Endocrine System

TUCOM-3rd ENDOCRINE SYSTEM Dr.
Zainab Samir Yahya
Introduction:
For the body to function properly, its various parts and organs must communicate
with each other to ensure that a constant internal environment (i.e., homeostasis) is
maintained. For example, neither the body temperature nor the levels of salts and
minerals (i.e., electrolytes) in the blood must fluctuate beyond preset limits.
Communication among various regions of the body also is essential for enabling the
organism to respond appropriately to any changes in the internal and external
environments. Two systems help ensure communication: the nervous system and the
hormonal (i.e., neuroendocrine) system. The nervous system generally allows rapid
transmission (i.e., within fractions of seconds) of information between different body
regions. Conversely, hormonal communication, which relies on the production and
release of hormones from various glands and on the transport of those hormones via the
bloodstream, is better suited for situations that require more widespread and longer
lasting regulatory actions. Thus, the two communication systems complement each
other. In addition, both systems interact:
Stimuli from the nervous system can influence the release of certain hormones and
vice versa.
Both systems rely on the release of chemicals that bind to specific receptors on their
target cells
They share many chemical messengers
 Called neurotransmitters in the nervous system
 Called hormones in the endocrine system
Both regulated primarily by negative feedback mechanisms
Common goal of both is to preserve homeostasis by coordinating and regulating
other cells, tissues, organs, and systems.
TUCOM-3rd ENDOCRINE SYSTEM Dr.Zainab Samir Yahya
Hormone: organic compound produced in animal bodies to regulate activity and

behavior /transported in tissue fluids such as blood or sap to stimulate specific cells or
tissues into action.
Endocrine gland: any of various glands, as the thyroid, adrenal, and pituitary glands,
that secretes hormones directly into the circulatory system.
Endocrine Tissue: found in organs that have other functions in addition to hormone
production.
Target cells: cells that have receptors for a particular hormone
Mechanisms of Intercellular Communication

Direct communication
- Transmission through gap junctions
- Ions, small solutes, lipid-soluble materials
- Distribution of effects is limited to adjacent cells of the same type that are
interconnected by connexons (proteins tunnels).
Paracrine communication
- Transmission through extracellular fluid
- Chemicals signals are Paracrines
- Distribution of effects is primarily limited to the local area (para=near)
where paracrine concentrations are relatively high; target cells must have
appropriate receptors.
Autocrine communication
- Through extracellular fluid as well
- Chemical signals are Autocrines
- Limited to same cell that secrets the chemical signal
Endocrine communication
- Transmission through the bloodstream
- Chemical Signals are hormones
- Target cells are mainly in other distant tissues and organs and must have
appropriate receptors.
Synaptic communication
- Transmission across synapses
- Chemical signals are neurotransmitters
- Effects are limited to very specific area; target cells must have appropriate
receptors.
Classification of hormones
Hormones can be classified according to their chemical nature, mechanism of action,
nature of action, their effects, and stimulation of Endocrine glands.
1. Classification by chemical nature of hormones
Hormones Source Example

Derived from cholesterol which
belong to a sex hormones, adrenal
Steroid hormones
chemical compounds known as cortex hormones
steroids
Hormones derived from the An example of a hormone
modification of amino acids are derived from tryptophan is
referred to as amine hormones. melatonin, while tyrosine
Amine hormones
Amine hormones are synthesized derivatives include thyroid
from the amino acids tryptophan hormones and
or tyrosine. catecholamines
These hormones are made up of
only few amino acid residues and
Peptide hormones they are usually present Oxytocin and vasopressin
themselves in form of a linear
chains
These hormones are build up from
large number of amino acid Insulin, glucagon,
Protein hormones
residues somatotropins
These are conjugated protein luteinizing hormones,

Glycoprotein bound to carbohydrate which follicle stimulating
hormones include galactose, mannose, hormones, thyroid
fructose stimulating hormones
Made up of small fatty acid
Eicosanoid hormones derivatives with a variety of Prostaglandins
arachidonic acid
2. Classification by, mechanism of action

a) Group I hormones
These are group of lipophilic hormones that are usually derived from cholesterol (except
T3 and T4). These hormones usually bind to intracellular receptors thereby forming
hormone-receptor complex. They are mostly found in general circulation in association
with transport proteins however they have relatively longer half-lives in hours or days.
Examples of these hormones are T3, T4, estrogen, progesterone and testosterone.
b) Group II hormones
These are hormones that bind to cell surface (plasma membrane) receptor before they
stimulate the release of certain molecules known as second messenger which will then
perform the biochemical function of these hormones. These hormones are transported in
free form and they usually possess short half-lives in minutes. Group II are further
subdivided into 3 categories based on the chemical nature of the second messenger:
i. Secondary messenger is cAMP: eg. Adrenocorticotropic hormone, FSH, LH,

PTH,ADH, calcitonin, glucagon
ii. Secondary messenger is cGMP: Atrial natriuretic peptide (ANP).
iii. Secondary messenger is phosphotidylinocitol/calcium or both:
Some hormones activate transmembrane receptors that activate the

enzyme phospholipase C attached to the inside projections of the receptors
(Table-1). This enzyme catalyzes the breakdown of some phospholipids in the
cell membrane, especially phosphatidylinositol bi- phosphate (PIP2), into two
different second messenger products: inositol triphosphate (IP3)
and diacylglycerol (DAG). The IP3mobilizes calcium ions from mitochondria
and the endoplasmic reticulum, and the calcium ions then have their own
second messenger effects, such as smooth muscle contraction and changes in
cell secretion.
Table-1: Hormones That Use the Phospholipase C Second Messenger System
Angiotensin II (vascular smooth muscle)

Catecholamines (α receptors)
Gonadotropin-releasing hormone (GnRH)
Growth hormone–releasing hormone (GHRH)
Oxytocin
Thyrotropin releasing hormone (TRH)
Vasopressin (V1 receptor, vascular smooth muscle)
DAG, the other lipid second messenger, activates the enzyme protein kinase C (PKC),
which then phosphorylates a large number of proteins, leading to the cell‘s response
(Figure). In addition to these effects, the lipid portion of DAG is arachidonic acid, which
is the precursor for the prostaglandins and other local hormones that cause multiple
effects in tissues throughout the body.
Another second messenger system operates in response to the entry of calcium into the
cells. Calcium entry may be initiated by changes in membrane potential that open
calcium channels or a hormone interacting with membrane receptors that open calcium
channels. On entering a cell, calcium ions bind with the protein calmodulin. This protein
has four calcium sites, and when three or four of these sites have bound with calcium,
the calmodulin changes its shape and initiates multiple effects inside the cell, including
activation or inhibition of protein kinases. Activation of calmodulin-dependent protein
kinases causes, via phosphorylation, activation or inhibition of proteins involved in the
cell‘s response to the hormone. For example, one specific function of calmodulin is to
activate myosin light chain kinase, which acts directly on the myosin of smooth muscle
to cause smooth muscle contraction.
3. Nature of hormones action

a. Local hormones—Paracrine, autocrine and synaptic are three types of local
hormone signaling. In paracrine signaling, hormones are released into the fluid
between cells (the interstitial fluid) and diffuse to nearby target cells. Hormones that
influence secretions or other processes on the same cells that released them are said
to be autocrine signalers. The more specialized synaptic signaling occurs between
neurons (the nerve cells that make up the nervous system) and between neurons and
muscle cells, allowing nerve cells to talk to each other and to muscles., for example,
hormone testosterone.
b. General hormones: Hormones released into the bloodstream from endocrine gland
cells and special cells in the hypothalamus (neurosecretory cells) travel throughout
the body looking for target cells. These hormones are similar to a television signal
in that they are broadcast everywhere but can only be picked up and read by a cell
with the right hormone receptor or antenna. These are hormones transported
through circulation to the distal target tissue/organ examples are thyroid hormones
and insulin.
c. Specific hormones: these hormones affect functions of specific organ e.g. FSH and
androgen.
4. Effect of hormones
a. Kinetic hormones—These hormones may cause muscle contraction, pigment
migration, glandular secretion and others, example of these hormones is
epinephrine
b. Metabolic hormones—These are hormones that mainly caused changes in the rate
of metabolism and balance the reaction examples include insulin, glucagon,
parathyroid hormones.
c. Morphogenetic hormones—These are hormones that mainly involved in growth
and differentiation in the body, examples are Follicle stimulation hormones,
luitenizing hormones and thyroid hormones.
5. Stimulation of Endocrine glands
a. Tropic hormones—These are hormones that stimulate other endocrine gland for
secretion examples are TSH which stimulate secretion of thyroid gland for the
production of thyroid hormones
b. Nontropic hormone—These are hormones that usually exert their effect on non-
endocrine target tissues examples of these hormone are Thyroid hormone which
increases the rate of oxygen consumption and metabolic activity of different cells in
the body.
Five major functions of hormones

1. Regulate metabolic processes (e.g. thyroid hormones).
2. Control the rate of chemical reactions (e.g. growth hormone).
3. Aid in the transport of substances across the cell membrane of target cells (e.g.
insulin and glucagon).
4. Regulate water and electrolyte balances (e.g. antidiurectic hormone, calcitonin, and
aldosterone).
5. Play a vital role in reproduction, growth and development (e.g. estrogens ,
progesterone, and testosterone)
Hormone Action
1. Most hormones adhere to the following action plan :
 endocrine gland synthesizes the hormone .
 Hormone diffuses into capillaries .
 Hormone is transported by blood or lymph toward target cells .
 Hormone diffuses out of capillaries at target tissue, and causes an effect in target
cells .
2. Each step of this action plan is highly specific and carefully controlled by the endocrine
and circulatory systems :
synthesis of hormone using protein or lipid anabolism.
secretion of hormone using exocytosis or diffusion .
transport of hormone in the blood or lymph (i.e. steroid hormones require a
―protein transporter‖ during the transport).
interaction between the hormone and target cell (i.e. protein hormones require
receptors at the cell membrane of target cells).
3. Effects in the target cells caused by hormone action
 A change in cell membrane permeability (e.g. insulin causes muscle cells to have
a higher permeability for glucose).
 A change in chemical reaction rate (e.g. growth hormone stimulates higher
chemical reaction rates in muscle and bone cells).
 Enzyme activation (e.g. epinephrine increases enzyme action in muscle cells).
 Activation of cell secretion (e.g. melanocytestimulating hormone activates more
melanin secretion from the melanocytes).
Actions of steroid hormones

1. Steroid hormones bind to a protein transporter during the transport in blood of
lymph .
2. When they have arrived at the target cells , the protein transporter (being fat-
insoluble) is repelled by the cell membrane, while the steroid hormone (being
fat-soluble) diffuses into the cytoplasm of target cell.
3. Steroid hormone also diffuses across the nuclear envelope and enters into the
nucleus of target cell.
4. Steroid hormone binds to a specific receptor located on a particular gene of
target cell‘s DNA.
5. This binding alters the genetic information within that gene, resulting in a new
messenger RNA (mRNA) being produced after transcription.
6. this new mRNA will be translated into a new protein (or enzyme) in the
cytoplasm of target cell .
7. the new protein or enzyme causes a specific effect to occur within the target
cells .
Action of protein hormones
1- A protein hormone is transported in the blood or lymph by itself, without a transporter .

