UNIT 10: INTRODUCTION TO THE

ENDOCRINE SYSTEM
BIOL2410 D01 Lecture Notes
A) Overview
The endocrine system is the second of the two control systems of
the body (the first being the nervous system), and as such has a
widespread impact on the operation of other organ systems. The
endocrine system helps to control body functions and regulate
homeostasis by circulating chemical signals, called hormones,
through the blood that act on target cells in all organs. Much like
in the nervous system, the principles of cell signaling and
communication covered in Unit 3 are critical to the proper
functioning of the endocrine system.
In this unit we will cover a general overview of the structure and
function of the endocrine system and its hormones and in Unit 11
we will look more closely at the action of specific hormones that
help to regulate growth and metabolism.
“EndoRadio” (Sarah Seburn)
A) Overview
1. What is a hormone?
2. Endocrine Glands and Hormones of the Human Body.
3. Classification & Synthesis of Hormones
4. Control of Hormone Secretion
5. Hormone Transport in the Blood
6. Mechanisms of Hormone Action
7. The Hypothalamus and Pituitary Gland
8. Hormone Interactions
9. Endocrine Pathologies

“EndoRadio” (Sarah Seburn)

 Fig. 7.2
B) What is a Hormone?
Ø Hormones are chemical signals that are secreted into the
blood by:
1. Endocrine glands – ductless glands whose only function is to
synthesize and secrete hormones.
Ø E.g.1: the pituitary gland secretes Growth Hormone (among
several other hormones)
Ø E.g.2: the
2. Isolated endocrine cells in other tissues/organs
Ø E.g.1: the Islets of Langerhans in the pancreas secrete insulin
and glucagon to regulate blood sugar
Ø E.g.2: the Leydig cells in the testes secrete testosterone
3. Neurons – secrete neurohormones that circulate in the
blood
Ø E.g.1: neurons in the hypothalamus secrete several different
“releasing hormones”, like Growth Hormone Releasing
Hormone (GHRH) that act on the anterior pituitary gland.
 Fig. 7.2
B) What is a Hormone?
Ø Properties of hormones:
1. More than one hormone can be produced in a single
endocrine gland
Ø E.g.1: the pituitary gland synthesizes and secretes 6 different
hormones.
Ø E.g.2: The pancreatic Islets of Langerhans contain two cell
types (! and " cells). " (beta) cells produce insulin, while
! (alpha) cells produce glucagon.
2. Different tissues can secrete the same hormone.
Ø E.g.1: The hypothalamus and the pancreas secrete
somatostatin (an inhibitory hormone).
3. A single hormone can act on multiple different target cells in
different organs.
Ø E.g.1: epinephrine and norepinephrine released by the
adrenal gland can act on cells in the heart, blood vessels,
airways of the respiratory tract, etc.
 Fig. 1.14b
B) What is a Hormone?
Ø Properties of hormones:
4. Multiple hormones can bind to receptors and produce responses
in a single target cell.
Ø E.g.1: norepinephrine, epinephrine, angiotensin, and vasopressin
can all act on the smooth muscle cells of blood vessels to regulate
blood flow and blood pressure.
Melatonin rhythms
5. Hormone secretion can vary over time and can be affected by
changes in the environment
Ø E.g.1: Circadian rhythms involved in release of cortisol and
melatonin. Cortisol secretion from adrenal gland peaks in the early
morning and decreases at night. Melatonin secretion from the
pineal gland peaks at night and decreases during the day.
6. Hormones have a half life =length of time required to reduce
hormone concentration in the blood by half.
a) Single amino acid derived hormones = minutes
b) Peptide and protein hormones = minutes to hours
Fig. 7.16
c) Steroid hormones = hours
 Fig. 7.2
B) What is a Hormone?
Ø General functions of hormones:
Ø Hormones control:
Ø Metabolism
Ø Reproduction
Ø Growth and development
Ø Water and electrolyte balance
Ø Digestion and absorption of nutrients
Ø Blood cell production and development
Ø Etc.
Ø i.e. hormones regulate homeostasis.

