Endocrine System

(Communication system)

– Less localized, slower, effects have longer duration

 when compared to the nervous system
– Exocrine glands (do not secrete in blood stream)
○ Secrete into tubules and ducts
Eg. Salivary glands, sweat glands, liver
– Endocrine glands
○ Secrete chemical messengers or hormones directly into blood
○ Ductless glands
○ Carried throughout body but affect specific target organs
○ Hormones
 Chemical messengers
 Most are proteins or steroids
 Produced in minute quantities (very powerful) and are later eliminated
through the kidney
 Cells of target organs have special receptors which are sensitive to a
specific hormone
 Functions:
• Cause changes in cell membrane to make the transport across the
membrane easier (permeability)
• Controls rate of enzyme action
• Causes cell to release chemicals
• Controls heart rate and respiration rate
 Released in response to nervous system or other hormones
○ Negative feedback maintains proper concentration (important for homeostasis)
 “response inhibits stimulus”
○ Malfunction causes hypoactivity (underactive) or hyperactivity (overactive) of
gland
○ Works along with the autonomic nervous system to maintain homeostasis

1. Thyroid Gland
– Small, bi-lobed gland in the neck around the trachea
– Produces triiodothyronine and thyroxine derived from the amino acid tyrosine
– Plays a major role in vertebrate development and maturation
– Thyroxine
○ Stimulates cellular respiration by increasing the rate of metabolism, therefore
increasing oxygen uptake by the cells.
(cellular respiration produces ATP used to speed up metabolism. With more
cellular respiration, there is more oxygen needed)
○ Stimulates growth and development of tissues
○ Maintains heat balance
– Hyperthyroidism
○ Excessive secretion of thyroid hormones
○ Causes high body temperature, sweating, weight loss, irritability, and high blood
pressure
– Hypothyroidism
○ Low secretion of thyroid hormones
○ Can cause cretinism in infants and weight gain
 Cretinism results in poor physical (dwarfism) and mental development
○ Lethargy and cold-intolerance in adults
○ In adults – “myxedema”
 Mental and physical lethargy
 Temperature drops 3-4˚C (always cold)
 Basometabolism drops 25-30%
• Reduced appetite but there is gain weight
○ Goiter
 Enlarged thyroid
 Caused by a dietary iodine deficiency and thyroid hormones cannot be
synthesized
– Calcitonin
○ Calcium homeostasis in blood: 9-11mg/100mL
↓ Negative feedback system:
○ A rise in blood Ca2+ causes thyroid to release calcitonin to lower Ca2+
concentration by:
 Stimulating calcium salt deposit in bone
 Reducing Ca2+ reabsorption in the kidneys
○ If Ca2+ falls below 9-11mg/100mL, parathyroid glands secrete parathyroid
hormone (PTH)
 Stimulates specialized bone cells called osteoclasts to degrade bone matrix
and release Ca2+ into blood
○ Calcium is an ion essential to the normal functioning of all cells:
 Healthy bones and teeth
 Muscle contraction
 Synaptic transmission
– Hormone regulation by the hypothalamus and pituitary through a negative feedback loop:
○ Thyroid stimulating hormone (TSH) from the anterior pituitary stimulates the
release of thyroid hormones
○ Thyroid stimulating hormone (TSH) is regulated by thyroid regulating hormone
(TRH) from the hypothalamus

1. Anterior Pituitary
– Endocrine cells manufacture hormones and secrete them into the circulation
– Controlled by hypothalamus (hormones sent from hypothalamus to anterior via portal
vein)
– Growth hormone (GH)
○ Stimulates growth of bone, muscles, organs, and cell metabolism
○ Active during years of childhood, adolescence and adult life
○ Declines with age and affects all tissues
○ Important for immune function
 Replacement therapy implicants
○ If someone took growth hormone therapy, they could live to 120-130 years of age
○ Hyperactivity
  Gigantism (childhood)
 Acromegaly (adults)
• Develops over many years
• Enlarged hands, feet, jaw
• Spacing of teeth due to the overgrowth of lower jaw
○ Hypoactivity
 Dwarfism
• No mental disorder, just physical
• Different from cretinism
1. Posterior Pituitary
– Neurosecretory cells in the hypothalamus synthesize antidiuretic hormone (ADH),
oxytocin, peptide hormones that are transported down the axons to the posterior pituitary
are stored
– Controlled by hypothalamus