2- When it has arrived at the target cell, the protein hormone binds with a specific
receptor embedded in the cell membrane of target cell. (The number of receptors
changes in response to the amount of hormone released -- ―up-regulation‖ refers to the
phenomenon where more receptors will be produced to respond to a deficiency of the
hormone; while ―down-regulation‖ refers to the process of producing less receptors to
respond to a large amount of hormone).
3- This binding activates a series of chemical reactions (―cascade reactions‖) in the
cytoplasm of target cell .
4- The product of these reactions is a substance known as the ―secondary messenger‖
(usually cyclic adenosine monophosphate or cAMP), which acts on behalf of the
protein hormone , causes a potent effect in the target cell (usually within the
cytoplasm).
5- Since protein hormones never diffuse to the DNA of target cells, no new proteins or
enzymes are made at the end .
Polypeptide and Protein Hormones Are Stored in

Secretory Vesicles Until Needed
Most of the hormones in the body are polypeptides and proteins. These hormones
range in size from small peptides with as few as 3 amino acids (thyrotropin-releasing
hormone) to proteins with almost 200 amino acids (growth hormone and prolactin). In
general, polypeptides with 100 or more amino acids are called proteins, and those with
fewer than 100 amino acids are referred to as peptides. Protein and peptide hormones
are synthesized on the rough end of the endoplasmic reticulum of the different endocrine
cells, in the same fashion as most other proteins (Figure). They are usually synthesized
first as larger proteins that are not biologically active (preprohormones) and are
cleaved to form smaller prohormones in the endoplasmic reticulum.
These are then transferred to the Golgi apparatus for packaging into secretory
vesicles. In this process, enzymes in the vesicles cleave the prohormones to produce
smaller, biologically active hormones and inactive fragments. The vesicles are stored
within the cytoplasm, and many are bound to the cell membrane until their secretion is
needed. Secretion of the hormones (as well as the inactive fragments) occurs when the
secretory vesicles fuse with the cell membrane and the granular contents are extruded
into the interstitial fluid or directly into the blood stream by exocytosis. Synthesis and
secretion of peptide hormones. The stimulus for hormone secretion often involves
changes in intracellular calcium or changes in cyclic adenosine monophosphate (cAMP)
in the cell.
In many cases, the stimulus for exocytosis is an increase in cytosolic calcium

concentration caused by depolarization of the plasma membrane. In other instances,
stimulation of an endocrine cell surface receptor causes increased cyclic adenosine
monophosphate (cAMP) and subsequently activation of protein kinases that initiate
secretion of the hormone. The peptide hormones are water soluble, allowing them to
enter the circulatory system easily, where they are carried to their target tissues.
Amine Hormones Are Derived from Tyrosine
The two groups of hormones derived from tyrosine, the thyroid and the adrenal
medullary hormones, are formed by the actions of enzymes in the cytoplasmic
compartments of the glandular cells. The thyroid hormones are synthesized and stored in
the thyroid gland and incorporated into macromolecules of the
protein thyroglobulin, which is stored in large follicles within the thyroid gland.
Hormone secretion occurs when the amines are split from thyroglobulin, and the free
hormones are then released into the blood stream. After entering the blood, most of the
thyroid hormones combine with plasma proteins, especially thyroxine-binding
globulin, which slowly releases the hormones to the target tissues.
Epinephrine and norepinephrine are formed in the adrenal medulla, which normally
secretes about four times more epinephrine than norepinephrine. Catecholamines are
taken up into preformed vesicles and stored until secreted. Similar to the protein
hormones stored in secretory granules, catecholamines are also released from adrenal
medullary cells by exocytosis. Once the catecholamines enter the circulation, they can
exist in the plasma in free form or in conjugation with other substances.
Transport of Hormones in the Blood
Water-soluble hormones (peptides and catecholamines) are dissolved in the plasma

and transported from their sites of synthesis to target tissues, where they diffuse out of
the capillaries, into the interstitial fluid, and ultimately to target cells.
Steroid and thyroid hormones, in contrast, circulate in the blood mainly bound to
plasma proteins. Usually less than 10 percent of steroid or thyroid hormones in the
plasma exist free in solution. For example, more than 99 percent of the thyroxine in the
blood is bound to plasma proteins. However, protein-bound hormones cannot easily
diffuse across the capillaries and gain access to their target cells and are therefore
biologically inactive until they dissociate from plasma proteins.
The relatively large amounts of hormones bound to proteins serve as reservoirs,

replenishing the concentration of free hormones when they are bound to target receptors
or lost from the circulation. Binding of hormones to plasma proteins greatly slows their
clearance from the plasma.
Onset of Hormone Secretion After a Stimulus,and Duration

of Action of Different Hormones
Some hormones, such as norepinephrine and epinephrine, are secreted within seconds
after the gland is stimulated, and they may develop full action within another few
seconds to minutes; the actions of other hormones, such as thyroxine or growth
hormone, may require months for full effect. Thus, each of the different hormones has
its own characteristic onset and duration of action—each tailored to perform its specific
control function.
Feedback Control of Hormone Secretion

Feedback circuits are at the root of most control mechanisms in physiology, and are
particularly prominent in the endocrine system. Hormone secretions in our body are
regulated by 2 feedback mechanisms to maintain their homeostasis in the blood: positive
and negative. A feedback loop mechanism is the one in which the secreted end product
itself controls its own production. Instances of positive feedback certainly occur, but
negative feedback is much more common. Negative feedback is seen when the output of
a pathway inhibits inputs to the pathway. The heating system in your home is a simple
negative feedback circuit. When the furnace produces enough heat to elevate
temperature above the set point of the thermostat, the thermostat is triggered and shuts
off the furnace (heat is feeding back negatively on the source of heat). When
temperature drops back below the set point, negative feedback is gone, and the furnace
comes back on. Feedback loops are used extensively to regulate secretion of hormones
in the hypothalamic-pituitary axis.
An important example of a negative feedback loop is seen in control of thyroid hormone

secretion[hypothalamic-pituitary-thyroidal (HPT) axis. The thyroid hormones
thyroxine and triiodothyronine T4 and T3) are synthesized and secreted by thyroid
glands and affect metabolism throughout the body. The basic mechanisms for control in
this system are:
• Neurons in the hypothalamus secrete thyroid releasing hormone (TRH), which

stimulates cells in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
• TSH binds to receptors on epithelial cells in the thyroid gland, stimulating synthesis
and secretion of thyroid hormones, which affect probably all cells in the body.
• When blood concentrations of thyroid hormones increase above a certain threshold,

TRH-secreting neurons in the hypothalamus are inhibited and stop secreting TRH. This
is an example of "negative feedback". Inhibition of TRH secretion leads to shut-off of
TSH secretion, which leads to shut-off of thyroid hormone secretion. As thyroid
hormone levels decay below the threshold, negative feedback is relieved, TRH secretion
starts again, leading to TSH secretion. In addition to these negative feedback loop, the
basal medial hypothalamus also integrates input from other brain centers about changes
in the environment, such as a change in temperature, to determine the appropriate level
of TSH-RH secretion. This allows the body to regulate secretion of thyroid hormones in
response to changes in the environment. Finally, the thyroid also receives input from the
autonomic nervous system via parasympathetic and sympathetic fibers to regulate its
hormone secretion directly.
In a few instances, positive feedback occurs when the biological action of the hormone
causes additional secretion of the hormone. One example of this is the surge
of luteinizing hormone (LH) that occurs as a result of the stimulatory effect of estrogen
on the anterior pituitary before ovulation. The secreted LH then acts on the ovaries to
stimulate additional secretion of estrogen, which in turn causes more secretion of LH.
Eventually, LH reaches an appropriate concentration and typical negative feedback
control of hormone secretion is then exerted.
Cyclical Variations Occur in Hormone Release
Superimposed on the negative and positive feedback control of hormone secretion are
periodic variations in hormone release that are influenced by seasonal changes, various
stages of development and aging, the diurnal (daily) cycle, and sleep. For example, the
secretion of growth hormone is markedly increased during the early period of sleep but
is reduced during the later stages of sleep. In many cases, these cyclical variations in
hormone secretion are due to changes in activity of neural pathways involved in
controlling hormone release.
Circadian rhythms: are physical, mental, and behavioral changes that follow a 24-hour
cycle. These natural processes respond primarily to light and dark and affect most living
things, including animals, plants, and microbes. Chronobiology is the study of circadian
rhythms. One example of a light-related circadian rhythm is sleeping at night and being
awake during the day. Circadian rhythms can influence important functions in our
bodies, such as:
 Hormone release
 Eating habits and digestion
 Body temperature
However, most people notice the effect of circadian rhythms on their sleep patterns. The
SCN controls the production of melatonin, a hormone that makes you sleepy. It receives
information about incoming light from the optic nerves, which relay information from
the eyes to the brain. When there is less light—for example, at night—the SCN tells the
brain to make more melatonin so you get drowsy.
Clearance of Hormones from the Blood
Two factors can increase or decrease the concentration of a hormone in the blood. One
of these is the rate of hormone secretion into the blood. The second is the rate of
removal of the hormone from the blood, which is called the metabolic clearance
rate. This is usually expressed in terms of the number of milliliters of plasma cleared of
the hormone per minute. To calculate this clearance rate, one measures
(1) the rate of disappearance of the hormone from the plasma (e.g., nanograms per
minute) and
(2) the plasma concentration of the hormone (e.g., nanograms per milliliter of plasma).
Then, the metabolic clearance rate is calculated by the following formula:
The usual procedure for making this measurement is the following: A purified
solution of the hormone to be measured is tagged with a radioactive substance. Then the
radioactive hormone is infused at a constant rate into the blood stream until the
radioactive concentration in the plasma becomes steady. At this time, the rate of
disappearance of the radioactive hormone from the plasma equals the rate at which it is
infused, which gives one the rate of disappearance. At the same time, the plasma
concentration of the radioactive hormone is measured using a standard radioactive
counting procedure. Then, using the formula just cited, the metabolic clearance rate is
calculated.
Hormones are cleared from the plasma in several ways, including
(1) metabolic destruction by the tissues.
(2) binding with the tissues.
(3) excretion by the liver into the bile.
(4) excretion by the kidneys into the urine.
For certain hormones, a decreased metabolic clearance rate may cause an excessively
high concentration of the hormone in the circulating body fluids. For instance, this
occurs for several of the steroid hormones when the liver is diseased because these
hormones are conjugated mainly in the liver and then ―cleared‖ into the bile.
Hormones are sometimes degraded at their target cells by enzymatic processes that
cause endocytosis of the cell membrane hormone-receptor complex; the hormone is then
metabolized in the cell, and the receptors are usually recycled back to the cell
membrane.
Most of the peptide hormones and catecholamines are water soluble and circulate freely
in the blood. They are usually degraded by enzymes in the blood and tissues and rapidly
excreted by the kidneys and liver, thus remaining in the blood for only a short time. For
example, the half-life of angiotensin II circulating in the blood is less than a minute.
Hormones that are bound to plasma proteins are cleared from the blood at much slower
rates and may remain in the circulation for several hours or even days. The half-life of
adrenal steroids in the circulation, for example, ranges between 20 and 100 minutes,
whereas the half-life of the protein-bound thyroid hormones may be as long as 1 to 6
days.
Mechanisms of Action of Hormones