Ø Hormones function by controlling the

1. rates of enzymatic reactions in cells
2. transport of ions or molecules across cell cell membranes
3. gene expression and protein synthesis.
C) Endocrine Glands and Hormones of the Body
Ø You should be able to list KNOW THIS FIGURE!!

the different endocrine

glands of the body, the
hormones they produce,
and the main effects of
those hormones as shown
in Figure 7.2

Fig 7.2
D) Classification & Synthesis of Hormones
Ø Hormones are classified based on their molecular chemical structure:
1. Peptide and Protein Hormones
Ø Hormones made from chains of amino acids
Ø Are mainly hydrophilic (water soluble), so can be transported in the blood dissolved in
the blood plasma. This prevents them from crossing the cell membrane, so they must
bind to cell membrane receptors (GPCRs or tyrosine kinase receptors) on target cells
and trigger signal transduction mechanisms that activate second messengers.
Ø Examples include: insulin, oxytocin, cholecyctoskinin (CCK), growth hormone (GH), etc.
2. Steroid Hormones
Ø Hormones made from modification of cholesterol
Ø Hydrophobic (lipid soluble) so must be transported in the blood bound to a carrier
protein. They can cross cell membranes and mainly have actions on receptors in the
cytoplasm or nucleus that directly trigger the transcription and translation for synthesis
of new proteins. However some have receptors in the cell membrane.
Ø Examples include: estrogen, testosterone, vitamin D3
D) Classification & Synthesis of Hormones
Ø Hormones are classified based on their molecular chemical structure:
3. Amine Hormones
Ø Hormones made from modification of the individual amino acids tyrosine or
tryptophan
Ø Hormones derived from tyrosine:
a) Thyroid Hormones (e.g. Thyroxine/ T4)
Ø control cellular metabolism
Ø Hydrophobic (lipid soluble) – must be transported in the blood bound to a carrier
protein; can cross the cell membrane and bind to receptors in the nucleus to directly
trigger transcription and translation (synthesis of new proteins).
b) Catecholamines (epinephrine and norepinephrine)
Ø Hormones secreted by the adrenal medulla involved in short term stress response (as
part of the fight-or-flight response).
Ø Hydrophilic (water soluble) – transported in the blood dissolved in plasma; bind to cell
membrane receptors and trigger second messenger systems via GPCRs
Ø Hormone derived from tryptophan = melatonin
 D) Classification & Synthesis of Hormones

KNOW THIS TABLE!!

Table 7.1
D) Classification & Synthesis of Hormones
Ø Peptide Hormone Synthesis and Secretion:
Ø Peptide hormones are created from large, inactive
precursor proteins called preprohormones.
Preprohormones contain one or several prohormone
amino acid sequences and a signal sequence that
helps move the protein into the lumen of the
endoplasmic reticulum where posttranslational
modifications will take place.
Ø For example, Prepro TRH (thyrotropin releasing
hormone) consists of a signal sequence, 6 copies of
TRH, and 6 peptide fragments. Cutting off the signal
sequence would form the inactive prohormone form of
TRH (pro-TRH).
D) Classification & Synthesis of Hormones
Ø Peptide Hormone Synthesis and Secretion:
Ø Types of posttranslational modification of
preprohormones:
1. Peptide cleavage (proteolysis) – cutting up the
preprohormone into its component parts.
2. Glycosylation – addition of a carbohydrate
3. Phosphorylation – addition of a phosphate group
4. Sulfation – addition of a sulfate
5. Amidation – addition of an amine group
6. Acetylation – addition of acetyl group from Acetyl
Coenzyme A (an intermediate in carbohydrate
metabolism) Postranslational modification of insulin (similar
to Fig. 7.3d):
7. Subunit aggregation – combining multiple subunit 1. Cleavage of signal sequence from preproinsulin
proteins together to form a larger protein complex and formation of disulfide bonds between the
(quaternary structure) B-chain and A-chain forms proinsulin
2. Cleavage of C-peptide from proinsulin froms
insulin.
D) Classification & Synthesis of Hormones
Ø Peptide Hormone Synthesis and Secretion:
Ø Steps:
1. Translation of mRNA by a ribosome on the
endoplasmic reticulum to form an inactive
preprohormone.
2. Enzymes cut off the signal sequence from the
preprohormone to form an inactive prohormone.
3. The prohormone passes through the ER and Golgi,
and undergoes postranslational modification.
4. The prohormone is packaged into a secretory vesicle
that contains enzymes that cleave the prohormone
into the active peptide hormones. The active
hormone is stored in the vesicles in the cell until the
cell is stimulated to release it.

Fig. 7.3
D) Classification & Synthesis of Hormones
Ø Peptide Hormone Synthesis and Secretion:
Ø Steps:
5. In response to a release signal exocytosis of the
active hormone from the vesicle occurs into the ISF
(interstitial fluid).
6. The hormone crosses the capillary wall (endothelium)
into the blood and is transported to the target cells.

Fig. 7.3
D) Classification & Synthesis of Hormones
Ø Steroid Hormone Synthesis and Secretion:
Ø Steroid hormones are synthesized from cholesterol in the adrenal cortex or gonads (ovaries
and testes). Unlike peptide and catecholamine hormones that can be stored in secretory
vesicles inside the cell, steroid hormones are lipophilic and immediately cross cell
membranes after being made (so they are not stored, but made on demand and then
diffuse out of the cell).

