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Endocrine System: Hormones & Functions

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Topics covered

  • positive feedback,
  • feedback mechanisms,
  • pituitary gland,
  • nervous system,
  • hormonal sensitivity,
  • hormonal synthesis,
  • chemical communication,
  • hormones,
  • endocrine system,
  • hormonal modulation
0% found this document useful (0 votes)
18 views22 pages

Endocrine System: Hormones & Functions

Uploaded by

Maersk Mckinney
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Topics covered

  • positive feedback,
  • feedback mechanisms,
  • pituitary gland,
  • nervous system,
  • hormonal sensitivity,
  • hormonal synthesis,
  • chemical communication,
  • hormones,
  • endocrine system,
  • hormonal modulation

Chapter 17: Functional Organization of the Characteristics of the endocrine system.

Endocrine System
 Composed of endocrine glands that secrete
Lecture Outline chemical messengers (hormones) into
 The endocrine system is one of the two circulatory system to their target tissues
major control systems of the body. (effectors) where they stimulate a specific
 Lipid-soluble hormones, such as steroid response.
hormones and thyroid hormones (a), as well  Works closely with the nervous system to
as water-soluble hormones, such as insulin achieve and maintain homeostasis.
and glucagon (b), control almost every
aspect of human physiology Comparison of the Nervous and Endocrine
Systems

Similarities
 Both systems have shared brain structures,
specifically the hypothalamus.
 May use same chemical messenger as
neurotransmitter and hormone.
 Two systems are cooperative to regulate
17.1 principles of chemical Communication
body processes.
 Neurotransmitters and hormones can affect
their targets through G protein-coupled
receptors.
Differences.
 Mode of transport.
 Speed of response.
 Duration of response.
 Modulation of signal intensity.

Signaling in Endocrine and Nervous System

(a) Amplitude - modulated system


The concentration of the hormones
determines the strength of the signal and the
magnitude of the response.
Classes of Chemical Messengers
 Autocrine chemical messengers
 Paracrine chemical messengers
Neurotransmitter
 Endocrine chemical messengers

Hormones

(b) Frequency - modulated system


The strength of the signal depends on
the frequency, not the size, of the action
potentials.

 The hormone needs to attach to its


receptor in order for the target cell to
react to it.
 Target Specificity Hormones bind
(physically connect) to receptor
Overview of Endocrine - Regulated Processes
proteins.

 Growth and development


 Metabolism
 Blood composition
 Reproduction
Control of Hormone Secretion

Humoral Stimuli
Some hormones are released when the
blood levels of certain chemicals change.

Neural Stimuli
Following an action potential, a neuron
releases a neurotransmitter into a synapse with
a hormone-producing cell that then secretes its
hormone.

Hormonal stimuli
Certain hormones are secreted in
response to another hormone.

Patterns of Hormone Secretion

Chronic hormone secretion.


 Maintenance of relatively constant
concentration of hormone.

Acute hormone secretion.


 Concentration changes suddenly and
irregularly.

Episodic hormone secretion.


 Secreted in a fairly predictable pattern.
Classes of Hormones 1 Regulation of Hormone Levels in the Blood

Lipid-soluble.
 Nonpolar, including steroids, amino acid
derivatives, thyroid hormone, and fatty acid
derivatives.

Negative feedback
 Most popular regulatory system. The
hormone itself inhibits the release of
hormones; self-limiting.
Water-soluble.
Positive feedback
 Polar, including proteins, peptides, and
 The hormone itself stimulates the release
amino acid derivatives.
of the hormone; this process is self-
perpetuating.
Negative Feedback by Hormones

 The anterior pituitary gland secretes a


tropic hormone
 The hormone from the target endocrine
cell travels to its target.
 The hormone from the target endocrine
cell also has a negative-feedback effect on
17.3 Transport and Metabolism of Hormones the anterior pituitary and hypothalamus
Effect of Binding Proteins and decreases secretion of the tropic
 Many hormones would be broken down hormone.
shortly after entering the bloodstream
because of the hydrolytic enzymes present
in the blood.
Positive Feedback by Hormones  Without binding proteins, lipid-soluble
hormones would quickly diffuse out of
 The anterior pituitary gland secretes a capillaries and be degraded by enzymes of
tropic hormone, which travels in the blood the liver or lungs or be filtered out by the
to the target endocrine cell. kidneys and unable to effectively regulate
 The hormone from the target endocrine their targets.
cell travels to its target.  Conjugation
 The hormone from the target endocrine  Water-soluble hormones are broken down
cell also has a positive-feedback effect on by enzymes called proteases in the
the anterior pituitary and increases bloodstream and the products removed by
secretion of the tropic hormone. the kidneys.