Hormone Receptors and Their Activation
The first step of a hormone‘s action is to bind to specific receptors at the target cell.
Cells that lack receptors for the hormones do not respond. Receptors for some hormones
are located on the target cell membrane, whereas other hormone receptors are located in
the cytoplasm or the nucleus. When the hormone combines with its receptor, this usually
initiates a cascade of reactions in the cell, with each stage becoming more powerfully
activated so that even small concentrations of the hormone can have a large effect.
Hormonal receptors are large proteins, and each cell that is to be stimulated usually has
some 2000 to 100,000 receptors. Also, each receptor is usually highly specific for a
single hormone; this determines the type of hormone that will act on a particular tissue.
The target tissues that are affected by a hormone are those that contain its specific
receptors.
The locations for the different types of hormone receptors are generally the following:
1. In or on the surface of the cell membrane. The membrane receptors are specific
mostly for the protein, peptide, and catecholamine hormones.
2. In the cell cytoplasm. The primary receptors for the different steroid hormones are
found mainly in the cytoplasm.
3. In the cell nucleus. The receptors for the thyroid hormones are found in the nucleus
and are believed to be located in direct association with one or more of the
chromosomes.
The Number and Sensitivity of Hormone Receptors Are Regulated
The number of receptors in a target cell usually does not remain constant from day to
day, or even from minute to minute. The receptor proteins themselves are often
inactivated or destroyed during the course of their function, and at other times they are
reactivated or new ones are manufactured by the protein-manufacturing mechanism of
the cell. For instance, increased hormone concentration and increased binding with its
target cell receptors sometimes cause the number of active receptors to decrease.
This down-regulation of the receptors can occur as a result of (1) inactivation of some of
the receptor molecules; (2) inactivation of some of the intracellular protein signaling
molecules; (3) temporary sequestration of the receptor to the inside of the cell, away
from the site of action of hormones that interact with cell membrane receptors; (4)
destruction of the receptors by lysosomes after they are internalized; or (5) decreased
production of the receptors. In each case, receptor down-regulation decreases the target
tissue‘s responsiveness to the hormone.
Some hormones cause up-regulation of receptors and intracellular signaling proteins;

that is, the stimulating hormone induces greater than normal formation of receptor or
intracellular signaling molecules by the protein-manufacturing machinery of the target
cell, or greater availability of the receptor for interaction with the hormone. When this
occurs, the target tissue becomes progressively more sensitive to the stimulating effects
of the hormone.
Endocrine glands
Endocrine system glands are spaced throughout the entire body. They release a wide
number of hormones which control the metabolism and function of other cells. Exocrine
glands, by comparison, secrete substances inside and outside of the body using ducts.
These two methods of transport mark the difference between exocrine and endocrine
glands.
While in the bloodstream, the hormones are able to travel through the body‘s circulatory
system to reach distant targets. Hormones, in turn, will carry out varied functions in the
body depending on the receptors they bind and the quantity of the hormone that is
present. These changes will reflect the balance of secretion and excretion of hormones in
the body. Their duration will depend on the hormone‘s inherent half-life and activity
levels.
Different endocrine glands with cell arrangement:-

Organ Division Cell arrangement/ function Hormone
1- Hypophysis Adenohypophysis
Pars distalis Cells in cords around large-bore
capillaries:
 Acidophils
for normal growth and development of Growth hormone
all body cells, especially muscle and
bone cells.
stimulates milk production in the prolactin (PRL) or
mammary glands. Lactogenic hormone
(LTH)
 Basophils
stimulates the adrenal cortex to secrete ACTH
mineralocorticoids, glucocorticoids, or
gonadocorticoids.
stimulates the thyroid gland to secrete TSH
thyroid hormones.
stimulates the production of egg cells FSH
and sperm in the gonads.
triggers ovulation and stimulates the LH
production of estrogens and
progesterone in female, and promotes
testosterone production in male.
Pars intermedia Mostly basophilic cells around cystic
cavities
ACTH
stimulates melanocytes in the epidermis MSH

and hair follicles to release melanin
pigment.
Pars tuberalis Narrow sleeve of basophilc cells around The specific

infundibulum. function of the cells
This region is an extension of the in the pars tuberalis,
glandular pituitary gland and its cells however, is not
resemble those of the pars intermedia clear.
and pars distalis.
Neurohypophysis
Pars nervosa Nerve fibers and supporting cells
(pituicytes)
stimulates uterine contraction during the Oxytocin
birth process, and activates milk
ejection from the mammary glands.
stimulates water reabsorption in kidney vasopressin

tubules. (produced in
hypothalamus)
Infundibulum Nerve fibers (traveling from ----------

hypothalamus to pars nervosa)
2- Pancreas Islet of Langerhans
α cells raise blood glucose level glucagon
β cells lower blood glucose level. insulin
δ cells helps regulate carbohydrate metabolism somatostation or
by inhibiting the secretion of glucagons. growth hormone
inhibiting hormone
(GHIH)
3- Digestive stomach stimulate stomach activities gastrin
organs small intestine stimulate gallbladder activities, and cholecystokinin
intestinal gastrin to regulate stomach (CCK)
activities.
4- Thyroid Follicles: Simple cuboidal to columnar
epithelium in spherical shells around
colloid
Principal cells\ promote normal T3 and T4

metabolism.
Parafollicular cell| lower blood calcium Thyrocalcitonin

and phosphate levels and regulate
digestive hormones.
5- Parathyroid Densely packed cords of polygonal PTH
cells (chief cells and oxyphilic cells)|
raise blood calcium level and lower
blood phosphate level.
6- Adrenal Cortex
Zona glomerulosa Columnar cells in rounded clusters\ it Aldosterone
raises blood levels of sodium and water,
and lowers blood potassium level.
Zona fasiculata Large, pale-staining polygonal cells in Glucocorticoids
columns| affect glucose or carbohydrate (Cortisone)
metabolism. Cortisol is the most
important hormone in this group, where
it is involved in carbohydrate, lipid and
protein metabolism , and also helps
fight stress and inflammation .
Zona reticularis Round cells in irregular cords\ Gonadocorticoids
supplement sex hormones from the (DHEA)
testes and ovaries and stimulate early
development of reproductive organs.
These hormones are male types (adrenal
androgens), namely testosterone , but
can be converted into female types,
such as estrogens, by the skin , liver,
and adipose tissues
Medulla Chromaffin cells= large round cells Norepinephrine and
with centrally located nucleus with epinephrine
prominent nucleus, often cytoplasmic
granules. Note large veins in center of
medulla.
Effects of these hormones resemble
sympathetic stimulation, where body
activities such as cardiac actions, blood
pressure , and breathing rate are
increased , while digestive processes are
decreased.
7-Thymus gland A diminishing gland (over time) located thymosin
between the lungs. secretes a group of
hormones to affect the production and
maturation of lymphocytes in body
defense
8- kidneys stimulate red blood cell production in Erythropoietin
the red bone marrow
9-Pineal gland regulate circadian rhythms which are melatonin
necessary to keep track of day/night
cycles, sleep/wake rhythm, menstrual
and ovarian cycles.
10- Testis develop secondary sexual testosterone
characteristics.
11- Ovary develop and maintain female sexual Estrogen

characteristics
help maintain ovarian and menstrual Progesterone
cycles, and pregnancy.
12-placenta maintain normal pregnancy . estrogen and
progesterone
13-Heart -regulate blood pressure. atrial natriuretic
(Cardiokines) -There is evidence that ANP is factor or Natriuretic
significantly elevated in patients with Peptides
left ventricular dysfunction which is ANP and BNP
independent of clinical symptoms, and
that the ANP levels in the circulation
are negatively correlated with ejection
fraction (EF)
The inflammatory response is thought Interleukins (1β, 6,

to be one of the most important 18, 33)
mechanisms in the process of
atherosclerosis. Abnormalities in the
levels of various inflammatory
cytokines have been found in patients
with acute coronary syndrome
cardioprotective factor that could Follistatin
protect cardiomyocytes and decrease
apoptosis induced by
ischemia/reperfusion (IR) injury
play a definite role in inducing Fibroblast Growth
angiogenesis, repairing impaired Factor 21(FGFs)
endothelial cells, and promoting
vascular smooth muscle cell
proliferation
a highly conserved factor closely Macrophage
related to the inflammatory response. migration inhibitory
MIF is released from necrotic factor (MIF)
cardiomyocytes after MI, and the levels
in circulation are rapidly increased after
stimulation since the cells produce and
store MIF before the inflammatory
response
promote angiogenesis, reverse Neuregulin (NRG)
myocardial remodeling, and improve
apoptosis and oxidative stress
a local factor in controlling vascular Adrenomedullin
tension, cardiac contractility, and renal
sodium excretion
elicit inhibitory effects on myocardial Protease Inhibitor

hypertrophy. 16
Chen et al. demonstrated that Ang-II Angiotensin-II

could also be produced by
cardiomyocytes and fibroblasts in the
heart, which elicits biological effects
through paracrine or autocrine
pathways
doi: 10.1016/j.yjmcc.2015.11.010.
14-Adipose tissue cytokines (cell signaling proteins) -Leptin