KNOW THIS DIAGRAM!!

§ What enzyme is required for the
production of both cortisol and
aldosterone?
§ What enzyme is required for the
production of Estradiol (i.e. estrogen)?
§ What molecule is a precursor for both
Testosterone and Estradiol?
§ What hormones secreted by the ovary,
testis and adrenal cortex are derived from
cholesterol?

Fig. 7.5
D) Classification & Synthesis of Hormones
Ø Amine Hormone Synthesis and Secretion:
Ø Amine hormones are synthesized from either:
1. Tryptophan
Ø E.g. Melatonin from the pineal gland – helps
to regulate body’s circadian rhythms.
Produced according to the amount of light a
person is exposed to (less light = more
melatonin). Plays a role in sleep-wake cycles.
2. Tyrosine
Ø E.g.1: Catecholamines are derived from a
single tyrosine, and so most behave like
peptide hormones
Fig. 7.6
Ø E.g.2: Thyroid Hormones (T3 and T4) are
derived from 2 tyrosine molecules, and so
behave like steroid hormones.
Fig. 7.5
E) Control of Hormone Secretion
Ø Involves endocrine reflex pathways:
1. Stimulus – change in the internal or external environment
2. Sensor – cells of the endocrine gland
3. Input signal – signal transduction pathway in endocrine cell
4. Integration – biochemical processes within the endocrine
gland
5. Output (efferent) signal = hormone released into blood
6. Target Cells – Hormone interacts with Target cell receptors –
leads to activation of second messenger systems or
activation of genes for transcription and translation.
7. Response – can be within the tissue and systemic = changes
caused by altering cellular activity
8. Negative feedback – Systemic change opposes the original
stimulus and shuts down signaling by the endocrine gland.
Fig. 7.7
E) Control of Hormone Secretion
Ø Involves endocrine reflex pathways:
Ø E.g. regulation of blood calcium levels
1. Stimulus – low blood calcium concentration
2. Sensor – cells of the parathyroid gland
3. Input signal – signal transduction pathways in parathyroid cells
4. Integration – biochemical processes within the parathyroid gland
5. Output (efferent) signal = parathyroid hormone released into
blood
6. Target Cells – Bone and kidney cells.
7. Response –
a) Tissue Response: Bone = increased resorption (bone break down);
kidney increases reabsorption of calcium (less lost in urine) and
increased calcitriol (vitamin D3) production which increases
absorption of calcium from the GI tract (ie. from the foods we eat)
b) Systemic response: increased plasma calcium concentration.
Fig. 7.7
E) Control of Hormone Secretion
Ø Involves endocrine reflex pathways:
Ø E.g. regulation of blood calcium levels
8. Negative feedback – higher plasma calcium levels feed back to
the parathyroid gland and become the new stimulus. Once
calcium levels are high enough, the parathyroid gland will no
longer be stimulated to secrete.

