Introduction to the
Endocrine System
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
About this Chapter
Function and purpose of hormones
Classification, structure, and synthesis of hormones
Pathways of nervous to endocrine regulation
Effects of hormone interactions
Pathologies of the endocrine system
Hormone evolution
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Hormones
Chemical messengers secreted into the blood by specialized cells
Processes that fall mostly under hormonal control include:
- Growth and Development,
- Metabolism,
- Regulation of the internal environment (temperature, water
balance, ions),
- Reproduction.
- Hormones act on their target cells in one of three basic ways:
(1) by controlling the rates of enzymatic reactions,
(2) by controlling the transport of ions or molecules across cell
membranes,
or (3) by controlling gene expression and the synthesis of
proteins.
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Anatomy Summary: Hormones
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Anatomy Summary: Hormones
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Anatomy Summary: Hormones
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Anatomy Summary: Hormones
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General Information on Hormones
Chemical Regulating Systems
Hormones
Depend on cell to cell communication molecules
Made in gland(s) or cells
Transported by blood
Distant target tissue receptors
Activates physiological response
Pheromones: organism to organism communication
Hormone Function
Control rates of enzymatic reactions, transport of ions or
molecules across cell membranes, and gene expression and
protein synthesis
Exert effects at very low concentrations
Bind to target cell receptors
Half-life indicates length of activity
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Hormones: Classification
Peptide or protein hormones
Molecular structure includes amino acid chains
Water soluble and lipophobic = bind to membrane cell receptor
short life-time but triggers rapid respondses
Steroid hormones
Molecular structure includes a cholesterol molecule.
Made only in few organs (adrenal gland, gonads, placenta)
Not water soluble, lipophobic
Enters the nucleus, affects transcription= genomic effect
Amine hormones
Small hormone derived from tryptophan and tyrosine
Catecholamines- epinephrine, norepinephrine, and dopamine are
neurohormones that are lipophobic
Thyroid hormones – T3, T4, Thyroxine, are lipophilic and bind
intracellular receptors
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Hormones: Peptides or Proteins
Preprohormone
Large, inactive- before being processed they may have
multiple copies of a peptide hormone
Prohormone
Post-translational modification - inactive
prehormones are cleaved by proteolytic enzymes
Peptide hormone-receptor complex
Signal transduction system -
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Peptide Hormone Synthesis,
Packaging, and Release
1 Messenger RNA on the 2 Enzymes in the 3 The prohormone 4 Secretory vesicles containing 5 The secretory 6 The hormone
ribosomes binds amino ER chop off the passes from the enzymes and prohormone vesicle releases moves into the
acids into a peptide chain signal sequence, ER through the bud off the Golgi. The enzymes its contents by circulation for
called a preprohormone. creating an Golgi complex. chop the prohormone into one exocytosis into transport to its
The chain is directed into inactive or more active peptides plus the extracellular target.
the ER lumen by a signal prohormone. additional peptide fragments. space.
sequence of amino acids.
Golgi complex
Endoplasmic reticulum (ER)
To target
Ribosome
Active hormone
Peptide
Transport fragment
vesicle 3
4 6
Secretory
vesicle 5
Release
Prohormone signal
Capillary
2 endothelium
1
Signal Cytoplasm ECF Plasma
sequence
Preprohormone
mRNA
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Peptide Hormone-Receptor Complex
Membrane receptors and signal
transduction for peptide hormones
Surface receptor
Hormone binds
Enzyme activation
Open channels
Second messenger
systems
Cellular response
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Steroid Hormones: Features
Cholesterol-derived- made only in a few organs,
synthesized as needed, not stored.
Lipophilic and can enter target cell -
Cytoplasmic or nuclear receptors (mostly) – binds
receptors intracellularly
Activate DNA for protein synthesis – receptor-
hormone complexes act as transcription factors.
Slower acting, longer half-life – because of it’s slow
rate of activation they do not mediate reflex
pathways.
Examples-
Cortisol, estrogen, and testosterone
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Steroid Hormones: Structure
Steroid hormones are derived from cholesterol
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Steroid Hormones: Action
1 Most hydrophobic Blood Steroid Cell surface receptor
steroids are bound vessel hormone
to plasma protein
carriers. Only 2a
unbound hormones Rapid responses
can diffuse into the 1
target cell.
