posterior pituitary
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Figure 16.5a The hypothalamus controls release of hormones from the pituitary gland in two different ways (1 of 2).
Slide 1
Hypothalamic neurons
synthesize oxytocin or
antidiuretic hormone (ADH).
Oxytocin and ADH are
stored in axon terminals in
the posterior pituitary.
When hypothalamic neurons
fire, action potentials arriving at
the axon terminals cause
oxytocin or ADH to be released
into the blood.
1
2
3
4
Oxytocin
ADH
Posterior lobe
of pituitary
Optic
chiasma
Infundibulum
(connecting stalk)
Hypothalamic-
hypophyseal
tract
Axon terminals
Posterior lobe
of pituitary
Paraventricular nucleus
Hypothalamus
Supraoptic
nucleus
Inferior
hypophyseal
artery
Oxytocin and ADH are
transported down the axons of
the hypothalamic- hypophyseal
tract to the posterior pituitary.
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Pituitary-hypothalamic Relationships
Anterior Lobe:
Vascular connection to hypothalamus
Hypophyseal portal system
Primary capillary plexus
Hypophyseal portal veins
Secondary capillary plexus
Carries releasing and inhibiting hormones to anterior
pituitary to regulate hormone secretion
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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).
Slide 1
Hypothalamic hormones
travel through portal veins to
the anterior pituitary where
they stimulate or inhibit
release of hormones made in
the anterior pituitary.
In response to releasing
hormones, the anterior
pituitary secretes hormones
into the secondary capillary
plexus. This in turn empties
into the general circulation.
GH, TSH, ACTH,
FSH, LH, PRL
Anterior lobe
of pituitary
When appropriately stimulated,
hypothalamic neurons secrete
releasing or inhibiting hormones
into the primary capillary plexus.
Hypophyseal
portal system
Primary capillary
plexus
Hypophyseal
portal veins
Secondary
capillary plexus
Superior
hypophyseal
artery
Anterior lobe
of pituitary
Hypothalamus
Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
CRH, GnRH, PIH.
A portal
system is
two
capillary
plexuses
(beds)
connected
by veins.
1
2
3
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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).
Slide 2
GH, TSH, ACTH,
FSH, LH, PRL
Anterior lobe
of pituitary
When appropriately stimulated,
hypothalamic neurons secrete
releasing or inhibiting hormones
into the primary capillary plexus.
Hypophyseal
portal system
Primary capillary
plexus
Hypophyseal
portal veins
Secondary
capillary plexus
Superior
hypophyseal
artery
Anterior lobe
of pituitary
Hypothalamus
Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
CRH, GnRH, PIH.
A portal
system is
two
capillary
plexuses
(beds)
connected
by veins.
1
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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).
Slide 3
Hypothalamic hormones
travel through portal veins to
the anterior pituitary where
they stimulate or inhibit
release of hormones made in
the anterior pituitary.
GH, TSH, ACTH,
FSH, LH, PRL
Anterior lobe
of pituitary
When appropriately stimulated,
hypothalamic neurons secrete
releasing or inhibiting hormones
into the primary capillary plexus.
Hypophyseal
portal system
Primary capillary
plexus
Hypophyseal
portal veins
Secondary
capillary plexus
Superior
hypophyseal
artery
Anterior lobe
of pituitary
Hypothalamus
Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
CRH, GnRH, PIH.
A portal
system is
two
capillary
plexuses
(beds)
connected
by veins.
1
2
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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).
Slide 4
Hypothalamic hormones
travel through portal veins to
the anterior pituitary where
they stimulate or inhibit
release of hormones made in
the anterior pituitary.
In response to releasing
hormones, the anterior
pituitary secretes hormones
into the secondary capillary
plexus. This in turn empties
into the general circulation.
GH, TSH, ACTH,
FSH, LH, PRL
Anterior lobe
of pituitary
When appropriately stimulated,
hypothalamic neurons secrete
releasing or inhibiting hormones
into the primary capillary plexus.
Hypophyseal
portal system
Primary capillary
plexus
Hypophyseal
portal veins
Secondary
capillary plexus
Superior
hypophyseal
artery
Anterior lobe
of pituitary
Hypothalamus
Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
CRH, GnRH, PIH.
A portal
system is
two
capillary
plexuses
(beds)
connected
by veins.
1
2
3
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Posterior Pituitary and Hypothalamic
Hormones
Oxytocin and ADH
Each composed of nine amino acids
Almost identical differ in two amino acids
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Oxytocin
Strong stimulant of uterine contraction
Released during childbirth
Hormonal trigger for milk ejection
Acts as neurotransmitter in brain