Fig. 7.7
E) Control of Hormone Secretion
Ø Stimuli acting on endocrine gland
may be a:
1. Humoral Stimulus:
Ø Stimulus = concentration of ions or
nutrients in the blood.
Ø E.g.1: increased blood glucose
levels after eating
carbohydrates.
Ø Pancreatic !cells (in the Islets of
Langerhans) detect blood glucose
levels and release insulin which
ultimately decreases blood glucose.
Ø E.g.2: low blood Ca++ levels
(see previous slide)
E) Control of Hormone Secretion
Ø Stimuli acting on endocrine gland
may be a:
2. Neural Stimulus:
Ø In complex neuroendocrine
pathways, the endocrine gland may
be stimulated by an autonomic
postganglionic neuron
Ø E.g.1: release of epinephrine
and norepinephrine from the
medulla of the adrenal gland.
Ø E.g.2: release of insulin from the
pancreas in response to an
autonomic reflex resulting from
activation of stretch receptors in
the digestive tract wall after
eating a meal.
E) Control of Hormone Secretion
Ø Stimuli acting on endocrine gland
may be a:
3. Hormonal Stimulus:
Ø When a hormone released from one
gland triggers the release of a
Note: A hormone that
hormone from another gland.
Ø E.g.1: Corticotropin Releasing
Hormone (CRH) secreted from
the hypothalamus in response
to stress triggers secretion of
Adrenocorticotropic Hormone
(ACTH) from the anterior
pituitary gland, which in turn
triggers the release of Cortisol
from the adrenal gland.
Fig. 7.11
F) Hormone Transport in Blood
Ø Once secreted, hydrophilic (water soluble) hormones, including
all peptide hormones and ~50% of catecholamines, travel in the
blood to target cells dissolved in the blood plasma (think
hydrophilic = loose in the plasma)
Ø Most hydrophobic (lipid soluble) hormones, including thyroid
hormones and steroid hormones, are not able to dissolve in the
plasma, so must be bound to a carrier protein in order to be
transported in the fluid environment of the blood plasma. Being
bound to a carrier protein extends the half-life of the hormone.
Ø Carrier proteins can be general to the hormone being
transported (e.g. albumins) or can be specific to an individual
hormone. Specific carriers include:
1. corticosteroid binding globulin that bind corticosteroids like cortisol. Fig. 7.5b
2. Thyroid binding globulin and transthyretin that bind to thyroid hormone.
3. Sex hormone binding globulin that binds to estradiol and testosterone.
G) Mechanisms of Hormone Action
Ø Hormones act by binding to receptors on target cells.
Ø The exact mechanism of action depends on the type of
receptor that the hormone binds to (membrane receptors,
intracellular receptors, etc.)
Ø Binding of the hormone to a receptor initiates a biochemical
response.
Ø Hormone action must be terminated
Ø the half-life indicates the length of activity
Ø Hormones can be inactivated and excreted through metabolic
processes.
G) Mechanisms of Hormone Action
Ø Peptide Hormone Action (also catecholamines):
1. The hormone binds to a receptor in the cell membrane and
activates signal transduction
Ø E.g.1: A GPCR with cAMP activity
Ø E.g.2: A tyrosine kinase receptor
2. Signal transduction results in activation of second messenger
systems that can cause
a) Phosphorylation of existing enzymes/proteins
b) Ion channel gating
c) Regulation of gene expression
G) Mechanisms of Hormone Action
Ø Steroid Hormone & Thyroid Hormone Action:
1. Carrier proteins release the hormone at at the
cell membrane.
2. Most steroid hormones diffuse into the cell and
bind to cytoplasmic or nuclear receptors.
a) Some steroid hormones bind to cell membrane
receptors that activate second messenger
systems.
3. The receptor hormone complex binds to DNA
and alters gene expression (either by activating
or suppressing gene transcription).
4. Activating genes results in transcription of an
mRNA that will move out of the nucleus,
associate with a ribosome where it will be
translated into a new protein.
G) Mechanisms of Hormone Action
Ø Steroid Hormone & Thyroid Hormone Action:
5. Creation of new proteins in the cells alters cell
activity which will create a tissue response that
leads to a systemic response.
UNIT 10: INTRODUCTION TO THE
ENDOCRINE SYSTEM
BIOL2410 D01 Lecture Notes
G) Mechanisms of Hormone Action
Ø Regulation of Hormone Receptors:
Ø Hormone levels can influence the response of
their target cells by regulating the abundance of
receptors and their affinity for the hormone.
Ø Types of receptor regulation:
1. Up regulation Low receptor density Increased receptor density
Ø A stimulus increases the synthesis of receptors for Weak response Increased sensitivity

a hormone thus increasing the sensitivity of the

target cell to that hormone. Can be triggered by
abnormally or chronically low hormone levels, in
which case the target cell attempts to enhance its
responsiveness to the low levels of hormone.
Ø E.g. Follicle Stimulating Hormone action on
ovarian cells causes them to synthesize more
receptors for Luteinizing Hormone, making the
cells more sensitive to LH. High receptor density Decreased receptor density
Strong response Decreased sensitivity
G) Mechanisms of Hormone Action
Ø Regulation of Hormone Receptors:
Ø Hormone levels can influence the response of
their target cells by regulating the abundance of
receptors and their affinity for the hormone.
Ø Types of receptor regulation:
2. Down regulation Low receptor density Increased receptor density
Ø A stimulus decreases the synthesis of receptors Weak response Increased sensitivity

for a hormone thus decreasing the sensitivity of

the target cell to that hormone. Can be triggered
by abnormally or chronically high hormone levels,
in which case the target cell attempts to diminish
its responsiveness to the excess hormone.
Ø E.g. Hyperinsulinemia – chronically high levels of
insulin reduces the number of insulin receptors in
cell membranes, making the cells less responsive
to insulin (insulin resistance). Can lead to High receptor density Decreased receptor density
Strong response Decreased sensitivity
development of Type 2 diabetes.
H) The Hypothalamus & Pituitary Gland
ØThe hypothalamus and the pituitary interact closely with one another as part of the
hypothalamic-pituitary axis (pathway).

Fig. 7.8
H) The Hypothalamus & Pituitary Gland
ØThe hypothalamus and the pituitary interact closely with one another as part of the
hypothalamic-pituitary axis (pathway).

