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PowerPoint® Lecture Slides
prepared by
Barbara Heard,
Atlantic Cape Community
Ninth Edition
College
Human Anatomy & Physiology
CHAPTER
16
The Endocrine
System
© Annie Leibovitz/Contact Press Images
© 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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Endocrine System: Overview
• Exocrine glands
– Nonhormonal substances (sweat, saliva)
– Have ducts to carry secretion to membrane
surface
• Endocrine glands
– Produce hormones
– Lack ducts
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
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
• Ovary (female)
• Testis (male)
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Chemistry of Hormones
• Two main classes
– Amino acid-based hormones
• Amino acid derivatives, peptides, and proteins
– Steroids
• Synthesized from cholesterol
• Gonadal and adrenocortical hormones
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
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
2. Lipid-soluble hormones (steroid and thyroid
hormones)
• Act on intracellular receptors that directly activate
genes
• Can enter cell
© 2013 Pearson Education, Inc.
Plasma Membrane Receptors and Secondmessenger Systems
• cAMP signaling mechanism:
1.
2.
3.
4.
Hormone (first messenger) binds to receptor
Receptor activates G protein
G protein activates adenylate cyclase
Adenylate cyclase converts ATP to cAMP
(second messenger)
5. cAMP activates protein kinases that
phosphorylate proteins
© 2013 Pearson Education, Inc.
Plasma Membrane Receptors and Secondmessenger 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
© 2013 Pearson Education, Inc.
Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones.
Slide 1
Recall from Chapter 3 that
G protein signaling mechanisms
are like a molecular relay race.
Hormone Receptor G protein Enzyme
2nd
(1st messenger)
messenger
1 Hormone (1st messenger)
binds receptor.
Extracellular fluid
Adenylate cyclase
G protein (Gs)
Receptor
5 cAMP activates
protein kinases.
cAMP
GTP
GTP
ATP
GDP
Inactive
protein
kinase
GTP
Active
protein
kinase
Triggers responses of
target cell (activates
enzymes, stimulates
cellular secretion,
opens ion channel, etc.)
Cytoplasm
2 Receptor
activates G
protein (Gs).
© 2013 Pearson Education, Inc.
3 G protein
activates
adenylate
cyclase.
4 Adenylate
cyclase converts
ATP to cAMP (2nd
messenger).
Plasma Membrane Receptors and Secondmessenger Systems
• PIP2-calcium signaling mechanism
– Involves G protein and membrane-bound
effector – phospholipase C
– Phospholipase C splits PIP2 into two second
messengers – diacylglycerol (DAG) and
inositol trisphosphate (IP3)
• DAG activates protein kinase; IP3 causes Ca2+
release
• Calcium ions act as second messenger
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Plasma Membrane Receptors and Secondmessenger Systems
– Ca2+ alters enzyme activity and channels, or
binds to regulatory protein calmodulin
– Calcium-bound calmodulin activates enzymes
that amplify cellular response
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones.
Extracellular
fluid
Steroid
hormone
Plasma
membrane
Cytoplasm
Receptor
protein
Nucleus
Slide 1
1 The steroid hormone
diffuses through the plasma
membrane and binds an
intracellular receptor.
Receptorhormone
complex 2 The receptorhormone complex enters the
nucleus.
Receptor
Binding region
DNA
mRNA
3 The receptor- hormone
complex binds a specific DNA
region.
4 Binding initiates
transcription of the gene to
mRNA.
5 The mRNA directs protein
synthesis.
New protein
© 2013 Pearson Education, Inc.
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-regulation—target cells form more
receptors in response to low hormone levels
– Down-regulation—target cells lose receptors
in response to high hormone levels
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Humoral Stimuli
• Changing blood levels of ions and
nutrients directly stimulate secretion of
hormones
• Example: Ca2+ in blood
– Declining blood Ca2+ concentration stimulates
parathyroid glands to secrete PTH
(parathyroid hormone)
– PTH causes Ca2+ concentrations to rise and
stimulus is removed
© 2013 Pearson Education, Inc.
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.
Capillary (low Ca2+
in blood)
Thyroid gland
(posterior view)
Parathyroid
glands
Parathyroid
glands
PTH
Stimulus: Low concentration of Ca2+ in
capillary blood.
Response: Parathyroid glands secrete
parathyroid hormone (PTH), which
increases blood Ca2+.
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Neural Stimuli
• Nerve fibers stimulate hormone release
– Sympathetic nervous system fibers stimulate
adrenal medulla to secrete catecholamines
© 2013 Pearson Education, Inc.
Figure 16.4b Three types of endocrine gland stimuli.