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ADH (Vasopressin)
Inhibits or prevents urine formation
Regulates water balance
Targets kidney tubules reabsorb more
water
Release also triggered by pain, low blood
pressure, and drugs
Inhibited by alcohol, diuretics
High concentrations vasoconstriction
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ADH
Diabetes insipidus
ADH deficiency due to hypothalamus or
posterior pituitary damage
Must keep well-hydrated
Syndrome of inappropriate ADH
secretion (SIADH)
Retention of fluid, headache, disorientation
Fluid restriction; blood sodium level
monitoring
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Anterior Pituitary Hormones
Growth hormone (GH)
Thyroid-stimulating hormone (TSH) or
thyrotropin
Adrenocorticotropic hormone (ACTH)
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Prolactin (PRL)
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Anterior Pituitary Hormones
All are proteins
All except GH activate cyclic AMP second-
messenger systems at their targets
TSH, ACTH, FSH, and LH are all tropic
hormones (regulate secretory action of
other endocrine glands)
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Growth Hormone (GH, or Somatotropin)
Produced by somatotropic cells
Direct actions on metabolism
Increases blood levels of fatty acids;
encourages use of fatty acids for fuel; protein
synthesis
Decreases rate of glucose uptake and
metabolism conserving glucose
Glycogen breakdown and glucose release
to blood (anti-insulin effect)
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Growth Hormone (GH, or Somatotropin)
Indirect actions on growth
Mediates growth via growth-promoting
proteins insulin-like growth factors
(IGFs)
IGFs stimulate
Uptake of nutrients DNA and proteins
Formation of collagen and deposition of bone
matrix
Major targetsbone and skeletal muscle
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Growth Hormone (GH)
GH release chiefly regulated by
hypothalamic hormones
Growth hormonereleasing hormone (GHRH)
Stimulates release
Growth hormoneinhibiting hormone (GHIH)
(somatostatin)
Inhibits release
Ghrelin (hunger hormone) also stimulates
release
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Homeostatic Imbalances of Growth
Hormone
Hypersecretion
In children results in gigantism
In adults results in acromegaly
Hyposecretion
In children results in pituitary dwarfism
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Figure 16.6 Growth-promoting and metabolic actions of growth hormone (GH).
Hypothalamus
secretes growth
hormonereleasing
hormone (GHRH), and
GHIH (somatostatin)
Anterior
pituitary
Inhibits GHRH release
Stimulates GHIH release
Inhibits GH synthesis
and release
Feedback
Indirect actions
(growth-
promoting)
Liver and
other tissues
Insulin-like growth
factors (IGFs)
Produce
Effects
Skeletal Extraskeletal
Fat
metabolism
Carbohydrate
metabolism
Direct actions
(metabolic,
anti-insulin)
Effects
Growth hormone (GH)
Increased cartilage
formation and
skeletal growth
Increased protein
synthesis, and
cell growth and
proliferation
Increased
fat breakdown
and release
Increased blood
glucose and other
anti-insulin effects
Increases, stimulates
Initial stimulus
Reduces, inhibits
Physiological response
Result
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Figure 16.7 Disorders of pituitary growth hormone.
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Thyroid-stimulating Hormone (Thyrotropin)
Produced by thyrotropic cells of anterior
pituitary
Stimulates normal development and
secretory activity of thyroid
Release triggered by thyrotropin-releasing
hormone from hypothalamus
Inhibited by rising blood levels of thyroid
hormones that act on pituitary and
hypothalamus