Fig. 7.8
H) The Hypothalamus & Pituitary Gland
ØEndocrine functions of the Hypothalamus:
Ø As part of the brain, the hypothalamus is composed of nervous
tissue (neurons and supporting glial cells).
Hypothalamic-
hypophysial
portal vessel (in
Ø Some hypothalamic neurons release neurohormones into the Infundibulum)

hypothalamic-hypophysial portal system (vessels connecting two

capillary beds) that connects to the anterior pituitary gland. These
neurohormones are trophic hormones that stimulate the Supraoptic Nucleus

production/release of hormones from the anterior pituitary.

Ø Some neurons from the supraoptic nucleus and paraventricular
Paraventricular
nucleus of the hypothalamus have axons that extend through the nucleus

infundibulum (stalk that connects the hypothalamus to the pituitary

Infundibulum
gland) into the posterior pituitary. The prohormones produced in
the cell bodies of these neurons are packaged into vesicles along
with proteolytic enzymes that will convert the prohormone into the
hormone. The vesicles migrate along the axon (a few mm/day) and
are stored in the axon terminals in the posterior pituitary gland.
H) The Hypothalamus & Pituitary Gland
ØEndocrine functions of the Hypothalamus:
Ø Trophic neurohormones secreted by hypothalamus
that act on the anterior pituitary:
1. Thyrotropin Releasing Hormone (TRH) – stimulates release
of thyroid stimulating hormone (TSH, thyrotropin) from
anterior pituitary.
2. Corticotropin Releasing Hormone (CRH) – stimulates
release of adrenocorticotropic hormone (ACTH) from
anterior pituitary
3. Growth Hormone Releasing Hormone (GHRH) – stimulates
release of growth hormone (GH) from anterior pituitary
4. Somatostatin – Inhibits release of Growth Hormone from
anterior pituitary
5. Gonadotrophin Releasing Hormone (GnRH) – stimulates
release of the gonadotropins, including Follicle Stimulating
Hormone (FSH) and Luteinizing Hormone (LH) from the Fig. 7.9
anterior pituitary.
H) The Hypothalamus & Pituitary Gland
ØEndocrine functions of the Hypothalamus:
Ø Nonapeptide (9 amino acid peptide) neurohormones
synthesized in hypothalamus (but released by
posterior pituitary):
1. Vasopressin
2. Oxytocin

Fig. 7.8
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
1. Separated in two parts:
a) Posterior pituitary
Ø Also known as the neurohypophysis or the pars nervosa
because it is made of neural tissue
Ø Stores and secretes the nonapeptide neurohormones produced
by neurons in the supraoptic and paraventricular nuclei of the
hypothalamus including:
i. Vasopressin (also known as antidiuretic hormone or ADH)
Ø Main functions include water homeostasis
ii. Oxytocin
Ø Main functions include uterine contractions during childbirth
(parturition) and milk ejection reflex (after birth)
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
1. Separated in two parts:
b) Anterior pituitary
Ø Also known as the adenohypophysis (prefix “adeno-” means
”gland”) or the pars distalis
Ø Secretes hormones that control growth, metabolism and
reproduction
Ø Trophic hormones secreted by the hypothalamus stimulate
the secretion of anterior pituitary hormones which include:
i. Follicle Stimulating Homone (FSH) Mnemonic for
remembering Anterior
ii. Leuteinizing Hormone (LH) Pituitary Hormones =
iii. Adrenocorticotropic Hormone (ACTH) FLAT PEG
iv. Thyroid Stimulating Hormone (TSH; thyrotropin)
v. Prolactin (PRL)
vi. Endorphin
vii. Growth Hormone (GH)
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
Note: Under normal
2. Hormones of the posterior pituitary (pars nervosa): conditions; signals
from baroreceptors
a) Vasopressin (ADH) tonically inhibit
vasopressin release.
Ø Stimulus for release: hypovolemia (low blood volume), hypernatremia
(high Na+ in blood); low blood pressure
i. Reduced plasma volume or increased Na+ intake à increases plasma
osmolality à increases osmoreceptor activity in vasopressin secreting
neurons of the hypothalamus à increases vasopressin release
ii. Reduced plasma volume à decreases arterial blood pressure à
decreases baroreceptor (pressure receptor) signaling à increases
vasopressin release.
Ø Target cells = cells of kidney tubules and vascular smooth muscle cells
Ø Receptors are all GPCRs:
Ø In kidney, activates GPCR phospholipase C signal transduction pathway
Ø In vascular smooth muscle activates a GPCR-adenylate cyclase-cAMP
signal transduction pathway.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
Note: Under normal
2. Hormones of the posterior pituitary (pars nervosa): conditions; signals
from baroreceptors
a) Vasopressin (ADH) tonically inhibit
vasopressin release.
Ø Main actions:
i. Increased water reabsorption in kidneys tubules/nephrons (brings
osmolality and pressure back into homeostatic range). Decreases the
volume of urine production and conserves water in the body.
ii. At high levels it causes vascular smooth muscle to contract
(vasoconstriction) which increases blood pressure.
Ø Vasopressin release is inhibited by alcohol consumption, which leads to
increased urine loss and dehydration.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
2. Hormones of the posterior pituitary (pars nervosa):
b) Oxytocin
Ø Stimulus for release::
i. Distension of birth canal (head of baby pressing on cervix of uterus)
ii. Infant suckling on nipple of breast
iii. Social bonding and positive physical contact (free hugs! J). For this
reason oxytocin is sometimes referred to as the “love” hormone.
Ø Target cells:
i. smooth muscle of uterus
ii. myoepithelial (smooth muscle) cells that surround secretory portions
of mammary glands
iii. neurons in hippocampus and amygdala of brain (areas involved in
social behaviour).
Ø Receptors are all GPCRs that activate different signal transduction
pathways depending on receptor location.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
2. Hormones of the posterior pituitary (pars nervosa):
b) Oxytocin
Ø Main actions:
i. Contractions of uterus that lead to child birth (parturition). See flow
chart for process.
ii. Milk ejection reflex – oxytocin causes myoepithelial cells to squeeze
the secretory cells in the mammary glands causing milk to move into
the ducts that lead to the nipple.
iii. Social behaviours – pair bonding (monogamy), social learning, ability
to recognize emotions correctly in other people, etc.
Ø Some studies have shown that an oxytocin nasal spray can help
improve certain markers of social behaviour in children with autism
spectrum conditions.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
KNOW THIS
DIAGRAM!
- Be able to
name the
hypothalamic
releasing
hormones, the
hormones of
the anterior
pituitary, their
endocrine and
non-endocrine
targets, and
their main
effects.