17.4 Hormone Receptors and Mechanisms of


Action

Half-Life of Hormones

 Hormone concentrations are stable in the


bloodstream, though some hormones are
more stable than others.
 Larger, more complex hormones are more
stable than smaller, simpler hormones.
 Half-life

Target Tissue Specificity and Response

 Portion of receptor molecule where


hormone binds is called binding site.
 Hormone/receptor site is specific
 The purpose of binding to target tissue is to
elicit a response by the target cell.
Elimination of Hormones from the
Bloodstream

 All hormones are destroyed either in


circulation or by enzymes at their target
cells.
Agonists and Antagonists  Large proteins, glycoproteins, polypeptides;
 Agonist – a drug with similar structure of a smaller molecules like epinephrine and
specific hormone that can bind to a norepinephrine.
hormone receptor and activate it.
 Antagonist – a drug that can bind to a
hormone receptor and inhibit its action.

Action of Nuclear Receptors 1

 After lipid-soluble hormones enter their


target cell they bind to their receptors.
Classes of Receptors 1
 Lipid-soluble hormones either bind to
Lipid-soluble hormones. cytoplasmic receptors and travel to the
 Bind to nuclear receptors. nucleus or bind to nuclear receptors.
 Lipid soluble and relatively small molecules
 React either with enzymes in the cytoplasm  Receptors that bind to DNA have fingerlike
or with DNA to cause transcription and projections that recognize and bind to
translation. specific nucleotide sequences in the DNA
 Thyroid hormones, testosterone, estrogen, called hormone-response elements. The
progesterone, aldosterone, and cortisol. combination of the hormone and its
receptor forms a transcription factor.

Classes of Receptors 2
Water-soluble hormones.
 Bind to membrane-bound receptors:
integral proteins with receptor site at
extracellular surface. ACTION OF NUCLEAR RECEPTORS 2
 Water-soluble or large-molecular-weight
hormones.  When the hormone-receptor complex
binds to the hormone-response element, it
regulates the transcription of specific binds to its membrane receptor that is
messenger RNA (mRNA) molecules. coupled to a 3 unit G protein that produces
 Newly formed mRNA molecules move to second messenger molecules when
the cytoplasm of the cell, and bind to activated.
ribosomes to be translated into specific
proteins.
 The new proteins produce the cell’s
response to the lipid-soluble hormone.

Common Second Messengers

Action of Membrane-Bound Receptors and


Signal Amplification

Types of membrane-bound receptors:


 Ligand-gated ion channels (covered in Chs. G Protein Structure and Function
9 & 11) subunits:
 G protein-coupled receptors
 Enzymatic receptors  Alpha (α) – type of α subunit determines
the specific cellular response.
 Beta (β) and gamma (γ) subunits
 Alpha subunit deactivated by GTPase by
removing a phosphate from the G T P and
the α subunit rejoins the β and γ subunits.

G Protein-Coupled Receptors
 GTP-binding proteins that allow for
transduction of an extracellular signal into
an intracellular signal through the use of
second messengers.

 In a second-messenger system, the


hormone is the first messenger, which
Activation of G Protein-Coupled Receptor G Protein-Coupled Receptors 2

 Inactive state, a GDP is bound to the α Alpha subunits that decrease cAMP
subunit and the three subunits form a
complex of G αβγ.  Activation inhibits adenylate cyclase which
results in a decrease in available cAMP.
 When activated by the hormone binding to  Phosphodiesterase breaks down the cA M
the receptor, the G D P on the α subunit is P that is available, further reducing the
replaced by G T P and the α subunit cAMP.
separates from the β and γ subunits. Each  Process used by epinephrine and
group can continue its role in cell prostaglandins.
regulation.

G Protein-Coupled Receptors 1

Αlpha subunits that increase cAMP

 Activation of adenylate cyclase converts


ATP to cAMP, a second messenger.
G Protein-Coupled Receptors 3
 cAMP binds to protein kinases, leading to
phosphorylation of other molecules,
affecting enzyme activity.

 Phosphodiesterase breaks down cAMP to


AMP; this pathway is used by hormones
like glucagon, epinephrine, ADH, LH, and
FSH.

Enzymatic Receptors 1

Guanylate Cyclase Receptors


 cGMP, a second messenger, is synthesized
in response to a hormone binding to a
membrane-bound receptor.
 Activates the enzyme, guanylate cyclase
that converts GTP to cGMP.
 cGMP activates specific enzymes as the
cell’s response.

Enzymatic Receptors 2

Receptor Tyrosine Kinases

 Insulin receptor is a receptor tyrosine


kinase of four subunits.

Decrease in Receptor Number

 Normally, receptor molecules are degraded


and replaced on a regular basis.
 Down-regulation - desensitization
 Rate at which receptors are synthesized
decreases in some cells after the cells are
exposed to a hormone.
 Combination of hormones and receptors
can increase the rate at which receptor
molecules are degraded.

Signal Amplification

 The rate and magnitude of a hormone’s


response are determined by the Increase in Receptor Number
mechanism of action at the receptor.
Up-Regulation
 Nuclear receptors activate protein
synthesis which can take several hours.  Some stimulus causes increase in synthesis
of receptors for a hormone, thus increases
 Hormones that use second messenger, sensitivity to that hormone.
respond quickly and with a greater
magnitude.
 For example, FSH stimulation of the ovary Synergistic Interactions
causes an increase of LH receptors. Ovarian
cells are now more sensitive to LH, even if  Two or more hormones exert their effects
the concentration of LH does not change. on a target tissue to greatly increase the
This causes ovulation. response.