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Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Target cells
Stimulates
Figure 16.8 Regulation of thyroid hormone secretion.
Inhibits
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Adrenocorticotropic Hormone
(Corticotropin)
Secreted by corticotropic cells of anterior
pituitary
Stimulates adrenal cortex to release
corticosteroids
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Adrenocorticotropic Hormone
(Corticotropin)
Regulation of ACTH release
Triggered by hypothalamic corticotropin-
releasing hormone (CRH) in daily rhythm
Internal and external factors such as fever,
hypoglycemia, and stressors can alter release
of CRH
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Gonadotropins
Follicle-stimulating hormone (FSH) and
luteinizing hormone (LH)
Secreted by gonadotrophs of anterior
pituitary
FSH stimulates gamete (egg or sperm)
production
LH promotes production of gonadal
hormones
Absent from the blood in prepubertal boys
and girls
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Gonadotropins
Regulation of gonadotropin release
Triggered by gonadotropin-releasing hormone
(GnRH) during and after puberty
Suppressed by gonadal hormones (feedback)
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Prolactin (PRL)
Secreted by prolactin cells of anterior
pituitary
Stimulates milk production
Role in males not well understood
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Prolactin (PRL)
Regulation of PRL release
Primarily controlled by prolactin-inhibiting
hormone (PIH) (dopamine)
Blood levels rise toward end of pregnancy
Suckling stimulates PRL release and
promotes continued milk production
Hypersecretion causes inappropriate
lactation, lack of menses, infertility in
females, and impotence in males
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Thyroid Gland
Composed of follicles that produce
glycoprotein thyroglobulin
Colloid (thyroglobulin + iodine) fills lumen
of follicles and is precursor of thyroid
hormone
Parafollicular cells produce the hormone
calcitonin
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Thyroid Hormone (TH)
Actually two related compounds
T
4
(thyroxine); has 2 tyrosine molecules + 4
bound iodine atoms
T
3
(triiodothyronine); has 2 tyrosines + 3
bound iodine atoms
Affects virtually every cell in body
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Thyroid Hormone
Major metabolic hormone
Increases metabolic rate and heat
production (calorigenic effect)
Regulation of tissue growth and
development
Development of skeletal and nervous systems
Reproductive capabilities
Maintenance of blood pressure
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Synthesis of Thyroid Hormone
Thyroid gland stores hormone
extracellularly
Thyroglobulin synthesized and discharged
into follicle lumen
Iodides (I

) actively taken into cell and

released into lumen
Iodide oxidized to iodine (I
2
),
Iodine attaches to tyrosine, mediated by
peroxidase enzymes
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Synthesis of Thyroid Hormone
Iodinated tyrosines link together to form T
3

and T
4

Colloid is endocytosed and combined with
lysosome
T
3
and T
4
are cleaved and diffuse into
bloodstream
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 1
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
2
3
4
5
6
7
Golgi
apparatus
Iodide (I)
Rough
ER
Capillary
Iodide (I

) is trapped
(actively transported in).
Lysosome
Lysosomal enzymes
cleave T
4
and T
3
from
thyroglobulin and hormones
diffuse into bloodstream.
Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
Iodinated tyrosines are
linked together to form T
3

and T
4
.
Iodide
is oxidized
to iodine.
Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
To peripheral tissues
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Thyro-
globulin
colloid
T
3

T
4

T
3

T
4

T
3

T
4

Iodine
DIT MIT
Colloid
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 2
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 3
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2
Iodide (I) Iodide (I

) is trapped
(actively transported in).
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 4
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2
Iodide (I) Iodide (I

) is trapped
(actively transported in).
Iodine
3
Iodide
is oxidized
to iodine.
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 5
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2
Iodide (I) Iodide (I

) is trapped
(actively transported in).
Iodine
3
Iodide
is oxidized
to iodine.
4
Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Thyro-
globulin
colloid
DIT MIT
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 6
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2
Iodide (I) Iodide (I

) is trapped
(actively transported in).
Iodine
3
Iodide
is oxidized
to iodine.
4
Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Thyro-
globulin
colloid
DIT MIT
5
Iodinated tyrosines are
linked together to form T
3

and T
4
.
T
3

T
4

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Figure 16.10 Synthesis of thyroid hormone.
Slide 7
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
Golgi
apparatus
Rough
ER
Capillary
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Colloid
2
Iodide (I) Iodide (I