Fig. 7.9
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
Ø 3 groups/families based on related structure:
a) Growth Hormones family
Ø Single polypeptides of 191 (GH) to 199 (PRL) amino acids, folded into
globular form by disulfide bonds.
i. Growth Hormone (GH) –
Ø Secretion is stimulated by GHRH and inhibited by somatostatin
(also known as Growth Hormone Inhibiting Hormone, GHIH) from
the hypothalamus
Ø Target cells include liver cells and cells of many tissues
Ø Main effects in liver: acts as a trophic hormone that stimulates the
release of IGFs (Insulin-like Growth Factors) that are released into
the blood (hormone)
Ø Main effects of GH and IGFs in all other tissues like bone, muscle,
etc. is growth and increased metabolism.

Fig. 7.10
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
Ø 3 groups/families based on related structure:
a) Growth Hormones family
Ø Single polypeptides of 191 (GH) to 199 (PRL) amino acids, folded into
globular form by disulfide bonds.
i. Prolactin (PRL) –
Ø Secretion is tonically inhibited by dopamine (also known as
Prolactin Inhibitory Hormone, PIH) from the hypothalamus. PRL
secretion therefore begins when dopamine secretion is inhibited.
Ø Main actions: influences development of mammary glands and
milk production in biologically female individuals (XX), while it
influences testosterone production and spermatogenesis in
biologically male individuals (XY).

Fig. 26.17
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
Ø 3 groups/families based on related structure:
b) Glycoprotein family:
Ø Have a large percentage of carbohydrates in their structure
Ø All composed of two protein subunits: ! and ". ! subunit has the
same amino acid sequence for all, but " subunit differs
Ø Includes the gonadotropins whose secretion is stimulated by GnRH
from the hypothalamus :
i. Follicle Stimulating Hormone (FSH) – stimulates follicle cells that
help to support gametogenesis (production of eggs and sperm) in
both biological sexes.
Ø In biologically female (XX) individuals – stimulates development
of granulosa cells of follicles in ovary that support oogenesis
and causes them to produce estrogen (in the form of estradiol). Fig. 26.6
Ø In biologically make (XY) individuals – stimulates and maintains
spermatogenesis.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
Ø 3 groups/families based on related structure:
b) Glycoprotein family:
Ø Have a large percentage of carbohydrates in their structure
Ø All composed of two protein subunits: ! and ". ! subunit has the
same amino acid sequence for all, but " subunit differs
Ø Includes the gonadotropins whose secretion is stimulated by GnRH
from the hypothalamus :
ii. Luteinizing Hormone (LH) –
Ø In biologically female (XX) individuals – stimulates release of
estrogen from ovaries, high levels stimulate ovulation, and also
stimulates production of progesterone from left over follicle after
ovulation.
Ø In biologically make (XY) individuals – stimulates testosterone Fig. 26.6
release from Leydig cells of the testes.
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis):
3. Hormones of the anterior pituitary (pars distalis):
Ø 3 groups/families based on related structure:
b) Glycoprotein family:
Ø Also includes
iii. Thyroid Stimulating Hormone (TSH; thyrotropin) –
Ø Stimulus for secretion is Thyrotropin Releasing
Hormone (TRH) from hypothalamus
Ø Main action is to stimulate thyroid gland to
synthesize and secrete the thyroid hormones (T3
= triiodothyronine and T4 = thyroxine).