Slide 1
Neural Stimulus
Hormone release caused
by neural input.
CNS (spinal cord)
Preganglionic
sympathetic
fibers
Medulla of
adrenal gland
Capillary
Stimulus: Action potentials in preganglionic
sympathetic fibers to adrenal medulla.
Response: Adrenal medulla cells secrete
epinephrine and norepinephrine.
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Figure 16.4c Three types of endocrine gland stimuli.
Hormonal Stimulus
Hormone release caused by another
hormone (a tropic hormone).
Hypothalamus
Anterior
pituitary
gland
Thyroid
gland
Adrenal Gonad
cortex (Testis)
Stimulus: Hormones from hypothalamus.
Response: Anterior pituitary gland secretes
hormones that stimulate other endocrine
glands to secrete hormones.
© 2013 Pearson Education, Inc.
Slide 1
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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Hormones in the Blood
• Hormones removed from blood by
– Degrading enzymes
– Kidneys
– Liver
• Half-life—time 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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Figure 16.5a The hypothalamus controls release of hormones from the pituitary gland in two different ways (1 of 2).
Slide 1
Paraventricular nucleus
Hypothalamus
Posterior lobe
of pituitary
Optic
chiasma
Infundibulum
(connecting stalk)
Hypothalamichypophyseal
tract
Supraoptic
nucleus
Inferior
hypophyseal
artery
Axon terminals
2 Oxytocin and ADH are
transported down the axons of
the hypothalamic- hypophyseal
tract to the posterior pituitary.
3 Oxytocin and ADH are
stored in axon terminals in
the posterior pituitary.
Posterior lobe
of pituitary
Oxytocin
ADH
© 2013 Pearson Education, Inc.
1 Hypothalamic neurons
synthesize oxytocin or
antidiuretic hormone (ADH).
4 When hypothalamic neurons
fire, action potentials arriving at
the axon terminals cause
oxytocin or ADH to be released
into the blood.
Pituitary-hypothalamic Relationships
• Anterior Lobe:
– Originates as outpocketing of oral mucosa
– Vascular connection to hypothalamus
• Hypophyseal portal system
–
–
–
–
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Primary capillary plexus
Hypophyseal portal veins
Secondary capillary plexus
Carries releasing and inhibiting hormones to anterior
pituitary to regulate hormone secretion
Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2).
Slide 1
Hypothalamus
Anterior lobe
of pituitary
Superior
hypophyseal
artery
2 Hypothalamic hormones
travel through portal veins to
the anterior pituitary where
they stimulate or inhibit
release of hormones made in
the anterior pituitary.
3 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
© 2013 Pearson Education, Inc.
Hypothalamic
neurons synthesize
GHRH, GHIH, TRH,
CRH, GnRH, PIH.
1 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
A portal
system is
two
capillary
plexuses
(beds)
connected
by veins.
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
© 2013 Pearson Education, Inc.
Anterior Pituitary Hormones
• Growth hormone (GH)
• Thyroid-stimulating hormone (TSH) or
thyrotropin
• Adrenocorticotropic hormone (ACTH)
• Follicle-stimulating hormone (FSH)
• Luteinizing hormone (LH)
• Prolactin (PRL)
© 2013 Pearson Education, Inc.
Anterior Pituitary Hormones
• All are proteins
• All except GH activate cyclic AMP secondmessenger systems at their targets
• TSH, ACTH, FSH, and LH are all tropic
hormones (regulate secretory action of
other endocrine glands)
© 2013 Pearson Education, Inc.
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)
© 2013 Pearson Education, Inc.
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 targets—bone and skeletal muscle
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Growth Hormone (GH)
• GH release chiefly regulated by
hypothalamic hormones
– Growth hormone–releasing hormone (GHRH)
• Stimulates release
– Growth hormone–inhibiting hormone (GHIH)
(somatostatin)
• Inhibits release
• Ghrelin (hunger hormone) also stimulates
release
© 2013 Pearson Education, Inc.
Homeostatic Imbalances of Growth
Hormone
• Hypersecretion
– In children results in gigantism
– In adults results in acromegaly
• Hyposecretion
– In children results in pituitary dwarfism
© 2013 Pearson Education, Inc.
Figure 16.6 Growth-promoting and metabolic actions of growth hormone (GH).