 Reproductive hormones act synergistically


with hypothalamic hormones to promote
synthesis of gonad-regulating tropic
hormones.

Hormone Interactions

Permissive Interactions Antagonistic Interactions


 Some hormones assist other hormones to
have a stronger response.  Some hormones work in the opposite way
from another to tightly regulate a response.
 Thyroid hormone promotes synthesis of
receptors for epinephrine in the heart.  Calcitonin and PTH regulate Ca^2+ blood
levels.

 Insulin and glucagon regulate blood


glucose levels.
Chapter 18: Endocrine Glands

Endocrine System
- consists of glands and cells that secrete
hormones into the blood.  Location: Below hypothalamus, connected
by infundibulum
Functions of endocrine system include:  Size: Pea-sized
 Placement: Sella turcica of sphenoid bone
 Regulation of metabolism – control rate of  Lobes:
nutrient utilization. -Prosterior (Neurohypophysis)
 Control of food intake and digestion – -Anterior (Adenohypophysis)
regulation of the level of satiation and the
breakdown of food into individual nutrients.
 Modulation of tissue development –
regulation of the development of tissues.
 Ion regulation – monitoring of blood pH
 Control of the water balance – regulation
of water balance
 Changes in heart rate and blood pressure
– regulation of the heart rate and blood
pressure
Anterior Pituitary
 Control of blood glucose and other
nutrients – regulation of glucose and other
nutrients in the blood.  Origin: Glandular epithelium
 Control of reproductive functions – control (adenohypophysis), from Rathke's pouch.
of the development.  Connection: Joins posterior pituitary at pars
 Uterine contractions and milk release - intermedia.
stimulation of uterine contractions during  Hypothalamic releasing/inhibiting
delivery and stimulation of milk release. hormones control anterior pituitary via
 Modulation of immune system function – hypothalamohypophysial portal system.
control of the production of immune cells.
Superior Pituitary
18.2 Pituitary Gland and Hypothalamus
 Origin: Hypothalamic outgrowth.
 Tissue: Nervous (neurohypophysis).
 Hormones: Neuropeptides.
 Hypothalamus produces hormones, stored
and released by posterior pituitary via
hypothalamohypophysial tract.

Relationship of the Pituitary Gland to the Brain:


The Hypothalamus
 Where nervous and endocrine systems
interact.
 Hypothalamus regulates secretions of
anterior pituitary.
 Posterior pituitary-extension of the
hypothalamus.
 Anterior pituitary produces nine major
hormones that regulate body functions.

Structure of the Pituitary Gland


Hypothalamic control of posterior pituitary:

 Hormones produced in neurons in


hypothalamus
 Axons form hypothalamohypophysial tract.
 Action potentials in these neurons cause Hormones of the Hypothalamus
hormone release.

Hypothalamic control of anterior pituitary:

 Blood vessels make up


hypothalamohypophysial portal system,
connect the areas.
 Hypothalamic releasing and inhibiting
hormones stimulate or inhibit anterior
pituitary hormone release.

Secretion of Posterior Pituitary Hormones

1. Stimulation of neurons within the Posterior Pituitary Hormones


hypothalamus controls the secretion of PPH
2. Action potentials are conducted by axons of  Antidiuretic hormone (A D H).
the hypothalamic neurons through the - Also called vasopressin.
hypothalamohypophysial tract. - regulates water balance. Increased
3. Action potentials cause the release of electrolyte concentration or decreased
hormones from axon terminals into the blood pressure stimulates ADH release,
circulatory system. which increases water reabsorption in
4. The hormones pass through the circulatory the kidneys.
system and influence the activity of their  Osmoreceptors - sense changes in the
target tissues. osmotic pressure of blood
 Baroreceptors- monitor blood pressure
Hypothalamic Control of the Anterior Pituitary  Oxytocin- known for its role in childbirth
and lactation