) is trapped
(actively transported in).
Iodine
3
Iodide
is oxidized
to iodine.
4
Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Thyro-
globulin
colloid
DIT MIT
5
Iodinated tyrosines are
linked together to form T
3

and T
4
.
T
3

T
4

6
Lysosome
Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 8
Thyroglobulin is synthesized and
discharged into the follicle lumen.
1
2
3
4
5
6
7
Golgi
apparatus
Iodide (I)
Rough
ER
Capillary
Iodide (I

) is trapped
(actively transported in).
Lysosome
Lysosomal enzymes
cleave T
4
and T
3
from
thyroglobulin and hormones
diffuse into bloodstream.
Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
Iodinated tyrosines are
linked together to form T
3

and T
4
.
Iodide
is oxidized
to iodine.
Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
To peripheral tissues
Colloid in
lumen of
follicle
Thyroid follicular cells
Tyrosines (part of thyroglobulin
molecule)
Thyro-
globulin
colloid
T
3

T
4

T
3

T
4

T
3

T
4

Iodine
DIT MIT
Colloid
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Transport and Regulation of TH
T
4
and T
3
transported by thyroxine-binding
globulins (TBGs)
Both bind to target receptors, but T
3
is ten
times more active than T
4

Peripheral tissues convert T
4
to T
3

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Transport and Regulation of TH
Negative feedback regulation of TH
release
Rising TH levels provide negative feedback
inhibition on release of TSH
Hypothalamic thyrotropin-releasing hormone
(TRH) can overcome negative feedback
during pregnancy or exposure to cold
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Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Target cells
Stimulates
Figure 16.8 Regulation of thyroid hormone secretion.
Inhibits
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Homeostatic Imbalances of TH
Hyposecretion in adultsmyxedema;
goiter if due to lack of iodine
Hyposecretion in infantscretinism
HypersecretionGraves' disease
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Figure 16.11 Thyroid disorders.
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Calcitonin
Produced by parafollicular (C) cells
No known physiological role in humans
Antagonist to parathyroid hormone (PTH)
At higher than normal doses
Inhibits osteoclast activity and release of Ca
2+

from bone matrix
Stimulates Ca
2+
uptake and incorporation into
bone matrix
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Parathyroid Glands
Four to eight tiny glands embedded in
posterior aspect of thyroid
Contain oxyphil cells (function unknown)
and parathyroid cells that secrete
parathyroid hormone (PTH) or
parathormone
PTHmost important hormone in Ca
2+

homeostasis
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Parathyroid Hormone
Functions
Stimulates osteoclasts to digest bone matrix
and release Ca
2+
to blood
Enhances reabsorption of Ca
2+
and secretion
of phosphate by kidneys
Promotes activation of vitamin D (by kidneys);
increases absorption of Ca
2+
by intestinal
mucosa
Negative feedback control: rising Ca
2+
in
blood inhibits PTH release
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Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.
Osteoclast activity
in bone causes Ca
2+