Fig. 23.5
H) The Hypothalamus & Pituitary Gland
ØThe pituitary gland (also called the hypophysis): Fig. 23.2

3. Hormones of the anterior pituitary (pars distalis):

Ø 3 groups/families based on related structure:
c) Proopiomelanocortin (POMC) family:
Ø A collection of peptide hormones all derived from the
polypeptide precursor proopiomelanocortin (POMC)
i. Adrenocorticotropic Hormone (ACTH) – stimulates release
of cortisol from the cortex of the adrenal gland.
ii. Melanocyte Stimulating Hormone (MSH) – acts on
melanocytes in the skin and stimulates them to produce
melanin (a pigment protein); also acts on hypothalamus to
suppress appetite and plays a role in the immune response
iii. Endorphins – “endogenous morphine”; these are naturally
occurring opioids that modulate responses to pain and
stress in the body
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
1. Long loop negative feedback:
Ø Peripheral endocrine gland (e.g. adrenal gland, thyroid gland, etc) produces
a hormone that suppresses secretion of anterior pituitary and hypothalamic
trophic hormones.
Ø This is the most dominant feedback mechanism

Fig. 7.11
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
1. Long loop negative feedback:
Ø Peripheral endocrine gland (e.g. adrenal gland, thyroid gland, etc) produces
a hormone that suppresses secretion of anterior pituitary and hypothalamic
trophic hormones.
Ø This is the most dominant feedback mechanism
Ø E.g.1: cortisol secreted by the adrenal cortex feeds back to decrease
secretion of CRH from the hypothalamus and ACTH from the pituitary
(effectively decreasing its own production – prevents hypersecretion of
cortisol). Fig. 7.11
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
1. Long loop negative feedback:
Ø E.g.2: thyroid hormones from the thyroid gland feed back to decrease the
release of TRH from the hypothalamus and TSH from the anterior pituitary
(effectively decreasing secretion of T3 and T4 themselves, which helps to
avoid hypersecretion).

Fig. 23.5
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
2. Short-loop negative feedback
Ø The hormone secreted by the pituitary acts on the hypothalamus to
reduce or inhibit production of the associated hypothalamic trophic
hormone.
Ø Secondary feedback mechanism

Fig. 7.11
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
2. Short-loop negative feedback
Ø The hormone secreted by the pituitary acts on the hypothalamus to
reduce or inhibit production of the associated hypothalamic trophic
hormone.
Ø Secondary feedback mechanism
Ø E.g.1: ACTH from the anterior pituitary acts on the hypothalamus to inhibit
production and secretion of CRH
Ø E.g.2: Growth Hormone from anterior pituitary decreases/inhibits release of
Fig. 7.11
GHRH from hypothalamus.
H) The Hypothalamus & Pituitary Gland
ØFeedback loops in Hypothalamic-Pituitary Pathways:
Ø In most feedback loops, the response of the affected tissue acts as
the feedback. In the hypothalamic-pituitary pathway the hormones
themselves act as the feedback (and the output signal). This is
because there are often multiple target tissues producing multiple
responses so there is no one response signal to monitor
Ø 3 types of feedback:
3. Ultra Short-loop negative feedback
Ø Occurs within the hypothalamus or pituitary
Ø Autocrine or paracrine signals from within the hypothalamus or
pituitary themselves reduce/inhibit the secretion of the hormones
they produce.
Ø Not well understood.
Ø E.g.1: TSH secreted in the pituitary can act in an autocrine/paracrine
manner to reduce production/secretion of TSH Fig. 7.11
 Permissiveness

I) Hormone Interactions
ØHormones can interact with one another to increase or
decrease the response of a target cell.
Ø3 types of hormone interactions:
Synergism

Antagonism
 Permissiveness

I) Hormone Interactions
ØHormones can interact with one another to increase or
decrease the response of a target cell.
Ø3 types of hormone interactions:
1. Permissiveness
Synergism

Ø One or more hormones permit or enhance the action of another

hormone at the target cell.
Ø Example: Permissive effect of Thyroid Hormones on Epinephrine
during lipolysis (breakdown of triglycerides into fatty acids and
monoglycerides)
Ø Epinephrine (Hormone A) weakly stimulates lipolysis Antagonism
Ø In the presence of thyroid hormones T3 and T4 (the permissive
hormones) the same amount of epinephrine strongly stimulates
lipolysis.
Ø How? T3 and T4 up regulate epinephrine receptors on the target
cells, increasing sensitivity that results in a stronger response
 Permissiveness