2
Protein
2 Steroid hormone carrier Nucleus
receptors are
typically in the Cytoplasmic
cytoplasm or receptor Nuclear
nucleus. receptor
DNA
2a Some steroid
hormones also Interstitial
bind to mem- fluid
brane receptors
that use second 3
Endoplasmic
messenger
systems to reticulum Transcription
Cell
create rapid produces mRNA
cellular membrane 5
responses. 4
New
proteins Translation
3 The receptor-
hormone complex
binds to DNA
and activates or 4 Activated genes create new 5 Translation produces new
mRNA that moves into the proteins for cell processes.
represses one or
more genes. cytoplasm.
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Steroid Hormones: Action
1 Most hydrophobic Blood Steroid Cell surface receptor
steroids are bound vessel hormone
to plasma protein
carriers. Only 2a
unbound hormones Rapid responses
can diffuse into the 1
target cell.
2
Protein
2 Steroid hormone carrier Nucleus
receptors are
typically in the Cytoplasmic
cytoplasm or receptor Nuclear
nucleus. receptor
2a Some steroid
hormones also Interstitial
bind to mem- fluid
brane receptors
that use second
messenger
systems to Cell
create rapid
cellular membrane
responses.
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Steroid Hormones: Action
1 Most hydrophobic Blood Steroid Cell surface receptor
steroids are bound vessel hormone
to plasma protein
carriers. Only 2a
unbound hormones Rapid responses
can diffuse into the 1
target cell.
2
Protein
2 Steroid hormone carrier Nucleus
receptors are
typically in the Cytoplasmic
cytoplasm or receptor Nuclear
nucleus. receptor
DNA
2a Some steroid
hormones also Interstitial
bind to mem- fluid
brane receptors
that use second 3
messenger
systems to Cell Transcription
create rapid produces mRNA
cellular membrane
responses. 4
3 The receptor-
hormone complex
binds to DNA
and activates or 4 Activated genes create new
represses one or mRNA that moves into the
more genes. cytoplasm.
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Steroid Hormones: Action
1 Most hydrophobic Blood Steroid Cell surface receptor
steroids are bound vessel hormone
to plasma protein
carriers. Only 2a
unbound hormones Rapid responses
can diffuse into the 1
target cell.
2
Protein
2 Steroid hormone carrier Nucleus
receptors are
typically in the Cytoplasmic
cytoplasm or receptor Nuclear
nucleus. receptor
DNA
2a Some steroid
hormones also Interstitial
bind to mem- fluid
brane receptors
that use second 3
Endoplasmic
messenger
systems to reticulum Transcription
Cell
create rapid produces mRNA
cellular membrane 5
responses. 4
New
proteins Translation
3 The receptor-
hormone complex
binds to DNA
and activates or 4 Activated genes create new 5 Translation produces new
mRNA that moves into the proteins for cell processes.
represses one or
more genes. cytoplasm.
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Amine Hormones: Features
Derived from one of two
amino acids
Tryptophan – double ring
amino acid
Tyrosine-single ring amino
acid
Ring structure-
Thyroid hormones- bind
intracellular receptors.
Catecholamines-
neurohormones that bind
cell membrane receptors
Epinephrine -
Norepinephrine -
Dopamine -
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Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
A fundamental principle of homeostasis is the importance of reflex
pathways in maintaining the internal environment.
Reflex pathways are a convenient way to classify hormones and simplify
learning the pathways that regulate their secretion.
All reflex pathways have similar components: a stimulus, a sensor, an input
signal, integration of the signal, an output signal, one or more targets, and a
response.
In endocrine and neuroendocrine reflexes, the output signal is a hormone or a
neurohormone. Some hormones have clear stimuli, other hormones have less
obvious stimuli or are secreted continuously, often with a circadian rhythm
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Endocrine Reflex Pathways
Stimulus
Hormones may have multiple stimuli
for their release and endocrine
cells act as the receptor
Afferent signal
input signal
Integration
The cells that make the hormone
must interpret the various signals
and decide how much to produce.