and PO
4
3-
release
into blood
Hypocalcemia
(low blood Ca
2+
)
PTH release from
parathyroid gland
Ca
2+
reabsorption
in kidney tubule
Activation of
vitamin D by kidney
Ca
2+
absorption
from food in small
intestine
Ca
2+
in blood
Initial stimulus
Physiological response
Result
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Homeostatic Imbalances of PTH
Hyperparathyroidism due to tumor
Bones soften and deform
Elevated Ca
2+
depresses nervous system and
contributes to formation of kidney stones
Hypoparathyroidism following gland
trauma or removal or dietary magnesium
deficiency
Results in tetany, respiratory paralysis, and
death
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Adrenal (Suprarenal) Glands
Paired, pyramid-shaped organs atop
kidneys
Structurally and functionally are two
glands in one
Adrenal medullanervous tissue; part of
sympathetic nervous system
Adrenal cortexthree layers of glandular
tissue that synthesize and secrete
corticosteroids
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Adrenal Cortex
Three layers of cortex produce the
different corticosteroids
Zona glomerulosamineralocorticoids
Zona fasciculataglucocorticoids
Zona reticularisgonadocorticoids
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Mineralocorticoids
Regulate electrolytes (primarily Na
+
and K
+
)
in ECF
Importance of Na
+
: affects ECF volume, blood
volume, blood pressure, levels of other ions
Importance of K
+
: sets RMP of cells
Aldosterone most potent mineralocorticoid
Stimulates Na
+
reabsorption and water
retention by kidneys; elimination of K
+
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Aldosterone
Release triggered by
Decreasing blood volume and blood pressure
Rising blood levels of K
+
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Mechanisms of Aldosterone Secretion
Renin-angiotensin-aldosterone mechanism:
decreased blood pressure stimulates kidneys to
release renin triggers formation of angiotensin
II, a potent stimulator of aldosterone release
Plasma concentration of K
+
: increased K
+

directly influences zona glomerulosa cells to
release aldosterone
ACTH: causes small increases of aldosterone
during stress
Atrial natriuretic peptide (ANP): blocks renin and
aldosterone secretion to decrease blood
pressure
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Figure 16.15 Major mechanisms controlling aldosterone release from the adrenal cortex.
Blood volume
and/or blood
pressure
K+ in blood
Stress Blood pressure
and/or blood
volume
Hypo-
thalamus
Heart
CRH
Anterior
pituitary
Direct
stimulating
effect
Initiates
cascade
that
produces
Renin
Angiotensin II
ACTH Atrial natriuretic
peptide (ANP)
Inhibitory
effect
Zona glomerulosa
of adrenal cortex
Enhanced
secretion
of aldosterone
Targets
kidney tubules
Absorption of Na
+
and
water; increased K
+
excretion
Blood volume
and/or blood pressure
Kidney
Primary regulators Other factors
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Homeostatic Imbalances of Aldosterone
Aldosteronismhypersecretion due to
adrenal tumors
Hypertension and edema due to excessive Na
+