Control of Antidiuretic Hormone (A D H) Secretion

 Detection: Osmoreceptors and


baroreceptors detect changes in blood
osmolality and pressure.
 Signal: Increased osmolality and decreased
pressure stimulate ADH-secreting neurons
 Transport: Action potentials travel to the
posterior pituitary.
 Release: ADH is released into the
 Neuropeptide Production: Neurons in the bloodstream.
hypothalamus produce releasing and  Kidney Action: ADH increases water
inhibiting hormones. reabsorption in the kidneys, leading to
 Portal System Transport: These hormones reduced urine volume and increased urine
are transported through the osmolality.
hypothalamohypophysial portal system to the
anterior pituitary. Control of Oxytocin Secretion
 Binding to Receptors: The hormones bind
to receptors on anterior pituitary cells.
 Anterior Pituitary Hormone Release: In
response to releasing hormones, the anterior
pituitary releases its own hormones into the
bloodstream
 Stretch of the uterus and the uterine cervix release of GH, while GHIH inhibits it.
stimulates oxytocin secretion.  Target Tissues: GH acts on target tissues,
 Action potentials are conducted by sensory including bone, muscle, and liver.
neurons.
 Action potentials are conducted by axons of
oxytocin-secreting neurons, where they Control Mechanisms of Growth Hormone:
increase oxytocin secretion.
 Oxytocin enters the circulation increasing  Stress and Low Blood Glucose: Increase
contractions of the uterus and milk GHRH release, leading to increased GH
letdown from the lactating breast. secretion.
 Circadian Rhythms: GH secretion follows a
Anterior Pituitary Hormone daily pattern, with peaks during sleep.
 Negative Feedback: Increased GH and
 Many are tropic hormones, which stimulate insulin-like growth factors (IGFs) inhibit
the secretion of other hormones from target GHRH release and stimulate GHIH release,
tissues. creating a feedback loop.
Includes:
 Growth hormone (GH) or somatotropin. Direct and Indirect Effects of GH:
 Prolactin
 Adrenocorticotropic hormone (ACTH).  Direct: GH binds to receptors on cells,
 Lipotropins. causing changes within the cells.
 Beta endorphins.  Indirect: GH stimulates the liver and skeletal
 Melanocyte-stimulating hormone (MSH). muscle to produce IGFs, which then promote
 Luteinizing hormone (LH). growth and development.
 Follicle-stimulating hormone (FSH).
 Thyroid-stimulating hormone (TSH).

Growth Hormone

 Stimulates uptake of amino acids; protein


synthesis.
 Stimulates breakdown of fats to be used as
an energy source and to promote growth and
protein synthesis.
 Stimulates synthesis of glycogen: glucose
sparing.
 Promotes bone and cartilage growth.
 Regulates blood levels of nutrients after a
meal and during periods of fasting. Growth Hormone and Growth Disorders
 GH Function: GH promotes growth and
development, particularly in bone and  GH's Direct Effect: GH stimulates
muscle. It also regulates blood nutrient levels gluconeogenesis, leading to the production
after meals and during fasting. of insulin-like growth factors (IGFs).
 GH Secretion Pathway:  IGFs' Role: IGFs stimulate growth in bone
 Hypothalamus: Releases growth hormone- and muscle, promoting bone length and
releasing hormone (GHRH) and growth muscle protein synthesis.
hormone-inhibiting hormone (GHIH).  Negative Feedback: GH and IGFs have a
 Anterior Pituitary: GHRH stimulates the negative feedback effect on the
hypothalamus, regulating their own secretion.

Growth Hormone Disorders:


 Hyposecretion: Leads to pituitary dwarfism increased Ca2+ concentration in cells of the
in children, characterized by short stature thyroid gland and ultimately stimulates the
with normal bone shapes and intelligence. production of T3 and T4.
 The production of TSH is regulated by TRH
 Hypersecretion: Causes gigantism in from the hypothalamus and negative
children and acromegaly in adults, resulting feedback from T3 and T4.
in excessive bone growth and other
complications.

Prolactin

 Prolactin's Function: Prolactin stimulates


milk production, enhances progesterone
secretion by the ovaries, and contributes to
regulating ion composition of blood, growth,
development, behavior, metabolism, and
immune function.
 Prolactin Secretion Regulation: Prolactin- This image is a textbook page about the
releasing hormone (PRH) stimulates
prolactin release, while prolactin-inhibiting
hormone (PIH) or dopamine inhibits it.
 Prolactin's Mechanism: Prolactin binds to
membrane-bound receptors, activating a
kinase that phosphorylates intracellular
proteins and triggers a cellular response.

Adrenocorticotropic Hormone (ACTH).

 ACTH: is a hormone produced by the


anterior pituitary gland.
 CRH (Corticotropin-releasing hormone): is
released from the hypothalamus and
stimulates the release of ACTH from the
anterior pituitary gland.
 ACTH: stimulates the adrenal cortex to
Thyroid-Stimulating Hormone (TSH) produce cortisol.
 Cortisol: is a glucocorticoid that helps
 TSH is a glycoprotein hormone that regulate stress and blood sugar levels.
stimulates the thyroid gland to produce and  Environmental stress: is a key stimulus for
release thyroid hormones T3 and T4. ACTH secretion.
 TSH receptors are located on the thyroid
gland and activate a signaling pathway that
increases intracellular cAMP levels, leading
to increased activity of phospholipase, which
opens Ca2+ channels. This results in
Thyroid gland.