Inhibits GHRH release
Stimulates GHIH release
Feedback
Anterior
pituitary
Hypothalamus
secretes growth
hormone–releasing
hormone (GHRH), and
GHIH (somatostatin)
Inhibits GH synthesis
and release
Growth hormone (GH)
Indirect actions
Direct actions
(growthpromoting)
(metabolic,
anti-insulin)
Liver and
other tissues
Produce
Insulin-like growth
factors (IGFs)
Effects
Effects
Skeletal
Extraskeletal
Fat
metabolism
Carbohydrate
metabolism
Increases, stimulates
Reduces, inhibits
Increased cartilage
formation and
skeletal growth
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Increased protein
synthesis, and
cell growth and
proliferation
Increased
fat breakdown
and release
Increased blood
glucose and other
anti-insulin effects
Initial stimulus
Physiological response
Result
Figure 16.7 Disorders of pituitary growth hormone.
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Figure 16.8 Regulation of thyroid hormone secretion.
Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Target cells
© 2013 Pearson Education, Inc.
Stimulates
Inhibits
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 corticotropinreleasing hormone (CRH) in daily rhythm
– Internal and external factors such as fever,
hypoglycemia, and stressors can alter release
of CRH
© 2013 Pearson Education, Inc.
Gonadotropins
• Follicle-stimulating hormone (FSH) and
luteinizing hormone (LH)
• Secreted by gonadotropic cells 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
• Two lateral lobes connected by median
mass called isthmus
• Composed of follicles that produce
glycoprotein thyroglobulin
• Colloid (fluid with thyroglobulin + iodine)
fills lumen of follicles and is precursor of
thyroid hormone
• Parafollicular cells produce the hormone
calcitonin
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Figure 16.9 The thyroid gland.
Hyoid bone
Thyroid cartilage
Common carotid
artery
Epiglottis
Colloid-filled
follicles
Follicular cells
Superior thyroid
artery
Inferior thyroid
artery
Isthmus of
thyroid gland
Trachea
Left subclavian
artery
Left lateral
lobe of thyroid
gland
Aorta
Parafollicular cells
Gross anatomy of the thyroid gland, anterior view
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Photomicrograph of thyroid gland
follicles (145x)
Thyroid Hormone (TH)
• Actually two related compounds
– T4 (thyroxine); has 2 tyrosine molecules + 4
bound iodine atoms
– T3 (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 (I2),
• Iodine attaches to tyrosine, mediated by
peroxidase enzymes
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Synthesis of Thyroid Hormone
• Iodinated tyrosines link together to form T3
and T4
• Colloid is endocytosed and vesicle is
combined with a lysosome
• T3 and T4 are cleaved and diffuse into
bloodstream
© 2013 Pearson Education, Inc.
Figure 16.10 Synthesis of thyroid hormone.
Slide 1
Thyroid follicular cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus
Rough
ER
Iodine
3 Iodide
is oxidized
to iodine.
2 Iodide (I–) is trapped
(actively transported in).
Iodide (I−)
T4
T3
Lysosome
DIT
MIT
Thyroglobulin
colloid
5 Iodinated tyrosines are
linked together to form T3
and T4.
T4
T3
T4
T3
To peripheral tissues
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6 Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
7 Lysosomal enzymes
cleave T4 and T3 from
thyroglobulin and hormones
diffuse into bloodstream.
Colloid in
lumen of
follicle
Transport and Regulation of TH
• T4 and T3 transported by thyroxine-binding
globulins (TBGs)
• Both bind to target receptors, but T3 is ten
times more active than T4
• Peripheral tissues convert T4 to T3
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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
© 2013 Pearson Education, Inc.
Figure 16.8 Regulation of thyroid hormone secretion.
Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Target cells
© 2013 Pearson Education, Inc.
Stimulates
Inhibits
Homeostatic Imbalances of TH
• Hyposecretion in adults—myxedema;
goiter if due to lack of iodine
• Hyposecretion in infants—cretinism
• Hypersecretion—most common type is
Graves' disease
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Figure 16.11 Thyroid disorders.
© 2013 Pearson Education, Inc.
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 Ca2+
from bone matrix
– Stimulates Ca2+ uptake and incorporation into
bone matrix
© 2013 Pearson Education, Inc.
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
• PTH—most important hormone in Ca2+
homeostasis
© 2013 Pearson Education, Inc.
Figure 16.12 The parathyroid glands.
Pharynx
(posterior
aspect)
Capillary
Thyroid
gland
Parathyroid
glands
Esophagus
Trachea
© 2013 Pearson Education, Inc.
Parathyroid
cells
(secrete
parathyroid
hormone)
Oxyphil
cells
Parathyroid Hormone
• Functions
– Stimulates osteoclasts to digest bone matrix
and release Ca2+ to blood
– Enhances reabsorption of Ca2+ and secretion
of phosphate by kidneys
– Promotes activation of vitamin D (by kidneys);
increases absorption of Ca2+ by intestinal
mucosa
• Negative feedback control: rising Ca2+ in
blood inhibits PTH release
© 2013 Pearson Education, Inc.
Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.
Hypocalcemia
(low blood Ca2+)
PTH release from
parathyroid gland
Osteoclast activity
in bone causes Ca2+
and PO43- release
into blood
Ca2+ reabsorption
in kidney tubule
Activation of
vitamin D by kidney
Ca2+ absorption
from food in small
intestine
Ca2+ in blood
Initial stimulus
Physiological response
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Result
Homeostatic Imbalances of PTH
• Hyperparathyroidism due to tumor
– Bones soften and deform
– Elevated Ca2+ 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
© 2013 Pearson Education, Inc.
Adrenal (Suprarenal) Glands
• Paired, pyramid-shaped organs atop
kidneys
• Structurally and functionally are two
glands in one
– Adrenal medulla—nervous tissue; part of
sympathetic nervous system
– Adrenal cortex—three layers of glandular
tissue that synthesize and secrete
corticosteroids
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Adrenal Cortex
• Three layers of cortex produce the
different corticosteroids
– Zona glomerulosa—mineralocorticoids
– Zona fasciculata—glucocorticoids
– Zona reticularis—gonadocorticoids
© 2013 Pearson Education, Inc.
Figure 16.14 Microscopic structure of the adrenal gland.
Hormones
secreted
Zona
glomerulosa
Aldosterone
Zona
fasciculata
Cortex
Adrenal gland
• Medulla
• Cortex
Capsule
Cortisol
and
androgens
Kidney
Medulla
Zona
reticularis
Adrenal
medulla
Drawing of the histology of the
adrenal cortex and a portion of
the adrenal medulla
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Epinephrine
and
norepinephrine
Photomicrograph (115x)
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.
Primary regulators
Blood volume
and/or blood
pressure
K+ in blood
Other factors
Stress
Blood pressure
and/or blood
volume
Hypothalamus
Kidney
Heart
CRH
Renin
Direct
stimulating
effect
Initiates
cascade
that
produces
Anterior
pituitary
Atrial natriuretic
peptide (ANP)
ACTH
Angiotensin II
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
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Homeostatic Imbalances of Aldosterone
• Aldosteronism—hypersecretion 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
• Hypersecretion—Cushing's
syndrome/disease
– Depresses cartilage and bone formation
– Inhibits inflammation
– Depresses immune system
– Disrupts cardiovascular, neural, and
gastrointestinal function
• Hyposecretion—Addison'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.
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Same patient with Cushing's
syndrome. The white arrow shows
the characteristic "buffalo hump" of
fat on the upper back.
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
Stress
Nerve impulses
Hypothalamus
CRH (corticotropinreleasing hormone)
Spinal cord
Corticotropic cells
of anterior pituitary
To target in blood
Preganglionic
sympathetic
fibers
Adrenal medulla
(secretes amino acid–
based hormones)
Catecholamines
(epinephrine and
norepinephrine)
Short-term stress response
• Heart rate 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
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ACTH
Mineralocorticoids
Adrenal cortex
(secretes steroid
hormones)
Glucocorticoids
Long-term stress response
• Kidneys retain
• Proteins and fats converted
sodium and water
to glucose or broken down
for energy
• Blood volume and
• Blood glucose increases
blood pressure
• Immune system
rise
supressed
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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Figure 16.18 Photomicrograph of differentially stained pancreatic tissue.
Pancreatic islet
•  (Glucagonproducing)
cells
•  (Insulinproducing)
cells
Pancreatic acinar
cells (exocrine)
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Glucagon
• Major target—liver
• Causes increased blood glucose levels
• Effects
– Glycogenolysis—breakdown of glycogen to
glucose
– Gluconeogenesis—synthesis 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
Tissue cells
Insulin
Stimulates
glycogen
formationw
Pancreas
Glucose
Glycogen
Blood
glucose
falls to
normal
range.
Liver
Stimulus
Blood
glucose level
Stimulus
Blood
glucose level
Blood
glucose
rises to
normal
range.
Pancreas
Glucose
Glycogen
Liver
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Stimulates
glycogen
breakdown
Glucagon
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 O2 transport; depression of nervous
system  coma and death possible
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Diabetes Mellitus: Signs
• Three cardinal signs of DM
– Polyuria—huge urine output
• Glucose acts as osmotic diuretic
– Polydipsia—excessive thirst
• From water loss due to polyuria
– Polyphagia—excessive 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
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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
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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-angiotensinaldosterone mechanism
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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
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Other Hormone-producing Structures
• 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
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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
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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
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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 bonedemineralizing effects of PTH
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