Excretion of K
+
leading to abnormal function of
neurons and muscle
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Glucocorticoids
Keep blood glucose levels relatively
constant
Maintain blood pressure by increasing
action of vasoconstrictors
Cortisol (hydrocortisone)
Only one in significant amounts in humans
Cortisone
Corticosterone
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Glucocorticoids: Cortisol
Released in response to ACTH, patterns of
eating and activity, and stress
Prime metabolic effect is gluconeogenesis
formation of glucose from fats and proteins
Promotes rises in blood glucose, fatty acids, and
amino acids
"Saves" glucose for brain
Enhances vasoconstriction rise in blood
pressure to quickly distribute nutrients to cells
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Homeostatic Imbalances of Glucocorticoids
HypersecretionCushing's
syndrome/disease
Depresses cartilage and bone formation
Inhibits inflammation
Depresses immune system
Disrupts cardiovascular, neural, and
gastrointestinal function
HyposecretionAddison's disease
Also involves deficits in mineralocorticoids
Decrease in glucose and Na
+
levels
Weight loss, severe dehydration, and hypotension
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Figure 16.16 The effects of excess glucocorticoid.
Patient before onset. Same patient with Cushings
syndrome. The white arrow shows
the characteristic buffalo hump of
fat on the upper back.
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Gonadocorticoids (Sex Hormones)
Most weak androgens (male sex
hormones) converted to testosterone in
tissue cells, some to estrogens
May contribute to
Onset of puberty
Appearance of secondary sex characteristics
Sex drive in women
Estrogens in postmenopausal women
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Gonadocorticoids
Hypersecretion
Adrenogenital syndrome (masculinization)
Not noticeable in adult males
Females and prepubertal males
Boys reproductive organs mature; secondary sex
characteristics emerge early
Females beard, masculine pattern of body hair;
clitoris resembles small penis
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Adrenal Medulla
Medullary chromaffin cells synthesize
epinephrine (80%) and norepinephrine
(20%)
Effects
Vasoconstriction
Increased heart rate
Increased blood glucose levels
Blood diverted to brain, heart, and skeletal
muscle
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Adrenal Medulla
Responses brief
Epinephrine stimulates metabolic
activities, bronchial dilation, and blood flow
to skeletal muscles and heart
Norepinephrine influences peripheral
vasoconstriction and blood pressure
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Adrenal Medulla
Hypersecretion
Hyperglycemia, increased metabolic rate,
rapid heartbeat and palpitations,
hypertension, intense nervousness, sweating
Hyposecretion
Not problematic
Adrenal catecholamines not essential to life
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Figure 16.17 Stress and the adrenal gland.
Short-term stress Prolonged stress
Nerve impulses
Spinal cord
Preganglionic
sympathetic
fibers
Adrenal medulla
(secretes amino acid
based hormones)
Catecholamines
(epinephrine and
norepinephrine)
Short-term stress response
Stress
Hypothalamus
Corticotropic cells
of anterior pituitary
To target in blood
CRH (corticotropin-
releasing hormone)
Adrenal cortex
(secretes steroid
hormones)
Mineralocorticoids Glucocorticoids
ACTH
Heart rate increases
Long-term stress response
Kidneys retain
sodium and water
Proteins and fats converted
to glucose or broken down
for energy
Blood glucose increases
Blood pressure increases
Bronchioles dilate
Liver converts glycogen to glucose and releases
glucose to blood
Blood flow changes, reducing digestive system activity
and urine output
Metabolic rate increases
Blood volume and
blood pressure
rise
Immune system
supressed
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Pineal Gland
Small gland hanging from roof of third ventricle
Pinealocytes secrete melatonin, derived from
serotonin
Melatonin may affect
Timing of sexual maturation and puberty
Day/night cycles
Physiological processes that show rhythmic variations
(body temperature, sleep, appetite)
Production of antioxidant and detoxification molecules
in cells
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Pancreas
Triangular gland partially behind stomach
Has both exocrine and endocrine cells
Acinar cells (exocrine) produce enzyme-rich
juice for digestion
Pancreatic islets (islets of Langerhans)
contain endocrine cells
Alpha () cells produce glucagon (hyperglycemic
hormone)
Beta () cells produce insulin (hypoglycemic
hormone)
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Glucagon
Major targetliver
Causes increased blood glucose levels
Effects
Glycogenolysisbreakdown of glycogen to
glucose
Gluconeogenesissynthesis of glucose
from lactic acid and noncarbohydrates
Release of glucose to blood
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Insulin
Effects of insulin
Lowers blood glucose levels
Enhances membrane transport of glucose into
fat and muscle cells
Inhibits glycogenolysis and gluconeogenesis
Participates in neuronal development and
learning and memory
Not needed for glucose uptake in liver,
kidney or brain

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Insulin Action on Cells
Activates tyrosine kinase enzyme receptor
Cascade increased glucose uptake
Triggers enzymes to
Catalyze oxidation of glucose for ATP
production first priority
Polymerize glucose to form glycogen
Convert glucose to fat (particularly in adipose
tissue)
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Figure 16.19 Insulin and glucagon from the pancreas regulate blood glucose levels.
Stimulates glucose
uptake by cells
Insulin
Stimulates
glycogen
formationw
Pancreas
Tissue cells
Glucose Glycogen
Liver
Blood
glucose
falls to
normal
range.
Stimulus
Blood
glucose level
Pancreas
Glucose Glycogen
Liver
Stimulates
glycogen
breakdown
Blood
glucose
rises to
normal
range.
Stimulus
Blood
glucose level
Glucagon
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Factors That Influence Insulin Release
Elevated blood glucose levels primary stimulus
Rising blood levels of amino acids and fatty
acids
Release of acetylcholine by parasympathetic
nerve fibers
Hormones glucagon, epinephrine, growth
hormone, thyroxine, glucocorticoids
Somatostatin; sympathetic nervous system