 The thyroid gland is one of the largest


endocrine glands.
 It is highly vascular and stores hormones.
 The thyroid gland is composed of follicles,
which are made up of follicular cells that
surround thyroglobulin/thyroid hormones.
 Between the follicles are parafollicular cells.
 Follicular cells secrete thyroglobulin into
the lumen of the follicle.
 Iodine is necessary for the production of T3
and T4 hormones.
 Parafollicular cells secrete calcitonin,
ACTH and related substances. which reduces Ca2+ in body fluids when Ca
levels are elevated.
 ACTH, MSH, endorphins, and lipotropins:
are all derived from the same large precursor
molecule called pro-opiomelanocortin
(POMC).
 Lipotropins: cause adipose cells to
catabolize fat.
 β-endorphins: act as an analgesic and are
produced during times of stress and exercise.
 MSH: causes melanocytes to produce more
melanin.

LH
and FSH.

 LH and FSH are glycoprotein hormones that


promote growth and function of the gonads.
 LH is luteinizing hormone, and FSH is
follicle-stimulating hormone.
 LH and FSH regulate the production of
gametes and reproductive hormones:
 Testosterone in males. Biosynthesis of Thyroid Hormones
 Estrogen and progesterone in females. Step 1: Iodide ions (I-) are actively transported into
thyroid follicle cells by a sodium-iodide symporter
(NIS).

Step 2: Thyroglobulin, containing tyrosine molecules,


is synthesized within the follicular cells.

Step 3: Iodide ions are oxidized to form iodine (I) and


attached to tyrosine molecules within thyroglobulin.
Step 4: Iodinated tyrosine molecules are formed, through a feedback loop, maintaining normal
either monoiodotyrosine (MIT) or diiodotyrosine (DIT). metabolism.

Step 5: Thyroid hormones T3 and T4 are synthesized Calcitonin


within the follicular lumen. T3 and T4 are stored
within the thyroid follicles, providing a reserve for 2-3 - Calcitonin, made by thyroid C cells, lowers
months. blood calcium by stopping bone breakdown
and increasing calcium excretion in urine.

Abnormal Thyroid Conditions

1. Hypothyroidism

- Hypothyroidism is a condition where the


thyroid gland is underactive and
produces insufficient thyroid hormones.
Symptoms include fatigue, weight gain,
and cold intolerance, often caused by
Hashimoto’s thyroiditis, iodine deficiency,
or thyroid surgery.

2. Hyperthyroidism

- Hyperthyroidism occurs when the


thyroid gland is overactive and produces
excess hormones, speeding up the
body’s metabolism. Symptoms include
weight loss, rapid heartbeat, and anxiety,
and it can be caused by Graves’ disease,
thyroid nodules, or thyroiditis.

3. Goiter
Thyroid Hormones
- A goiter is the abnormal enlargement of
- T3 and T4 hormones from the thyroid control the thyroid gland, sometimes causing
metabolism and energy use. T4 is more visible neck swelling. It may lead to
abundant, but T3 is more potent and active difficulty swallowing or breathing and
in cells. often results from iodine deficiency,
autoimmune diseases, or nodules.
Effects of T3 and T4

- These hormones regulate energy production,


body temperature, and support growth. They 4. Thyroid Nodules
help the body use glucose, fats, and proteins
- Thyroid nodules are lumps in the
for energy.
thyroid gland, which can be benign or
Effects of Hyposecretion and Hypersecretion malignant. Often asymptomatic, they
may cause difficulty swallowing if large
- Low thyroid hormones (hyposecretion) cause and are typically caused by hormonal
fatigue, weight gain, and cold intolerance. changes, iodine deficiency, or thyroid
Excess thyroid hormones (hypersecretion) cancer.
lead to weight loss, anxiety, and heat
sensitivity.

Regulation of Thyroid Hormone Secretion 5. Thyroiditis

- The hypothalamus, pituitary, and thyroid - Thyroiditis is the inflammation of the


work together to balance T3 and T4 levels thyroid gland, leading to either
temporary hyperthyroidism or
hypothyroidism. Symptoms include
thyroid pain, fatigue, and weight
changes, caused by autoimmune
disorders, infections, or postpartum
hormonal shifts.

Parathyroid Glands

Location: Four small glands located behind


the thyroid gland in the neck.

Function: Regulate calcium levels in the


blood and maintain bone health.

Hormone Produced: Parathyroid hormone


(PTH), which increases blood calcium levels.

Importance: Essential for maintaining stable


calcium and phosphorus levels in the body,
which are crucial for various bodily functions,
including muscle contraction and nerve
signaling.

Causes and Symptoms of Hyposecretion and


Hypersecretion of PTH

 Hypoparathyroidism

Cause: Accidental removal of the parathyroid


glands during a thyroidectomy.

Functions of Parathyroid Hormone (PTH) Symptoms:

 Increases Blood Calcium Levels: Raises - Hypocalcemia


calcium concentration in the bloodstream. - Increased neuromuscular excitability,
potentially leading to tetany,
 Stimulates Bone Resorption: Promotes the
laryngospasm, and death from
breakdown of bone tissue to release calcium.
asphyxiation.
 Enhances Intestinal Absorption: Increases
- Flaccid heart muscle, which can lead to
calcium absorption from the digestive tract
cardiac arrhythmia.
by activating vitamin D.
- Diarrhea
 Reduces Renal Excretion: Decreases the
amount of calcium excreted by the kidneys,
allowing for more calcium retention.
 Regulates Phosphorus Levels: Decreases  Hyperparathyroidism
reabsorption of phosphate in the kidneys,
helping to balance calcium and phosphorus Causes: Abnormal parathyroid function, often
levels. due to adenomas, hyperplasia, or carcinomas.
Secondary hyperparathyroidism can also occur
due to conditions that reduce blood calcium
levels.