(adipokines) secreted by adipose tissue. Some -Adiponectin
contribute to an obesity-related low- -Apelin
grade state of inflammation or to the -chemerin
development of metabolic syndrome, a -interleukin-6 (IL-6)
constellation of diseases including, but -monocyte
not limited to, type 2 chemotactic protein-
diabetes, cardiovascular 1 (MCP-1)
disease and atherosclerosis. The first -plasminogen
adipokine to be discovered was leptin in activator inhibitor-
1994.Since that time, hundreds of 1 (PAI-1)
adipokines have been discovered. -retinol binding
protein 4 (RBP4)
-tumor necrosis
factor-alpha (TNFα)
-omentin
15-skeletal muscle fibers) in Receptors for myokines are found on -Myostatin

muscle response to muscular muscle, fat, liver, pancreas, bone, heart, -Interleukins
cells(myokines) contractions immune, and brain cells.The location of (1,6,10,15)
these receptors reflects the fact that -Brain-derived
myokines have multiple functions. neurotrophic
Foremost, they are involved in exercise- factor (BDNF)
associated metabolic changes, as well as -Decorin
in the metabolic changes following -Irisin
training adaptation. They also
participate in tissue regeneration and
repair, maintenance of healthy bodily
functioning, immunomodulation; and
cell signaling, expression and
differentiation
16-Hepatokine proteins produced regulation of metabolic diseases such - angiotensin
by liver cells as diabetes and fatty liver - IGF-1 (Insulin-like
(hepatocytes) Growth Factor 1)
are secreted into Adropin

the circulation and -Fetuin-A
function -Fetuin-B
as hormones across -Sex hormone-
the organism. binding
globulin (SHBG)
-Hepassocin
17-Lungs Bronchoconstriiction -angiotensin
Bronchodilation - vasoactive lung
Vasodilation peptide "VLP"
Vasoconstriction -Prostaglandins
- Vasoactive
polypeptides
- Bradykinin
- (nor-epinephrine,
- histamine
Hypothalamus and Pituitary Gland
 The hypothalamus is a small organ situated in the bran below the thalamus, which
controls the secretion of the pituitary gland.
 The hypothalamus is attached to the pituitary gland by a small stalk called the
infundibulum, and it is considered the connecting link between the endocrine
system and the nervous system.
 The cells of the hypothalamus alone secrete about nine different hormones, out of
which seven hormones are involved in the regulation of the pituitary gland.
 The hormones produced in the hypothalamus are termed inhibiting or releasing

hormones.
 The pituitary gland is often referred to as the master gland but, in fact, it plays more
of a ‗middle-management‘ role; many of its actions are directed by the
hypothalamus
 Secretion of the hypothalamic releasing and inhibiting hormones is determined by

multiple sensory inputs, which continually monitor the changing physiological
status of the body. Multiple parameters monitored continuously and in real time
include temperature, pH, solute concentrations and current levels of circulating
hormones. The hypothalamus functions as the key bridge between the nervous and
endocrine systems, but many of the interactions between the two remain poorly
understood.
 The pituitary gland is a small pea-shaped organ measuring about 1-1.5 cm in

diameter, which occurs in the hypophyseal fossa of the sphenoid bone in the skull.
 The pituitary gland can be differentiated into two anatomically and functionally
separate parts; anterior pituitary and posterior pituitary.
 The anterior pituitary, also called adenohypophysis, is composed of epithelial cell.
 The anterior pituitary accounts for approximately 70-80% of the total mass of the
gland and includes two major parts:
Pars distalis – larger, bulbous portion
Pars tuberalis – highly vascular sheath wrapped around the infundibular stalk.
A third (intermediate) region of the pituitary gland is often recognisable; this
is known as the pars intermedia and is usually present as a thin band of tissue
that marks the point where the anterior and posterior pituitaries fuse.
 The anterior pituitary is supplied with a portal system that ensures the circulation of
hormones produced by the gland.
 Adenohypophysis - based on grouping of all regions composed of glandular tissue

This includes the... pars distalis pars intermedia pars tuberalis. The pars distalis
forms the largest proportion of the gland and functions as the overall regulator of
peripheral endocrine function by synthesizing and secreting at least 4 major trophic
hormones.
 The cells in the adenohypophysis secrete two classes of hormones: (1) direct acting
and (2) trophic. Direct acting hormones include growth hormone (GH) and prolactin
from the pars distalis, and melanocyte stimulating hormone (MSH) from the pars
intermedia. Trophic hormones include adrenocorticotrophic hormone (ACTH),
thyroid stimulating hormone (TSH), luteinizing hormone (LH) and follicle
stimulating hormone (FSH).
 Neurohypophysis - based on grouping of all regions composed of neural or

neurosecretory tissue This includes the median eminence infundibular stalk pars
nervosa ( infundibular process).
 The secretion of the anterior pituitary is influenced by the releasing hormone

produced by the hypothalamus.
 The posterior pituitary is composed of neural tissue, which is triggered by an action

potential that originates in the cell body of the hypothalamus.
 The hormones of the posterior pituitary are synthesized in the nerve cell bodies and
are transported along the axons to be stored in the axon terminals. The nerve stimuli
from the hypothalamus regulate exocytosis of the vesicles to release the hormones
into the bloodstream.
 Posterior pituitary (neurohypophysis) – neural tissue extends from the

hypothalamus through the infundibulum into a larger, bulbous region called the pars
nervosa; this forms the bulk of the posterior pituitary
 The overall secretion of hormones by the pituitary is regulated by a negative

feedback mechanism.
 Usually, there is one cell type for each major hormone formed in the anterior
pituitary gland. With special stains attached to high-affinity antibodies that bind
with the distinctive hormones, at least five cell types can be differentiated provides
a summary of these cell types, the hormones they produce, and their physiological
actions. These five cell types are:
1. Somatotropes—human growth hormone (hGH)
2. Corticotropes—adrenocorticotropin (ACTH)
3. Thyrotropes—thyroid-stimulating hormone (TSH)
4. Gonadotropes—gonadotropic hormones, which include both luteinizing hormone

(LH) and folliclestimulating hormone (FSH)
5. Lactotropes—prolactin (PRL).
 Hypothalamus communicates with the rest of the body via three routes:
Bloodstream: Hypothalamus receives blood mainly from the hypophyseal

artery, a branch of the anterior cerebral artery. All the blood from the
hypothalamus is drained into the hypothalamohypophyseal system of veins
and distributed to the pituitary gland. From the pituitary gland, the blood is
drained via the hypophyseal vein.
Nervous connections The nervous connections can be divided into afferent and
efferent fibers.
Endocrine connections Hypothalamus uses the bloodstream to communicate
with the pituitary gland. These connections of the hypothalamus are called the
bloodstream or endocrine connections. The cells of the pituitary gland release
hormones in response to the regulating factors or hormones released by the
hypothalamus. These regulatory factors reach the pituitary gland via the
hypophyseal portal system of veins.
Hypothalamus- Hormone released by the Effect of the hormone

releasing hormone anterior pituitary in
response
Growth hormone Growth hormone (GH) Goes directly to long bones and the big
releasing hormone muscles to stimulate growth.
(GHRH)
Somatostatin Growth hormone (GH) which also affects bone and muscle growth
but has the opposite effect as that of GHRH
Gonadotropin-releasing Follicle-stimulating Travels to gonads. In males, LH causes the
hormone (GnRH) hormone (FSH) testes to make testosterone; FSH controls
and luteinizing hormone sperm production. In females, LH and FSH
(LH) control the menstrual cycle and trigger the
release of an egg from the ovary (ovulation).
Corticotropin-releasing Adrenocorticotropic Travels to adrenal glands. Causes adrenal
hormone (CRH) hormone glands to release the stress
(ACTH) hormone cortisol and
regulate metabolism and immune response.
Thyrotropin-releasing Thyroid-stimulating Travels to thyroid gland. Causes thyroid to
hormone (TRH) hormone (TSH) release thyroxine (T4) and triiodothyronine
(T3).
Prolactin Releasing Prolactin (PRL) stimulate release of PRL from lactotropes
Hormone ( PRLH) and is believed to be an important regulator
related to photoperiodic effects on PRL
release
Dopamine (inhibition) Prolactin (PRL) a substance that functions primarily as a
neurotransmitter but also has some hormonal
effects, such as repressing lactation until it is
needed after childbirth.
Functions of Hypothalamus:
1. Autonomic Control The most important function of the hypothalamus is to integrate
the endocrine system and the autonomic nervous system. Hypothalamus acts as a
higher center for controlling the autonomic functions of the brain stem and spinal
cord. The stimulation of the posterior and lateral nuclei of the hypothalamus has been
shown to cause a sympathetic response. On the other hand, the stimulation of the
anterior nucleus and the preoptic area influences parasympathetic responses in the
body.
2. Endocrine Control Hypothalamus produces releasing factors or inhibitory factors for
controlling the hormones released by the pituitary gland. These factors include:
 Growth hormone-releasing hormone and inhibiting hormone also called
somatostatin
 Prolactin releasing hormone and inhibiting hormone
 Corticotropin-releasing hormone
 Thyrotropin-releasing hormone
 Luteinizing hormone-releasing hormone
These factors promote or inhibit the release of hormones from the anterior pituitary.
The release of these factors from the hypothalamus is controlled by positive and
negative feedback mechanisms depending on the levels of a particular hormone in
blood.
3. Secretion of Hormones Hypothalamus not only secretes the regulating factors but
also secretes two important hormones; vasopressin and oxytocin. Although these
hormones are released from the posterior pituitary, they are actually produced by the
neurons in the hypothalamus and are stored in the axonal endings present in the
posterior pituitary
4. Temperature Regulation Temperature regulation is another important function of the

hypothalamus. The anterior part of the hypothalamus controls processes that dissipate
heat from the body. Its stimulation causes dilation of blood vessels and sweating,
which causes a decrease in body temperature. Contrary to this, stimulation of the
posterior part of the hypothalamus results in vasoconstriction of the skin blood
vessels and inhibition of sweating resulting in conservation of body temperature.
5. Controlling Emotions and Behavior Being a part of the limbic system hypothalamus
also controls the emotions and behavior of a person. It is believed that the
hypothalamus integrates all the afferent information from other areas of the brain and
brings about the physical expression of emotion. Stimulation of the lateral area of the
hypothalamus is associated with the feelings of rage whereas the stimulation of the
medial area results in feelings of passivity.
6. Regulation of Food and Water Intake Hypothalamus is also the site of the hunger
center and satiety center in the brain. The stimulation of the lateral region of the
hypothalamus stimulates hunger and results in the intake of food. This region is
termed as hunger center. On the other hand, stimulation of the medial region of the
hypothalamus inhibits eating and results in reduced food intake. This is termed as the
satiety center of the brain.
Primary hormones secreted by the hypothalamus

include:
1. Anti-diuretic hormone (ADH): This hormone increases water absorption into the
blood by the kidneys.
2. Corticotropin-releasing hormone (CRH): CRH sends a message to the anterior
pituitary gland to stimulate the adrenal glands to release corticosteroids, which help
regulate metabolism and immune response.
3. Gonadotropin-releasing hormone (GnRH): GnRH stimulates the anterior pituitary to

release follicle stimulating hormone (FSH) and luteinizing hormone (LH), which
work together to ensure normal functioning of the ovaries and testes.
4. Growth hormone-releasing hormone (GHRH) or growth hormone-inhibiting
hormone (GHIH) (also known as somatostain): GHRH prompts the anterior pituitary
to release growth hormone (GH); GHIH has the opposite effect. In children, GH is
essential to maintaining a healthy body composition. In adults, it aids healthy bone
and muscle mass and affects fat distribution.
5. Oxytocin: Oxytocin is involved in a variety of processes, such as orgasm, the ability
to trust, body temperature, sleep cycles, and the release of breast milk.
6. Prolactin-releasing hormone (PRH) or prolactin-inhibiting hormone (PIH) (also
known as dopamine): PRH prompts the anterior pituitary to stimulate breast milk
production through the production of prolactin. Conversely, PIH inhibits prolactin,
and thereby, milk production.
7. Thyrotropin releasing hormone (TRH): TRH triggers the release of thyroid
stimulating hormone (TSH), which stimulates release of thyroid hormones, which
regulate metabolism, energy, and growth and development.
Hormonal Regulation of Pituitary Function