Efferent signal
Out put signal=hormone
Physiological action
Negative feedback
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Simple Endocrine Reflex Pathways
for PTH and Insulin
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Many Endocrine Reflexes Involve the Nervous System
The nervous system and the endocrine system overlap in both structure
and function.
Stimuli integrated by the central nervous system influence the
release of many hormones through efferent neurons (ex. Insulin release).
In addition, specialized groups of neurons secrete neurohormones,
and two endocrine structures are incorporated in the anatomy of the brain:
the pineal gland and the pituitary gland.
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The Pituitary Gland Anatomy
The pituitary gland sits in a protected pocket of bone, connected to the
brain by a thin stalk.
The anterior pituitary is a true endocrine gland that secretes six classic
hormones. Trophic Neurohormones from the hypothalamus control release of
the anterior pituitary hormones. The hypothalamic hormones reach the anterior
pituitary through
Copyright a Education,
© 2007 Pearson specialized region
Inc., publishing ofCummings
as Benjamin the circulation called a portal system.
Figure 7-11
The Pituitary Gland: Two Fused
Posterior
pituitary
produces
1.
Vasopressin
(also called
ADH)
2. Oxytocin
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The Hypothalamic-Hypophyseal Portal System
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The Pituitary Gland: Two Fused
Hormones of the hypothalamic-anterior pituitary pathway
The hormones of the anterior pituitary control so many vital functions that the
pituitary is often called the master gland of the body.
The anterior pituitary
hormones control
metabolism, growth,
and reproduction, all
very complex
processes
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Feedback Loops Are Different in the
Hypothalamic-Pituitary Pathway
The most complex endocrine reflexes because
they involve three integrating centers: the
hypothalamus, the anterior pituitary, and the
endocrine target of the pituitary hormone.
Feedback in these complex pathways follows a
pattern that described previously. Instead of the
response acting as the negative feedback signal,
the hormones themselves are the feedback
signal.
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Endocrine Control
Three levels
Hypothalamic
stimulation—from CNS
Pituitary stimulation—
from hypothalamic trophic
hormones
Endocrine gland
stimulation—from
pituitary trophic hormones
Long-loop feedback
Short-loop feedback
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Hormone Interactions
Synergism
Multiple stimuli—more
than additive
Permissiveness
Need second hormone to
get full expression
Antagonism
Glucagons opposes insulin
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Endocrine Pathologies
Hormone disease is caused by an imbalance due to either excess or deficiency or
abnormal responsiveness
Hypersecretion: excess hormone causes exaggerated effects
Tumors (benign or cancerous) of glandular tissues
Exogenous sources- most sources are medications or supplements, can cause
gland atrophy
Grave’s disease—high secretion of thyroxin-
Hyposecretion: deficient hormone
Most often low levels cause increased trophic hormone levels
Goiter— low secretion of thyroxin
Diabetes—low secretion of insulin
Abnormalities related to hormone response
Target tissues do not respond to the hormone correctly
Downregulation- high hormone levels may result in a decrease of receptors as it
happens in Hyperinsulinemia
Receptor abnormalities- the receptors may not function due to a genetic
mutation as it happens in Testicular feminization syndrome
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Diagnosis of endocrine pathologies may be simple or complicated,
depending on the complexity of the reflex.
Ex: a simple endocrine reflex, parathyroid hormone. If there is too
much or too little hormone, the problem can arise in only one
location: the parathyroid glands.
However, with complex hypothalamic-pituitary- endocrine gland
reflexes, the diagnosis can be much more difficult.
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If a pathology (deficiency or excess) arises in the last endocrine
gland in a reflex, the problem is considered to be a primary
pathology.
Ex: if a tumor in the adrenal cortex begins to produce excessive amounts
of cortisol, the resulting condition is called primary hypersecretion.
If dysfunction occurs in one of the tissues producing trophic
hormones, the problem is a secondary pathology.
Ex: if the pituitary is damaged because of head trauma and ACTH
secretion diminishes, the resulting cortisol deficiency is considered to be
secondary hyposecretion of cortisol.