Symptoms:

- High blood calcium levels, which can lead


to calcium deposits in the body and
weakened bones.

- Neuromuscular system less excitable,


potentially leading to muscular weakness. Hormones of the Adrenal Medulla.

- Increased force of contraction of cardiac - Hormones of the Adrenal Medulla: The


muscle, which can lead to cardiac arrest adrenal medulla secretes neuropeptides:
during contraction, and constipation. epinephrine (80%) and norepinephrine
(20%).
Adrenal Glands - Combine with adrenergic membrane-
bound receptors.
 Adrenal Glands: Also called the suprarenal
glands because they are near superior poles Alpha-adrenergic receptors with several
of kidneys; retroperitoneal. subclasses.
 Medulla: Formed from neural crest;
sympathetic. Secretes epinephrine and
norepinephrine.
 Cortex: Formed from mesoderm; consists of
three zones.

- Cause calcium channels to open, cause the


release of calcium ions from endoplasmic
reticulum by activating phospholipase
enzymes, open K+ channels, decrease
cAMP synthesis, or stimulate synthesis of
eicosanoids such as prostaglandin.

Beta-adrenergic receptors with several subtypes.

Zones of the Adrenal Cortex - All increase cAMP synthesis.

Cortex: three zones from superficial to deep. Actions of Adrenal Medulla Hormones
 Zona glomerulosa -produces Adrenal Medulla Hormones:
mineralocorticoids
 Zona fasciculate – produces - These hormones prepare the body for
glucocorticoids physical activity, but their effects are
 Zona reticularis – produces adrenal short-lived as they are rapidly
androgens metabolized.

Epinephrine:

- Increases blood glucose levels by


stimulating the breakdown of glycogen
to glucose in the liver.
- Increases breakdown of glycogen in
muscle cells, which gives glucose for
muscle use.
- Increases fat breakdown in adipose - Secreted when blood pressure is low.
tissue, releasing fatty acids into the - Increase sodium reabsorption by the
blood which can be metabolized by kidneys, leading to increased blood volume
tissues for energy. and blood pressure.
- Stimulate potassium excretion into the
Epinephrine and norepinephrine: urine.
- Increase hydrogen ion excretion into the
- Increase heart rate and force of
urine.
contraction.
- Cause blood vessels to constrict in skin,
kidneys, gastrointestinal tract, and other  Glucocorticoids (Zona fasciculata):
- Cortisol is the main hormone.
- Involved in metabolic, developmental, and
anti-inflammatory responses.
- Increase lipid breakdown, reduce glucose
and amino acid uptake in skeletal muscle,
stimulate gluconeogenesis in the liver, and
increase protein degradation.
- Increase blood glucose levels and
glycogen deposits in cells.

 Cortisol’s Roles:
- Helps tissues mature and develop.
viscera.
- Reduces inflammation and immune
response.

Regulation of Adrenal Medulla Secretion  Cortisol Secretion:


- Low blood sugar and stress trigger the
Adrenal Medulla Secretion Triggers:
release of CRH from the hypothalamus.
- Stress - CRH stimulates the pituitary to release
- Physical activity ACTH.
- Low blood glucose levels - ACTH stimulates the adrenal cortex to
release cortisol.
Mechanism: - Cortisol has a negative feedback loop,
controlling its own production.
- These triggers activate the
hypothalamus, which in turn increases  Cortisol’s Effects on Tissues:
activity in the sympathetic nervous - Affects glucose metabolism in peripheral
system. tissues.
Result: - Suppresses immune responses.
- Reduces the need for epinephrine and
- The sympathetic nervous system norepinephrine.
stimulates the adrenal medulla to
release epinephrine and norepinephrine  Adrenal Androgens (Zona reticularis):
into the bloodstream. - These are weak androgens that are
converted to testosterone by peripheral
tissues.
- They stimulate the growth of pubic and
axillary hair.
- In females, they contribute to sexual drive.

Hormones of
Adrenal Gland

Hormones of Adrenal Cortex

 Mineralocorticoids (Zona glomerulosa):


- Aldosterone is the main hormone.
Mineralocorticoids: Regulate mineral balance,  Major target tissues: liver, adipose,
mainly sodium and potassium. skeletal muscle, and satiety center of
Glucocorticoids: Affect metabolism, especially hypothalamus.
glucose levels.  Insulin – decreases blood glucose
Adrenal Androgens : Weak male hormones that  Glucagon – increases blood glucose;
influence hair growth and sexual drive. promotes release of glucose.