Regulation of the various trophic hormones from the cells of the pars distalis is through
a complex interplay of different inputs. These include positive and negative feedback
from the peripheral target tissues, stimulation or inhibition by hormones secreted from
the hypothalamus and also modulation through hormones secreted from other organs.
The major regulatory hormones are listed in Table, but there are many other hormones
that modulate pituitary function.
Pituitary hormone Major releasing factors Major inhibitory factors
Prolactin Prolactin releasing factor Dopamine

Growth hormone GH releasing hormone Somatostatin
Thyroid stimulating TSH releasing hormone T3 and T4 (thyroid

hormone hormones), prolactin,
somatostatin
LH and FSH Gonadotrophin releasing Estrogen, androgens,

hormone (GnRH), activin inhibin
Adrenocorticotrophic Corticotrophin releasing Cortisol, corticosterone

hormone hormone (adrenal cortical
hormones)
Hormones of the hypothalamus and pituitary gland
1. Growth Hormone
As its name suggests, the primary function of GH is to promote bodily growth.

Most famously, GH promotes the widening of the growth plates in the epiphyses of
the long bones of the skeleton, which results in elongation of the major bones of the
arms and legs, progressively increasing height. GH also enhances amino acid
uptake from the blood into cells, increasing the rate of protein synthesis in tissues
such as muscle; this is why it is known as an anabolic hormone. Thyroid hormones
T3 and T4 (thyroxin), which regulate metabolism, are necessary for GH to exert its
effects efficiently. The anabolic effects of GH are also enhanced by the presence of
other anabolic hormones such as testosterone. As well as promoting bone and
muscle growth, GH also stimulates the growth of many of the major internal
organs. Growth hormone exerts Much of Its effect through intermediate substances
called Somatomedins (also called Insulin-Like Growth Factors)
GH secretion is regulated by two hormones produced by the hypothalamus: Growth

hormone-releasing hormone stimulates the release of GH; Growth hormone-
inhibiting hormone (GHIH) acts antagonistically to inhibit the release of GH
(Table). Deficiency of GH during childhood may result in pituitary dwarfism; this
is characterized by below-average growth and, commonly, an underdeveloped
bridge of the nose and prominent forehead. Unlike achondroplastic dwarfism (a
genetic disorder), pituitary dwarfism, although associated with reduced height, is
characterized by normal bodily proportions. Recombinant human GH is available
to treat children who are deficient in GH. It is usually injected subcutaneously once
a day, and growth rate and potential side-effects then carefully monitored. Elevated
secretion of GH in childhood often leads to gigantism, in which rapid growth of the
long bones can result in an adult height of >2.4m. Elevated secretion of GH in
adults, after their epiphyseal growth plates have fused, can lead to acromegaly, in
which the hands, feet and some facial features (particularly the lower jawbone) can
grow abnormally large and usually out of normal proportion.
2. Prolactin
(lactogenic hormone) initiates milk secretion (lactation) in breast tissue. By itself,

prolactin has only a weak effect, but during pregnancy prolactin levels increase and
it acts synergistically with other hormones – including oestrogens, progesterone
and cortisol to promote the enlargement and engorgement of the breasts in
preparation for lactation. It has been hypothesized that the release of prolactin is
regulated and fine-tuned by the antagonistic actions of a prolactinreleasing
hormone and a prolactin-inhibiting hormone, both of which are thought to be
produced by the hypothalamus. Hyper secretion can disrupt normal menstrual
cycles in female and causes impotence in male; and hyposecretion causes poor milk
production in female (Table).
3. Tropic hormones
Tropic hormones have a stimulating effect on other endocrine glands, inducing
the synthesis and secretion of the target hormone(s). Four major tropic hormones
are synthesized and secreted by the anterior pituitary, as described below.
Thyroid-stimulating hormone (thyrotrophin)
TSH stimulates the thyroid gland to secrete the iodine-containing hormones T3 and
T4. These are primarily responsible for regulating metabolism, with T3 being the
more potent. Most cell types in the body have internal receptors for T3 and T4.
These hormones are also vital for growth and development, and play key roles in
the normal functioning of the cardiovascular, respiratory, skeletal and central
nervous systems. The release of TSH is regulated by thyrotropin-releasing
hormone, which is produced by the hypothalamus (Table). The fine tuning of T3
and T4 release is regulated by negative feedback, through the sequential secretions
of the hypothalamus, anterior pituitary and thyroid gland. Hypersecretion causes
Grave‘s disease, and hyposecretion causes cretinism in children and myxedema in
adults.
Adrenocorticotrophic hormone (adrenocorticotropin)
ACTH primarily regulates the production and secretion of cortisol from the
adrenal cortex (outer portion of the adrenal gland). Cortisol is a long-term stress
hormone and a steroidal hormone synthesized from cholesterol. It is referred to as a
glucocorticoid because it is produced by the adrenal cortex and influences the
concentration of glucose in the blood. Following periods of chronic stress
(including classic biological stressors such as starvation or physical injury), the
hypothalamus releases corticotropin-releasing hormone. This initiates the release of
ACTH from the anterior pituitary and, subsequently, stimulates the release of
cortisol from the adrenal cortex (Table). Cortisol plays a key role in regulating
metabolism and, during periods of food deprivation, stimulates the breakdown of
protein and fat to generate glucose for use as fuel in glucose-dependent tissues,
such as the brain. This process is called gluconeogenesis (literally, the creation of
new glucose). Cortisol also influences the sleep/ wake cycle, mood and behavior,
and has potent anti-inflammatory/immunosuppressant properties. ACTH also helps
to regulate the release of other steroid hormones produced by the adrenal cortex,
including aldosterone (which regulates the concentration of sodium and potassium
in the blood) and the group of testosterone-like hormones known as androgens. The
complex interplay between the hypothalamus, anterior pituitary and the adrenal
cortex is referred to as the HPT axis and will be examined in detail in part 4 of this
series. ACTH is also part of the melanocortin group of hormones, which influence
skin pigmentation. Hypersecretion causes Cushing‘s disease, while hyposecretion
is rare.
Melanocyte-stimulating hormone (MSH)
MSH is synthesized by the pars intermedia region of the pituitary gland. Although
this region marks the boundary where the anterior and posterior portions of the
pituitary gland fuse, it is generally considered part of the anterior pituitary. The
pars intermedia atrophies (shrinks) with age and, in adults, may only be present as a
vestigial remnant or, in some cases, is not recognizable at all. MSH exists in a
range of structurally similar forms known as melanocortins, which are all small
peptides.
As implied by its name, MSH stimulates the pigment-producing cells

(melanocytes) in the epidermis to release the dark pigment known as melanin,
which is largely responsible for skin color. All races are thought to have similar
numbers of melanocytes in their epidermis; it is the relative activity of these cells
and the amount of melanin they synthesis and release that ultimately determines
skin color. Melanocytes can synthesis MSH when exposed to the ultraviolet (UV)
light in sunlight. This is essential to protect the actively dividing cells of the
epidermis from the harmful effects of UV, known to cause DNA damage that can
lead to mutations and, potentially, skin cancers. Melanin is excellent at absorbing

UV wavelengths of light and, as it accumulates in the epidermis the skin, darkens
and develops a protective suntan. During pregnancy, levels of MSH tend to
increase, which, together with changes to the sex hormones oestrogen and
progesterone, often leads to hyper-pigmentation around the eye sockets,
cheekbones, lips and forehead. This is known as melasma or ‗the mask of
pregnancy‘; these pigmented areas usually fade gradually after childbirth. ACTH
(described above) is another hormone that can influence skin pigmentation through
the direct stimulation of melanocytes. This is particularly true of certain forms of
Cushing‘s syndrome, in which excess ACTH often causes regions of dark,
hyperpigmented skin
Gonadotrophin
These act on the gonads (testes and ovaries) to stimulate the production of sex
hormones and sperm or ova in males and females respectively (see below). The
main gonadrotrophins are FSH and LH; the release of both is regulated by
gonadotropin-releasing hormone, which is produced by the hypothalamus (Table
1). In females, each month FSH initiates the development of immature follicles in
the ovaries. As each follicle enlarges, it secretes the female sex hormone oestrogen,
before maturing into a Graafian follicle, a fluid-filled, pressurized sac containing a
mature ovum (egg), primed and ready to rupture. Ovulation is triggered by LH,
which initiates rupturing of the follicle and ovarian wall; this explosive event
propels the ovum into its adjacent fallopian tube. Following ovulation, the remnants
of the Graafian follicle collapse to form a structure known as the corpus luteum
(yellow body). This produces the second major female sex hormone, progesterone,
which maintains the integrity of the endometrial lining of the uterus to allow for the
implantation of a fertilized ovum. Despite their names being reflective of the role
played in the female ovarian cycle, FSH and LH also play crucial roles in male
reproductive physiology. FSH is essential in stimulating spermatogenesis, where
diploid cells (containing 46 chromosomes) undergo meiotic division to produce
vast numbers of haploid spermatozoa (each containing 23 chromosomes). FSH also
stimulates the activity of Sertoli cells (nurse cells) in the testes; these provide
nutrition to the developing spermatozoa, allowing maturation into viable gametes
that are capable of fertilization. LH stimulates the interstitial cells (Leydig cells) of
the testes to synthesis and release the male sex hormone testosterone. This powerful
anabolic steroid stimulates skeletal muscle development, growth of facial and body
hair, expansion of the larynx (causing the deepening of the voice) and
spermatogenesis, and is largely responsible for the male sex drive. The role of the
gonadotropins and male and female sex hormones will be discussed further in part
7 of this series.
Hormones of the posterior pituitary