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Primary and Secondary Pathologies
Primary and
Secondary
hypersecreti
ons are
caused by
abnormalitie
s of different
glands
along the
hormone
release path
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Problem
Graves’ Disease
Ben Crenshaw, a 33-year-old professional golf player had won the Masters Tournament
only a year ago, but now something was not right. He was tired and weak, had been
losing weight, and felt hot all the time. He attributed his symptoms to stress, but his
family thought otherwise. At their urging, he finally saw a physician. The diagnosis?
Graves’ disease, which results in an overactive thyroid gland.
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Shaped like a butterfly, the thyroid gland straddles the trachea just below the
Adam’s apple. Responding to hormonal signals from the hypothalamus and
anterior pituitary, the thyroid gland concentrates iodine, an element found in
food (most notably as an ingredient added to salt), and combines it with the
amino acid tyrosine to make two thyroid hormones, thyroxine and
triiodothyronine. These thyroid hormones perform many important functions
in the body, including the regulation of growth and development, oxygen
consumption, and the maintenance of body temperature.
Q1: a. To which of the three classes of hormones do the thyroid
hormones belong?
b. If a person’s diet is low in iodine, predict what happens to thyroxine
production.
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Thyroid hormone production is regulated by thyroid stimulating hormone (TSH),
a hormone secreted by the anterior pituitary. The production of TSH is in turn
regulated by the neurohormone thyrotropin-releasing hormone (TRH) from the
hypothalamus.
Q2: a. In a normal person, when thyroid hormone levels in the blood
increase, will negative feedback increase or decrease the secretion of
TSH?
b. In a person with a hyperactive gland that is producing too much thyroid
hormone, would you expect the level of TSH to be higher or lower than in
a normal person?
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Ben Crenshaw was diagnosed with Graves’ disease, one form of
hyperthyroidism. The goal of treatment is to reduce thyroid hormone activity,
and Ben’s physician offered him several alternatives. One treatment involves
drugs that prevent the thyroid gland from using iodine. Another treatment is a
single dose of radioactive iodine that destroys the thyroid tissue. A third
treatment is surgical removal of all or part of the thyroid gland. Ben elected
initially to use the thyroid-blocking drug. Several months later he was given
radioactive iodine.
Q3: Why is radioactive iodine (rather than some other radioactive
element, such as cobalt) used to destroy thyroid tissue?
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Graves’ disease is one form of thyroid gland hyperactivity. For this reason,
people with Graves’ disease have elevated thyroxine levels in the blood. Their
TSH levels are very low.
Q4: If levels of TSH are low and thyroxine levels are high, is Graves’
disease a primary disorder or a secondary disorder (one that arises as a
result of a problem with the anterior pituitary or the hypothalamus)?
Explain your answer.
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Researchers have learned that Graves’ disease is an autoimmune disorder in
which the body fails to recognize its own tissue. In this condition, the body
produces antibodies that mimic TSH and bind to the TSH receptor, turning it on.
This false signal “fools” the thyroid gland into overproducing thyroid hormone.
More women than men are diagnosed with Graves’ disease, perhaps because
of the influence of female hormones on thyroid function. Stress and other
environmental factors have also been implicated in hyperthyroidism.
Q5: Antibodies are proteins that bind to the TSH receptor. From that
information, what can you conclude about the cellular location of the TSH
receptor?
Q6: In Graves’ disease, why doesn’t negative feedback shut off thyroid
hormone production before it becomes excessive?
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Dexamethasone is a drug used to suppress the secretion of
adrenocorticotrophic hormone (ACTH) from the anterior
pituitary. Two patients with hypersecretion of cortisol are given
dexamethasone. Patient A’s cortisol secretion falls to normal as
a result, but patient B’s cortisol secretion remains elevated.
Draw maps of the reflex pathways for these two patients and use
the maps to determine which patient has primary
hypercortisolism.
Explain your reasoning.
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The following graph shows plasma TSH concentration in three
groups of subjects. Which pattern would be consistent with the
following pathologies? Explain your reasoning.
(a) primary hypothyroidism
(b) primary hyperthyroidism
(c) secondary hyperthyroidism
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