Cortisol - The primary stress hormone, increases


sugar, also called glucose, in the bloodstream,
enhances the brain’s use of glucose and increases
the availability of substances in the body that repair EFFECTS OF INSULIN AND GLUCAGON ON
tissues. THEIR TARGET TISSUES

Regulation of Cortisol Secretion  Skeletal Muscle, Cardiac Muscle, Cartilage,


- is mainly controlled by three intercommunicating Bone, Fibroblasts, Leukocytes, Mammary
regions of the body: Glands

 Hypothalamus in the brain Insulin Response:


 Pituitary gland
 Adrenal glands - Increases glucose uptake
- Promotes glycogen synthesis
- Increases amino acid uptake

18.6 PANCREAS Glucagon Response:

- Little effect (skeletal muscle lacks glucagon


receptors)

 Liver

Insulin Response:

Location: Along the small intestine and stomach; - Increases glycogen synthesis
retroperitoneal. - Promotes glucose use for energy (glycolysis)

Exocrine Function: Produces pancreatic digestive Glucagon Response:


juices. - Rapid glycogen breakdown (glycogenolysis)
Endocrine Function: Consists of pancreatic islets. - Releases glucose into the blood
- Stimulate glucose production
Composed of: (gluconeogenesis)
- Increase fat metabolism, makes ketones
- Alpha cells (20%); secrete glucagon
- Beta cells (75%); secrete insulin  Adipose Cells:
- Delta cells; secrete somatostatin
Insulin Response:

EFFECTS OF INSULIN AND GLUCAGON ON - Increases glucose uptake


THEIR TARGET TISSUES - Promotes glycogen, lipid, and fatty acid
synthesis
 Regulate nutrients, amino acids and - Inhibits breakdown of fats (lipase)
glucose.
Glucagon Response:
- Breaks down lipids (lipolysis) at high glycogen.
concentrations 5. Blood glucose level drops back to the normal
- Mostly inactive under normal conditions range.
6. Homeostasis is restored.
 Nervous System:

Insulin Response:

- Little effect, except for increasing glucose


uptake in the satiety center (regulates
hunger)

Glucagon Response:

- No effect

REGULATION OF PANCREATIC HORMONE


SECRETION

Insulin Secretion:

- Increased by: Hyperglycemia, certain amino


acids, parasympathetic activity, and GI
hormones.
Hormonal Regulation of Nutrient Utilization
- Decreased by: Hypoglycemia, sympathetic
activity, somatostatin, and during fasting.  After a meal, insulin levels increase and
glucagon, cortisol, GH, and epinephrine
decrease.
Glucagon Regulation:  These hormones regulate blood glucose
levels through negative feedback.
- Low blood glucose increases glucagon
release, while high levels reduces it.

- Some amino acids can also increase Hormonal Regulation During Exercise
glucagon secretion.
 During exercise, epinephrine and glucagon
increase blood glucose levels.
REGULATION OF INSULIN SECRETION
 Long-term exercise is regulated by cortisol
1. Blood glucose is within its normal range. and GH.
2. Blood glucose level increases above normal
range.  Hormones of the Reproductive System
3. The pancreas releases insulin in response to Testes produce testosterone
elevated blood glucose, along with digestive (spermatogenesis, secondary sex
hormones and parasympathetic signals. characteristics) and inhibin (inhibits FSH).
4. Tissues take in glucose when insulin binds to
them, and the liver and muscles store it as  Ovaries produce estrogen and
progesterone (sex organ development,
menstrual cycle), inhibin (inhibits FSH), and
relaxin (pelvic flexibility).

Hormones of the Pineal Gland

 Pineal gland secretes melatonin (regulates


sleep cycles, inhibits GnRH) and arginine
vasotocin (regulates reproduction in some
animals).
Regulation of Melatonin Secretion from the Pineal
Gland

 Melatonin secretion is regulated by light:


darkness increases secretion, light
decreases it.

 Melatonin influences sleep cycles and


inhibits GnRH.

Common questions

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Lipid-soluble hormones, such as steroids and thyroid hormones, are nonpolar and small, allowing them to diffuse through cell membranes and bind to nuclear receptors within target cells. This enables them to cause transcription and translation, leading to long-term changes . They require transport proteins in the bloodstream due to their solubility properties, which protects them from rapid degradation by hydrolytic enzymes . In contrast, water-soluble hormones, such as proteins and peptides, are polar and bind to membrane-bound receptors. This distinction necessitates second messenger systems for signal transduction, allowing for rapid and amplified cellular responses .

Insulin and glucagon have opposing roles in glucose homeostasis. Insulin, secreted by pancreatic beta cells, lowers blood glucose by promoting tissue glucose uptake and storage as glycogen, primarily in the liver and muscles . It also enhances lipid and protein synthesis. In contrast, glucagon, secreted by alpha cells, raises blood glucose levels by stimulating glycogen breakdown (glycogenolysis) and glucose production (gluconeogenesis) in the liver . Insulin secretion is stimulated by hyperglycemia, certain amino acids, and parasympathetic activity, while glucagon release is triggered by hypoglycemia and certain amino acids. This intricate feedback mechanism ensures that blood glucose levels remain within a narrow range, critical for cellular energy supply and overall metabolic balance .