Two major hormones are released from the posterior pituitary:
Antidiuretic hormone (ADH)

Oxytocin.
These hormones are synthesized in the cell bodies of neurons in the hypothalamus and
transported down the axons of the neurons running through the infundibulum. ADH and
oxytocin are concentrated and stored in the pars nervosa (Fig), before being released into
the blood when required. Both are peptide hormones and, as they are produced by
neurons, they are often called neuropeptides.
1. Oxytocin
Oxytocin is released into the blood at high concentration towards the end of the
gestational period and initiates parturition (childbirth) by stimulating contractions of the
myometrium (muscular layer of the uterus). Oxytocin secretion is regulated by a positive
feedback mechanism, whereby increased oxytocin stimulates more-powerful myometrial
contractions, which in turn stimulate the release of more oxytocin. This is possible
because the uterine wall has receptors that monitor the strength of myometrial
contractions and generate nerve impulses (action potentials) that are relayed back to the
hypothalamus. Oxytocin also stimulates the ‗letdown reflex‘ in lactating mothers; here
the smooth muscle linings of the milk ducts in the breast contract, making milk available
to the baby during suckling. Again, this is regulated by positive feedback, with the
mechanical stimulation of the baby‘s suckling action triggering the release of more
oxytocin. Oxytocin is often referred to as ‗the love hormone‘ because it plays an
important role in promoting mother/baby bonding; it is also thought to facilitate pair
bonding between partners. Evidence is also emerging that oxytocin has other
psychological effects, such as reducing anxiety, and promoting maternal behavior.

Disorders are rare and have no known effects, except in some hyposecretion cases, weak
labor contraction is reported.
2. Antidiuretic Hormone (ADH)
Antidiuretic hormone ADH plays a vital role in regulating fluid balance and blood
pressure. Specialized osmoreceptors located in the hypothalamus continually monitor
the solute concentration of the blood. When the body loses water (for example, through
sweating during exercise or following vomiting and diarrhoea) dehydration may occur
and the plasma solute concentration rises. This is detected by the hypothalamic
osmoreceptors, which initiate the release of ADH from the posterior pituitary. ADH
primarily acts on the kidneys, increasing the volume of fluid absorbed from the renal
filtrate back into the blood. This reduces the volume of urine produced (hence the name
antidiuretic hormone), resulting in the urine being darker and more highly concentrated.
By increasing fluid reabsorption back into the blood, ADH helps normalise the solute
concentration of the blood.
ADH is also released after a drop in blood volume or pressure. By promoting water
reabsorption in the kidney, ADH increases blood volume, which then starts to increase
blood pressure. This normalisation of blood pressure is further enhanced by ADH acting
as a powerful vasopressor (which promotes the constriction of blood vessels). ADH-
induced vasoconstriction, particularly in the peripheral arterioles (small arteries), further
increases and normalises blood pressure. As a result, ADH is also known as vasopressin,
particularly in the United States. Reduced secretion of ADH can lead to diabetes
insipidus (DI). Patients with DI cannot concentrate their urine, resulting in polyuria.
Large volumes of urine (3-20L/ day) are usually produced; if not treated, this can lead to
severe dehydration. DI is rare, affecting around 1 in 25,000 people; two major types are
recognised:
Neurogenic or central DI is caused by the undersecretion (hyposecretion) of ADH by

the posterior pituitary. This is most often due to trauma (commonly head injuries),
tumours affecting the hypothalamus or pituitary or, more rarely, infections
Nephrogenic DI is a rarer form, in which patients usually have normal ADH
synthesis and secretion, but their kidneys are insensitive to the effects of ADH – most
commonly due to kidney disease or drug-induced kidney damage.
DI requires careful management. Initially patients may be severely dehydrated, feel

nauseous and shivery, and experience headache; careful monitoring of water intake and
urine output, with ongoing assessment of urine and blood concentration, is essential.
Neurogenic DI is usually treated with desmopressin, a synthetic analogue of ADH that
acts on the kidneys in the same way to concentrate the urine and increase blood volume.
Treatment of nephrogenic DI is more complex and depends on the underlying cause of
the disease.
pineal gland
The pineal gland was described as the ―Seat of the Soul‖ by Renee Descartes and it is
located in the center of the brain. pineal gland, also called conarium, epiphysis
cerebri, pineal organ, or pineal body, endocrine gland found in humans that is the source
of melatonin, a hormone derived from tryptophan that plays a central role in the
regulation of circadian rhythm (the roughly 24-hour cycle of biological activities
associated with natural periods of light and darkness). The pineal gland has a rich supply
of adrenergic nerves (neurons sensitive to the adrenal hormone epinephrine) that greatly
influence its function. Microscopically, the gland is composed of pinealocytes (rather
typical endocrine cells except for extensions that mingle with those of adjacent cells)
and supporting cells that are similar to the astrocytes of the brain. In adults, small
deposits of calcium often make the pineal body visible on X-rays. (The pineal gland
eventually becomes more or less calcified in most people.) Both melatonin and
its precursor, serotonin, which are derived chemically from the alkaloid substance
tryptamine, are synthesized in the pineal gland. Along with other brain sites, the pineal
gland may also produce neurosteroids. Dimethyltryptamine (DMT), a
hallucinogenic compound , is chemically similar to melatonin and serotonin and is

considered to be a trace substance in human blood and urine.
Thyroid Gland
The thyroid gland is one of the most body important endocrine glands, is a butterfly-
shaped. It is situated in the neck below Adam's apple. Though its size can differ, based
on each person's size and iodine intake. Thyroid generally weighs approximately 15-20
grams (Fig.). It is consist of right and left lobe that lie on either side of the trachea. The
right and left lobes are connected via a thin strip of thyroid tissue called the isthmus.
Neighboring structures involve the esophagus and the carotid artery ,that is the main
blood supply to the head and neck.
Thyroid gland has a rich blood supply made up of two main arteries on each side;
superior and inferior thyroid gland arteries. Veins exhausting the thyroid gland tend to
run along with the arteries. The lymphatic discharge from the thyroid gland is to lymph
nodes situated near the esophagus and trachea. The lymphatic drainage transmit extra
fluid from the body back to heart and are filtered by lymph nodes in the center part of
the neck next to the thyroid and to lymph node in the side of the neck along the jugular
vein. These lymph nodes are important in cases of thyroid cancer.
Two nerves interested in speech path behind every thyroid lobe on either side of the
neck. The recurrent laryngeal nerves, that look like guitar strings, enter the voice box
(larynx) near thyroid. These nerves shift the vocal cords to control the voice. Injury at
one nerve causes a whisper-type hoarseness. Injury at both recurrent laryngeal nerves
can cause the airway to lock down leading to difficulty breathing.
The thyroid gland is the only endocrine gland that can store large quantities of its
secretory products, lasting up to 100 days.
Into microscopically level, there are three primary features of the thyroid
follicles, follicular cells and parafollicular cells. Initially, discovered by Geoffrey
Webster in 1664. Thyroid follicles are small spherical groupings of cells which play
major role in thyroid functions. They contain a rim which has a rich blood supply, nerve
and lymphatic which surrounds a core of colloid which contains generally of
thyroglobulin Tg. Thyroglobulin is synthesized in the rough endoplasmic reticulum
(rER) and Golgi apparatusand follows the secretory pathway to enter the colloid in the
lumen of the thyroid follicle by exocytosis. Tg is a large glycoprotein molecule

comprised of two subunits, each containing 5496 amino acids). It includes
approximately 140 tyrosyl residues. The core of a follicle is surrounded by a single layer
of follicular cells. When stimulated by TSH, these secrete THs T3 and T4. They do this
through transferring and metabolizing the Tg contained in colloid. Follicular cells differ
in shape from flat to columnar to cuboid, relying on how active they are. Diffused
between follicular cells and in spaces among spherical follicles are other type of thyroid
cells called parafollicular cells or C cells that secrete calcitonin.
Thyroid Hormones (THs)

THs are chemical substances produced by thyroid gland. This gland utilizes iodine to
produce THs, that are important to the function of each cell in the body. The two most
important THs are thyroxine T4 and triiodothyronine T3. The main form of TH in blood
is thyroxine T4. T3 is three to four times more active than T4. The main product of
thyroid gland is T4, where T3 is produced ten times less. Although some T3 is created in
thyroid, approximately 80% is produced out of the gland, mainly by conversion of T4 in
kidneys and liver. Nervous system is able to convert T4 to T3. In tissues most of effects
of T4 result from conversation to T3, so T4 is a pro-hormone. T3 is derived from T4 by
deiodination in peripheral tissues, kidneys ,liver and muscles, catalyzed by deiodinases
(5'-iodinase). Deiodination can also create reverse T3 (rT3) that is physiologically

inefficient. Three deiodinase D families are known and are described as isoforms type I,
II and III. Type I deiodinase is the main enzyme in kidneys and liver. Type II enzyme is
present in the heart, the skeletal muscle, CNS, fat and thyroid. Type III deiodinase
isoform is present in placenta and fetal tissue. Moreover, a degradation of rT3 and T3
result in formation of several diiodothyroxine (T2). Metabolic role of T2 isomers is
poorly know and is unclear in human beings. T3 is supposed to be the most
metabolically active thyroid hormones. Thyroid gland also produces the
hormone calcitonin that is included in calcium metabolism and stimulating osteoblast to
insert calcium to the bone.
Target cell Effect Mechanism

Heart Cronotropic Increase number of adrenergic receptor.
Inotropic Enhanced responses to circulating catecholamine
Adipose tissue Catabolic Stimulate lipolysis
Muscle Catabolic Increase protein breakdown

Bone Developmental Promote normal growth and skeletal development
Nerve system Developmental Promote normal brain development.