I) Hormone Interactions
ØHormones can interact with one another to increase or
decrease the response of a target cell.
Ø3 types of hormone interactions:
2. Synergism
Synergism

Ø The combined effect of the action of 2 or more hormones on a

target cell is greater than the sum of their individual action on the
target cell.
Ø Example: The synergism of glucagon and epinephrine and cortisol
to raise blood glucose levels.
Ø Glucagon and epinephrine and cortisol all increase blood Antagonism
glucose levels on their own, but all together blood glucose can
increase even further than the sum of three individual effects.
Ø How? Amplification of intracellular effects of second messenger
systems (glucagon + epinephrine) combined with synthesis of
new proteins (cortisol) increases the response..
I) Hormone Interactions
ØHormones can interact with one another to increase or
decrease the response of a target cell.
Ø3 types of hormone interactions:
2. Synergism
Ø The combined effect of the action of 2 or more hormones on a
target cell is greater than the sum of their individual action on the
target cell.
Ø Example: The synergism of glucagon and epinephrine and cortisol
to raise blood glucose levels.
Ø Glucagon and epinephrine and cortisol all increase blood Fig. 7.12
glucose levels on their own, but all together blood glucose can
increase even further than the sum of three individual effects.
Ø How? Amplification of intracellular effects of second messenger
systems (glucagon + epinephrine) combined with synthesis of
22 mg is more than the additive
new proteins (cortisol) increases the response. effective of the two hormones (15
mg/100 mL blood)
 Permissiveness

I) Hormone Interactions
ØHormones can interact with one another to increase or
decrease the response of a target cell.
Ø3 types of hormone interactions:
3. Antagonism
Synergism

Ø The actions of one hormone reduce the effectiveness or

oppose the action of another hormone on the target cell –
can be direct or indirect.
Ø Competitive inhibition – Antagonist binds to the same
target cell receptor without activating it.
Ø Functional antagonists – have opposing physiological Antagonism
actions (e.g. insulin and glucagon).
Ø Example: Effects of insulin and glucagon.
Ø Insulin (Hormone X) decreases plasma glucose levels by
increasing uptake and use by cells, while glucagon (Hormone Y)
increases plasma glucose levels by promoting glycogenolysis
(break down of glycogen stored in cells) and release of glucose
J) Endocrine Dysfunction & Pathologies
1. Hypersecretion = excess hormone
Ø Primary pathology (hypersecretion) = problem
with last endocrine gland in a complex pathway
(e.g. for hypersecretion of cortisol it would be the
adrenal gland that actually produces/ secretes the
hormone in question)
Ø Secondary pathology (hypersecretion) = problem
with the pituitary gland
Ø Tertiary pathology (hypersecretion) = problem
with the hypothalamus (rare)
Ø Usually caused by a benign tumor (adenoma) or KNOW THIS DIAGRAM!
exogenous treatment (i.e. injections of hormone) What are the signs of a
primary, secondary, or
Ø Normally treated by administering a drug that tertiary hypersecretion?
inhibits production/secretion
Fig.7.14
Ø Example: Hypercortisolism
J) Endocrine Dysfunction & Pathologies Fig.7.15

2. Hyposecretion = deficient hormone

Ø Can also be Primary or secondary
↑ ↑/normal
Ø Usually caused by atrophy of the endocrine
Short Loop
gland that produces the hormone Negative
Feedback
ØNormally treated though hormone ↓ ↑
replacement therapy
ØE.g. a treatment for Type 1 Diabetes in which the
pancreas does not produce insulin, is insulin ↓ ↓
injections.
ØExample: Hypocortisolism

KNOW THIS DIAGRAM! No negative feedback by

What are the signs of a No negative feedback cortisol increases CRH and
primary, secondary, or because ACTH and ACTH release, but short loop
tertiary hypersecretion? Cortisol are low feedback is intact and keeps
CRH within normal range
J) Endocrine Dysfunction & Pathologies
3. Abnormal Receptors/Response
ØTarget cell may lack the necessary receptors (e.g. due to
down regulation) to bring about the proper response.
ØE.g. hyperinsulinemia
ØTarget cell receptors may have mutations that prevent
hormone from binding.
ØE.g. Androgen insensitivity syndrome – mutation in gene
for androgen receptors in the biologically make fetus that
renders them nonfunctional.
ØTarget cell may lack the biochemical machinery for
proper signal transduction in cell.
ØE.g. pseudohypoparathyroidism – involves mutation that
leads to defective G-protein
ØTarget cell responsiveness is also altered naturally