Chronic secretion patterns involve the constant release of hormones at relatively stable levels, important for maintaining homeostatic processes such as basal metabolic rate, as seen with thyroid hormones . Acute secretion involves sudden hormone release in response to specific stimuli, critical for managing immediate physiological demands like stress responses or blood glucose regulation, as insulin is released in response to hyperglycemia . Episodic secretion is characterized by regular bursts of hormone release, often in circadian rhythms or in response to cyclic changes like the menstrual cycle, as observed with gonadotropin-releasing hormones . These varied patterns allow the endocrine system to respond adaptively to both continuous and fluctuating environmental inputs.

Lipid-soluble hormones, such as steroid hormones, can diffuse across the cell membrane and bind to intracellular receptors, either in the cytoplasm or nucleus. Once bound, the hormone-receptor complex binds to specific DNA sequences called hormone-response elements, initiating transcription of target genes and resulting in protein synthesis. This leads to long-term cellular effects . In contrast, water-soluble hormones cannot penetrate the cell membrane and bind to external membrane-bound receptors. These receptors, often coupled with G proteins, activate intracellular second messengers like cAMP, leading to rapid but short-lived cellular responses by modifying the activity of existing proteins through phosphorylation .

Hyperparathyroidism, often resulting from adenomas, leads to elevated parathyroid hormone (PTH) levels, causing hypercalcemia. This condition results in calcium deposits in soft tissues, weakened bones, reduced neuromuscular excitability, and increased cardiac contraction forces; it may lead to muscular and cardiac complications, and digestive issues like constipation . Hypoparathyroidism, frequently due to accidental gland removal, results in hypocalcemia, increasing neuromuscular excitability. Symptoms include tetany, potential airway obstruction, and unstable cardiac rhythms, posing critical clinical challenges. These conditions require careful management to prevent severe physiological consequences and ensure balanced calcium levels .

Cortisol secretion is regulated through the hypothalamic-pituitary-adrenal (HPA) axis. When stress or low blood sugar levels occur, the hypothalamus releases corticotropin-releasing hormone (CRH). CRH stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH), which then acts on the adrenal cortex to promote cortisol synthesis and secretion. As cortisol levels rise, they exert negative feedback on both the hypothalamus and pituitary, reducing the release of CRH and ACTH, thus maintaining hormone homeostasis . This layered feedback loop enables precise regulation of cortisol, ensuring adequate response to stress while preventing excessive hormone accumulation that could disrupt cellular function .

The adrenal cortex is derived from mesodermal tissue and consists of three zones that produce different types of corticosteroids: mineralocorticoids (e.g., aldosterone) from the zona glomerulosa, glucocorticoids (e.g., cortisol) from the zona fasciculata, and adrenal androgens from the zona reticularis. These hormones regulate electrolyte balance, metabolism, and secondary sexual characteristics . The adrenal medulla, formed from neural crest tissue, secretes catecholamines (epinephrine and norepinephrine) in response to sympathetic nervous system activation, primarily preparing the body for 'fight or flight' responses by increasing heart rate and blood glucose levels .

G protein-coupled receptors (GPCRs) amplify hormonal signals by activating intracellular second messengers, such as cyclic AMP (cAMP) or inositol triphosphate (IP3), which then initiate a cascade of downstream effects involving multiple proteins. For example, once a hormone binds to its GPCR and activates the associated G protein, adenylate cyclase is stimulated to convert ATP into cAMP, which activates protein kinases. These kinases phosphorylate various proteins, considerably amplifying the original signal . This amplification ensures that even low concentrations of hormones can elicit significant physiological responses, impacting processes like metabolism, growth, and cardiac function .

Hormone levels in the bloodstream are primarily regulated by negative and positive feedback mechanisms. Negative feedback involves the hormone itself inhibiting its release by affecting upstream control points, such as the anterior pituitary or hypothalamus, thus maintaining homeostasis by ensuring hormone levels do not exceed or fall below physiological norms; for example, cortisol regulates its own production via negative feedback loops . Positive feedback, while less common, involves the hormone promoting further secretion as seen during childbirth with oxytocin, enhancing labor contractions. These mechanisms enable the endocrine system to dynamically adjust hormone output in response to changing physiological demands, thereby stabilizing conditions within the body .

Epinephrine and norepinephrine, released by the adrenal medulla in response to stress, exert their effects via adrenergic receptors. These hormones increase heart rate and cardiac output, redirect blood flow to essential tissues by vasoconstriction in non-essential areas, and elevate blood glucose by promoting glycogen breakdown in the liver and muscle . Beta-adrenergic receptors predominantly increase cAMP synthesis, enhancing cardiac output and energy mobilization, while alpha-adrenergic receptors modulate vascular constriction and smooth muscle responses. These molecular actions prepare the body for 'fight-or-flight' scenarios by optimizing energy use and reinforcing requisite physiological responses to stressors .

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