GUT Metabolic Increased rate of carbohydrate absorption.
Lipoprotein Metabolic Formation of LDL receptors
Others Calorigenic Stimulated oxygen consumption by metabolically
active tissue (exception: testes, uterus, lymph nodes).
Increase metabolic rate

Table of physiologic effects of thyroid hormones
Type Percent
thyroxine-binding globulin
70%
(TBG)
transthyretin or Thyroxine-Binding Prealbumin (TTR or TBPA) 10-15%
Albumin 15-20%
Table of Thyroid Hormones Transport
Iodide Transport (Iodide Trapping)

The primary stage in the synthesis of thyroid hormones THs is the transfer of iodides
I− from blood to thyroid glandular cells and follicles. As shown in figure.
Iodide (I–) is brought across thyrocytes' basal membrane by membrane bound NIS
(Na- I− Symporter) that derives its energy from a Na+-K+ ATPase, permits thyroid
gland to maintain a concentration of free iodide 30 to 40 times as high as in plasma.
Thyroid gland condenses and uses only a fraction of the iodide I− provided it for
hormone synthesis, and the rest returns to the extracellular fluid pool. Sodium-Iodide
Symporter NIS work is promoted physiologically by TSH. In spite of salivary, gastric,
and breast tissues express NIS and condense iodide to a minimum range than thyroid,
these tissues don't organify or storage iodide and their NIS actions are not induce by
TSH. Big amounts of iodide suppress together NIS action and NIS gene expression, act
for mechanisms of iodine autoregulation. NIS activity is also prevents by perchlorate
that has been used to treat hyperthyroid and has been involved as an environmental
inhibitor of thyroid functions.
Thyroid Hormones Synthesis And Secretion

1. Iodide ions from diet delivered to thyroid gland and taken up by follicle cells.
2. Enzymes convert iodide ions to iodine atoms and attach them to tyrosine portions
of thyroglobulin molecule.
3. Thyroxine (T4 ), with four iodine atoms and triiodothyronine (T3 ), with three
iodine atoms are produced and stored in thyroglobulin.
4. Follicle cells remove thyroglobulin from follicle by endocytosis.
5. Lysosomal enzymes break down thyroglobulin, releasing thyroid hormones and
amino acids into cytoplasm. Amino acids used to synthesize more thyroglobulin.
6. T4 (90 percent of thyroid secretions) and T3diffuse across basement membrane and
enter bloodstream .
7. 75 percent of T4 and 70 percent of T3 molecules travel in the blood attached to
transport proteins (thyroid-binding globulins). Hormones are released by proteins
gradually. Most of the rest of T4 and T3 attach to transthyretin or albumin –
Bloodstream contains 1 week of reserve supply.
Figure: Synthesis and Secretion of Thyroid Hormones
Disorders of the Thyroid Gland

As discussed at the top, dietary iodine is wanted for the synthesis of T 3 and T4. But,
for numerous of the world‘s people, foods don't supply adequate levels of this mineral,
because the amount differ fit to soil level in which the food was grown. Dietary iodine
deficiency may result to reduce the ability for synthesize T 3 and T4, leading to a
diversity of severe disorders. When T3 and T4 cannot be synthesized, TSH is secreted in
large amounts. As a result of this hyperpromoting, thyroglobulin Tg raise in the thyroid
follicles, rising their charges of colloid. The accumulation of colloid raises the size of
the thyroid, this case called a goiter. A goiter is one and only a visual indication of the
deficiency. Another iodine deficiency disorders have weaken growth and development,
low fertility and infant death. Furthermore, iodine deficiency ID is the first cause of
preventable mental lag worldwide. Neonatal hypothyroid (called also cretinism) is
identify via cognitive deficits, short frame and occasionally deafness and mutism in the
adults and children born for mothers who were iodine-deficient through pregnancy.
1. Hyperthyroidism
Hyperthyroidism is the condition that occurs due to excessive production of thyroid
hormone by the thyroid gland or too much release of THs from thyroid gland, results
from thyroid inflammation and/or damage. Signs and symptoms vary between people
and may include irritability, muscle weakness, high metabolic rate, sensitivity to heat,
restless ness, hyperactivity, weight loss , protruding eyes , sleeping problems, a fast
heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor,
and weight loss. Graves' disease (Auto antibodies ,against self, bind TSH receptors on
thyroid cell membranes , mimicking action of TSH, over stimulating gland) is the cause
of about 50% to 80% of the cases of hyperthyroidism. Other causes include multinodular
goiter, toxic adenoma, inflammation of the thyroid, eating too much iodine and too
much synthetic thyroid hormone.
The diagnosis may be suspected based on signs and symptoms and then confirmed
with blood tests. Typically blood tests show a low thyroid stimulating hormone (TSH)
and raised T3 or T4. Radioiodine uptake by the thyroid, thyroid scan and TSI antibodies
may help determine the cause. The mechanism of this disorder is thyroid-stimulating
immunoglobulin recognize and bind to the thyrotropin receptor (TSH receptor) which
stimulates the secretion of thyroxine (T4) and triiodothyronine (T3). Thyroxine receptors
in the pituitary gland are activated by the surplus hormone, suppressing additional
release of TSH in a negative feedback loop. The result is very high levels of circulating
thyroid hormones and a low TSH level.
2. Hypothyroidism
Hypothyroidism is a highly thyroid trouble in which thyroid gland is hypoactive or
non-active. It is more often shown in women than men. It can cause a number of
symptoms, such as poor ability to tolerate cold, a feeling of tiredness, constipation,
depression and weight gain. Occasionally there may be swelling of the front part of the
neck due to goiter. TSH level is the best test for detecting hypothyroidism. Increase TSH
level emphasizes the diagnosis of hypothyroid in most patients. T3 and T4 levels are
generally low.
Hashimoto’s disease : Auto antibodies (against self) attack thyroid cells,

producing hypothyroidism . The plurality of patients with Hashimoto's HS have
thyroglobulin antibodies (Anti-Tg Abs) and/or thyroid peroxidase antibodies
(Anti-TPO Abs). These antibodies cause ruin of thyroid cells that lead to little
cells producing thyroid hormones THs. Risk agents for Hashimoto's thyroiditis
involved female gender, private history of another autoimmune diseases and an
autoimmune thyroiditis family history or another autoimmune diseases
Hypothyroidism (infantile) : cretinism - shunted growth, abnormal bone
formation , mental retardation , low body temperature , sluggishness.
Hypothyroidism (adult) : Myxedema - low metabolic rate, sensitivity to cols,
sluggishness, poor appetite , swollen tissue , mental dullness.
Simple goiter : Deficiency of thyroid hormone due to iodine deficiency ; because
no thyroid hormones inhibit pituitary release of TSH, thyroid is over stimulated
and enlarges, but functions below normal (hypothyroidism).
Chance of being hypothyroidism relies on the size of thyroid gland removed

(thyroidectomy) and any following thyroid disease. Removing the entire thyroid gland
will cause hypothyroidism even patients whose have only comprise half the thyroid
extracted are at a giant risk of developing hypothyroid than common people.
Radioactive iodine treatment (RAI treatment) is given to damage thyroid tissue
(especially for GD and thyroid cancer). The higher dosage, mean the greater chance of
enhancing hypothyroidism. However, even less doses may produce hypothyroidism,
whereas diagnostic radioactive thyroid scans don't produce hypothyroidism.
Parathyroid gland anatomy

 Two pairs embedded in posterior surface of the thyroid gland
 Contain two cell populations
1. Oxyphil cells (no known functions)
2. Parathyroid (principal) cells
 Produce parathyroid hormone (PTH) – Increases calcium levels in
extracellular fluids
 Monitor calcium levels in blood (like thyroid C cells)
– When calcium levels fall below normal, PTH is release
– Causes increase in calcium levels.

Calcium homeostasis: normal blood calcium range is (8.5-11) mg/dL
Effects of parathyroid hormone on peripheral Tissues:
Disorders f the parathyroid glands

 Hyperparathyroidism : fatigue , muscular weakness , painful joints, altered
mental functions, depression, weight loss, bone weakening , increased PTH
secretion over stimulates osteoclasts.
cause : Tumor
Treatment : Remove Tumor , correct bone deformities .
 Hypoparathyroidism : muscle cramps and seizures . Decreased PTH secretion
reduces osteoclast activity , diminishing blood calcium ion concentration .
cause : inadvertent surgical removal; injury .
Treatment : calcium salt injections , massive doses of vitamin D.
Adrenal gland
The adrenal glands are endocrine glands located just above the kidneys. and produce a
variety of hormones including adrenaline and the steroids aldosterone and cortisol. Each
gland has an outer cortex which produces steroid hormones and an inner medulla.
Chromaffin cells, also pheochromocytes, are neuroendocrine cells found mostly in the
medulla of the adrenal glands in mammals. Serve a variety of functions such as serving
as a response to stress, monitoring carbon dioxide and oxygen concentrations in the
body, maintenance of respiration and the regulation of blood pressure.
1. Adrenal Cortex
outer portion of the adrenal gland which is attached to the superior surface of the
kidney.
Divided into 3 regions, from outside to inside : Zona glomerulosa, Zona
fasciculate , and Zona reticularis.
Secretes over 30 steroid-based substances and several steroid hormones, all

crucial for normal homeostasis .
Zona glomerulosa secretes mineralocorticoids which help regulate the levels of
minerals such as sodium, potassium, and magnesium. Aldosterone is the most
important hormone in this group, where it raises blood levels of sodium and
water, and lowers blood potassium level.
Zona fasciculate secretes glucocorticoids which affect glucose or carbohydrate
metabolism. Cortisol is the most important hormone in this group, where it is
involved in carbohydrate, lipid and protein metabolism , and also helps fight
stress and inflammation . [Hyposecretion causes Addison‘s disease , and
hypersecretion causes Cushing‘s syndrome].
Zona reticularis secretes gonadocorticoids which supplement sex hormones from
the testes and ovaries and stimulate early development of reproductive organs.
These hormones are male types (adrenal androgens), namely testosterone , but can
be converted into female types, such as estrogens, by the skin , liver, and adipose
tissues[Hyposecretion causes congenital adrenal hyperplasia, and hypersecretion
causes gynecomastia in male].
2. Adrenal Medulla
inner portion of the adrenal gland.
Made of modified nerve tissue that is under direct regulation of sympathetic nerves
of the autonomic nervous system.
Contains glandular cells called chromaffin cells which secrete 2 closely related
hormones -- Epinephrine (or adrenaline) and Norepinephrine (or noradrenaline).
Effects of these hormones resemble sympathetic stimulation, where body activities
such as cardiac actions, blood pressure , and breathing rate are increased , while
digestive processes are decreased. [No known effects are due to hyposecretion of
these, but hypersecretion can caused hypertension, increased blood glucose level ,
and high heart rate].
They are in close proximity to pre-synaptic sympathetic ganglia of the sympathetic
nervous system which releases aceylcholine which further excites post-synaptic
sympathetic neurons/ chromaffin cells and releases the neurotransmitter
noradrenaline (also called norepinephrine). The action of noradrenaline on a
particular gland or muscle in excitatory is some cases, inhibitory in others.
Once a sensory input is received, the stress response may take either or both of two
forms, which act via different systems one acting quickly (within seconds) via
sympathetic nervous impulses and the monoamines adrenaline and noradrenaline,
and the second acting more slowly (within minutes or hours) via corticosteroids.
The stress system. Processing and coping with stressful situations requires the
engagement of complex mechanisms that integrate brain and body. The response to
stressful stimuli is articulated by a wide diversity of brain structures that collectively
are able to detect or interpret events as either real or potential threats (stressors). The
perception of these events as stressors involves different networks depending whether
it is a physical or psychological stressor. The identification of a stressor leads to
activation of two major constituents of the stress system and the release of its final
mediating molecules. The sympathetic-adreno-medullar (SAM) axis, secretes
noradrenaline and norepinephrine and the hypothalamus-pituitary-adrenal (HPA)
axis{describes the interaction between the hypothalamus, pituitary gland, and adrenal
glands}, secretes glucocorticoids .
Once these axes are activated in response to a given stressor, they will generate a
coordinated response that starts within seconds and might last for days, providing
quick responses enabling both, an appropriated strategy, almost immediately, and
homeostasis restoration. To accomplish this, the stress response systemically
promotes energy mobilization, metabolic changes, activation of the immune system
and suppression of the digestive and reproductive systems. More specifically in the
brain, the stress response induces short- and long-term effects through non-genomic,
genomic and epigenetic mechanisms. These central effects, combined with
proinflammatory signaling, lead to alterations in cellular excitability as well as
synaptic and neuronal plasticity. Collectively, these body-brain effects mediate
alterations in physiology and behavior that enable adaptation and survival.
Addison's disease
The overwhelming majority of cases of Addison's disease (hypoadrenocorticism) are