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Homeostatic Imbalances of Insulin
Diabetes mellitus (DM)
Due to hyposecretion (type 1) or hypoactivity (type 2)
of insulin
Blood glucose levels remain high nausea higher
blood glucose levels (fight or flight response)
Glycosuria glucose spilled into urine
Fats used for cellular fuel lipidemia; if severe
ketones (ketone bodies) from fatty acid metabolism
ketonuria and ketoacidosis
Untreated ketoacidosis hyperpnea; disrupted heart
activity and O
2
transport; depression of nervous
system coma and death possible
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Diabetes Mellitus: Signs
Three cardinal signs of DM
Polyuriahuge urine output
Glucose acts as osmotic diuretic
Polydipsiaexcessive thirst
From water loss due to polyuria
Polyphagiaexcessive hunger and food
consumption
Cells cannot take up glucose; are "starving"

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Homeostatic Imbalances of Insulin
Hyperinsulinism:
Excessive insulin secretion

Causes hypoglycemia
Low blood glucose levels
Anxiety, nervousness, disorientation,
unconsciousness, even death

Treated by sugar ingestion

2013 Pearson Education, Inc.
Table 16.4 Symptoms of Insulin Deficit (Diabetes Mellitus)
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Ovaries and Placenta
Gonads produce steroid sex hormones
Same as those of adrenal cortex
Ovaries produce estrogens and progesterone
Estrogen
Maturation of reproductive organs
Appearance of secondary sexual characteristics
With progesterone, causes breast development and cyclic
changes in uterine mucosa
Placenta secretes estrogens, progesterone, and
human chorionic gonadotropin (hCG)
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Testes
Testes produce testosterone
Initiates maturation of male reproductive
organs
Causes appearance of male secondary
sexual characteristics and sex drive
Necessary for normal sperm production
Maintains reproductive organs in functional
state
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Other Hormone-producing Structures
Adipose tissue
Leptin appetite control; stimulates
increased energy expenditure
Resistin insulin antagonist
Adiponectin enhances sensitivity to insulin

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Other Hormone-producing Structures
Enteroendocrine cells of gastrointestinal
tract
Gastrin stimulates release of HCl
Secretin stimulates liver and pancreas
Cholecystokinin stimulates pancreas,
gallbladder, and hepatopancreatic sphincter
Serotonin acts as paracrine

2013 Pearson Education, Inc.
Other Hormone-producing Structures
Heart
Atrial natriuretic peptide (ANP) decreases
blood Na
+
concentration, therefore blood
pressure and blood volume
Kidneys
Erythropoietin signals production of red
blood cells
Renin initiates the renin-angiotensin-
aldosterone mechanism
2013 Pearson Education, Inc.
Other Hormone-producing Structures
Skeleton (osteoblasts)
Osteocalcin
Prods pancreas to secrete more insulin; restricts
fat storage; improves glucose handling; reduces
body fat
Activated by insulin
Low levels of osteocalcin in type 2 diabetes
perhaps increasing levels may be new treatment
Skin
Cholecalciferol, precursor of vitamin D
2013 Pearson Education, Inc.
Thymus
Large in infants and children; shrinks as age
Thymulin, thymopoietins, and thymosins
May be involved in normal development of T
lymphocytes in immune response
Classified as hormones; act as paracrines

Other Hormone-producing Structures
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Developmental Aspects
Hormone-producing glands arise from all three
germ layers
Most endocrine organs operate well until old age
Exposure to pesticides, industrial chemicals,
arsenic, dioxin, and soil and water pollutants
disrupts hormone function
Sex hormones, thyroid hormone, and
glucocorticoids are vulnerable to the effects of
pollutants
Interference with glucocorticoids may help
explain high cancer rates in certain areas
2013 Pearson Education, Inc.
Developmental Aspects
Ovaries undergo significant changes with
age and become unresponsive to
gonadotropins; problems associated with
estrogen deficiency occur
Testosterone also diminishes with age, but
effect is not usually seen until very old age
2013 Pearson Education, Inc.
Developmental Aspects
GH levels decline with age - accounts for
muscle atrophy with age
TH declines with age, contributing to lower
basal metabolic rates
PTH levels remain fairly constant with age,
but lack of estrogen in older women
makes them more vulnerable to bone-
demineralizing effects of PTH