due to a primary failure of the adrenals. While a deficiency of sex hormones aren't
often clinically significant in our patients, a deficiency of aldosterone, the product of
the zona glomerulosa, and cortisol, a product of the zona fasciculata, can be
significant and life threatening. In the absence of aldosterone, sodium and potassium
become disregulated, causing hyponatremia and hyperkalemia. In addition to the
direct life threatening effects of these electrolyte disorders, volume depletion
associated the electrolyte imbalances can cause hypovolemic shock. Absence of
cortisol can initially be more subtle: causing malaise, inappetance, and failure to
thrive. However, with prolonged cortisol deficiency and stress, weakness, significant
gastrointestinal ulceration, and anorexia can result.
Cushing's syndrome
Cushing's syndrome is the opposite of Addison's: it is an excess of cortisol. However,

other levels of the adrenal cortex are usually not significantly affected, therefore,
electrolytes are normal. The excess cortisol is either the result of a functional adrenal
tumor (primary Cushing's) or a functional pituitary tumor (secondary Cushing's:
pituitaty dependant, or PDH) resulting in an excess of ACTH. This causes bilateral
adrenal enlargement in contrast to primary Cushing's syndrome, when only the
affected adrenal is enlarged.
Pancreas
 The only gland that is both exocrine and endocrine in physiology.

 In its exocrine aspect, 99% of its mass is composed of cells called acini which
secrete digestive enzymes and fluids into the small intestine through the pancreatic
ducts.
 In its endocrine aspect, 1% of its mass is little groups of cells called islets of
langerhans (or pancreatic islets) which secrete hormones to regulate blood glucose
level.
 in each pancreatic islet , alpha cells (α cells) secrete glucagons to raise blood
glucose level.
 beta cells (β cells) secrete insulin to lower blood glucose level. [Hyposecretion
causes diabetes mellitus where excessive glucose is present in urine, and
hypersecretion causes hyperinsulinism].
 delta cells (δ cells) secrete somatostation or growth hormone inhibiting hormone
(GHIH) which helps regulate carbohydrate metabolism by inhibiting the secretion
of glucagons.
 Regulation of blood glucose

1- Insulin is produced in the beta cells of the Islets of Langerhans. Its primary purpose
to lower blood glucose levels; in fact, insulin is the only blood sugar-lowering
hormone in the body. To this end, insulin promotes the formation of storage forms of
energy (e.g., glycogen, proteins, and lipids) and suppresses the breakdown of those
stored nutrients. Accordingly, the target organs of insulin are primarily those that are
specialized for energy storage, such as the liver, muscles, and adipose tissue.
Specifically, insulin has the following metabolic effects:
Promotes glucose uptake into cells and its conversion into glycogen, stimulates
the breakdown of glucose, and inhibits gluconeogenesis
Stimulates the transport of amino acids into cells and protein synthesis in
muscle cells, thereby lowering the levels of amino acids available for
gluconeogenesis in the liver
Increases fat synthesis in the liver and adipose tissue, thereby lowering the
levels of glycerol, which also can serve as a starting material for
gluconeogenesis.
The release of insulin is controlled by various factors, including blood glucose levels;
other islet hormones (e.g., glucagon); and, indirectly, other hormones that alter blood
glucose levels (e.g., GH, glucocorticoids, and thyroid hormone).
2- The second blood-sugar–regulating pancreatic hormone is glucagon, which is

produced in the alpha cells of the Islets of Langerhans. Glucagon increases blood
glucose levels; accordingly, its main actions generally are opposite to those of
insulin. For example, glucagon increases glycogen breakdown and gluconeogenesis
in the liver as well as the breakdown of lipids and proteins.
The release of glucagon is regulated by many of the same factors as is insulin‘s
release, but sometimes with the opposite effect. Thus, an increase in blood glucose
levels stimulates insulin release but inhibits glucagon release. A finely tuned balance
between the activities of insulin and glucagon is essential for maintaining blood sugar
levels. Accordingly, disturbances of that balance, such as an insulin deficiency or an
inability of the body to respond adequately to insulin, result in serious disorders, such
as diabetes mellitus.
Ovary
The female sex organ that also serves as an endocrine gland.
Contains follicular cells in its secondary and mature follicles, where they secrete
Estrogen to develop and maintain female sexual characteristics, to regulate ovarian
and menstrual cycles, to maintain pregnancy, and to develop secondary sexual
characteristics. [Both hyposecretion and hypersecretion will have broad effects in
female reproduction].
Also contains degenerating scar tissue called corpus luteum which contain lutein
cells that secrete Progesterone to help maintain ovarian and menstrual cycles, and
pregnancy. [Discorders are similar to those for estrogens].
Testis
 The male sex organ that also serves as an endocrine gland.
 Contains interstital cells (or leydig‘s cells) that secrete testosterone to develop
secondary sexual characteristics. [Both hyposecretion and hypersecretion and will
have broad effects in male reproduction].
The hypothalamic–pituitary–gonadal axis (HPG) axis

The hypothalamic–pituitary–gonadal axis (HPG axis, also known as the
hypothalamic–pituitary–ovarian/testicular axis) refers to the hypothalamus, pituitary
gland, and gonadal glands as if these individual endocrine glands were a single entity.
Because these glands often act in concert, physiologists and endocrinologists find it
convenient and descriptive to speak of them as a single system.
The HPG axis plays a critical part in the development and regulation of a number of
the body's systems, such as the reproductive and immune systems. Fluctuations in
this axis cause changes in the hormones produced by each gland and have various
local and systemic effects on the body.
The axis controls development, reproduction, and aging in human. Gonadotropin-

releasing hormone (GnRH) is secreted from the hypothalamus by GnRH-expressing
neurons. The anterior portion of the pituitary gland produces luteinizing hormone
(LH) and follicle-stimulating hormone (FSH), and the gonads produce estrogen and
testosterone.
The End…
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Endocrine System

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Endocrine System

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TUCOM-3rd ENDOCRINE SYSTEM Dr.

Zainab Samir Yahya

Hormone: organic compound produced in animal bodies to regulate activity and

Mechanisms of Intercellular Communication

1. Classification by chemical nature of hormones

Hormones Source Example

These are conjugated protein luteinizing hormones,

2. Classification by, mechanism of action

i. Secondary messenger is cAMP: eg. Adrenocorticotropic hormone, FSH, LH,

iii. Secondary messenger is phosphotidylinocitol/calcium or both:

Some hormones activate transmembrane receptors that activate the

Table-1: Hormones That Use the Phospholipase C Second Messenger System

Angiotensin II (vascular smooth muscle)

3. Nature of hormones action

Five major functions of hormones

Actions of steroid hormones

Action of protein hormones

1- A protein hormone is transported in the blood or lymph by itself, without a transporter .

Polypeptide and Protein Hormones Are Stored in

In many cases, the stimulus for exocytosis is an increase in cytosolic calcium

Amine Hormones Are Derived from Tyrosine

Transport of Hormones in the Blood

Water-soluble hormones (peptides and catecholamines) are dissolved in the plasma

The relatively large amounts of hormones bound to proteins serve as reservoirs,

Onset of Hormone Secretion After a Stimulus,and Duration

Feedback Control of Hormone Secretion

An important example of a negative feedback loop is seen in control of thyroid hormone

• Neurons in the hypothalamus secrete thyroid releasing hormone (TRH), which

• When blood concentrations of thyroid hormones increase above a certain threshold,

Cyclical Variations Occur in Hormone Release

Clearance of Hormones from the Blood

Hormones are cleared from the plasma in several ways, including

(1) metabolic destruction by the tissues.

(2) binding with the tissues.

(3) excretion by the liver into the bile.

(4) excretion by the kidneys into the urine.

Mechanisms of Action of Hormones

The Number and Sensitivity of Hormone Receptors Are Regulated

Some hormones cause up-regulation of receptors and intracellular signaling proteins;

Different endocrine glands with cell arrangement:-

stimulates melanocytes in the epidermis MSH

Pars tuberalis Narrow sleeve of basophilc cells around The specific

stimulates water reabsorption in kidney vasopressin

Infundibulum Nerve fibers (traveling from ----------

Principal cells\ promote normal T3 and T4

Parafollicular cell| lower blood calcium Thyrocalcitonin

11- Ovary develop and maintain female sexual Estrogen

The inflammatory response is thought Interleukins (1β, 6,

elicit inhibitory effects on myocardial Protease Inhibitor

Chen et al. demonstrated that Ang-II Angiotensin-II

14-Adipose tissue cytokines (cell signaling proteins) -Leptin

15-skeletal muscle fibers) in Receptors for myokines are found on -Myostatin

are secreted into Adropin

Hypothalamus and Pituitary Gland

 The hormones produced in the hypothalamus are termed inhibiting or releasing

 Secretion of the hypothalamic releasing and inhibiting hormones is determined by

 The pituitary gland is a small pea-shaped organ measuring about 1-1.5 cm in

 The anterior pituitary, also called adenohypophysis, is composed of epithelial cell.

 Adenohypophysis - based on grouping of all regions composed of glandular tissue

 Neurohypophysis - based on grouping of all regions composed of neural or

 The secretion of the anterior pituitary is influenced by the releasing hormone

 The posterior pituitary is composed of neural tissue, which is triggered by an action