1. Adrenal Cortex
– Essential to life
– Hyperactivity
○ Adrenal viralism
 Female develops masculine physical and psychological characteristics
• Increase in body hair, increase in muscle bulk, voice deepends
 Ovaries and uterus do not develop (because of the presence of
testosterone)
– Hypoactivity
○ Addison’s Disease
 Can lead to death
 Faulty carbohydrate metabolism
• Blood glucose drops
 Kidneys fail to reabsorb salt
• Blood pressure decreases
 Losing volume because salt goes into the nephron, and the
water follows
 Sex functions fail
– Secretes sex hormones
– Adrenal glands are redundant glands since their secretions are secreted by other parts of
the body
– Adrenal medulla mediates short-term responses to stress
○ Stress stimulates the hypothalamus
○ Hypothalamus activates adrenal medulla via nerve impulses from the spinal cord
and sympathetic nerves
○ Medulla secretes epinephrine (adrenaline) which can cause:
 Increase heart rate, blood pressure, alertness
 Decrease digestive system activities, urine output
 Changes in blood flow patterns
 Dilates bronchioles
 Liver converts glycogen to glucose and releases glucose to blood
– Adrenal cortex controls more prolonged responses to stress
○ Stress stimulates hypothalamus
 ○ Hypothalamus causes the release of adrenocorticotropic hormone (ACTH) from
the anterior pituitary
○ ACTH causes the adrenal cortex to release steroid hormones:
 Mineralocorticoids (eg. Aldosterone)
• Stress reponse (increased transport):
 Retention of sodium and water by kidneys
 Increased blood volume and blood pressure
 Glucocorticoids (eg. Cortisol)
• Stress response (more energy):
 Increased blood sugar
 Proteins and fats broken down for energy
1. Pancreas
– In exocrine system: for digestion
– In endocrine system: for blood sugar metabolism (glucose, glycogen)
– Islets of Langerhans
○ Small clusters of cells scattered throughout the pancreas
○ Composed of alpha ɑ and beta ß cells
 ɑ cells secrete glucagon
 ß cells secrete insulin
– Insulin
○ Isolated by Canadians Banting and Best (1922)
○ Hypoactivity
 Diabetes Mellitus Type I (“no insulin at the door”)
• Cells cannot use glucose and liver cannot store it
• Cannot produce insulin
• Autoimmune disorder – immune system attacks the pancreas and
destroys insulin producing cells (ß cells)
• Occurs during childhood
• Second leading cause of blindness
• Treated with insulin therapy
 Cannot be taken as a pill because it will be broken down in
digestion
 Needle, bag, spray
 Islet Cell Transplants:
• Side effects:
 Kidney/heart failure
 Peripheral nerve damage
• Insulin injections provide some blood sugar regulation, but do not
prevent serious complications
• Transplants could replace the body’s natural mechanism in
monitoring and producing insulin
• Holds potential to reverse effects of diabetes
• Main barrier:
 Immune system rejection – current anti-rejection drugs are
toxic/harmful to islet function and immune suppression
leaves recipients susceptible to invading microbes
• Edmonton Protocol
  Uses combination of 3 drugs to prevent rejection and
prevents diabetes from returning
 Success depends on new methods of isolating and
transplanting pancreatic cells
 Islet cells extracted from donor
 Infused with recipient’s liver by way of a large vein
 Uses ultrasound to see vein leading into liver
 Skin is frozen
 Syringe used to put in new cells
 Liver used to regenerate itself by rebuilding vessels and
cells which connect to new islet cells
 Gestational Diabetes
• Temporary condition that occurs in 2-4% of pregnancies
• Increases risk of Type II diabetes in mother and child
 Because of a lack of insulin, blood glucose levels increase which leads to
hyperglycemia
 Diabetes Mellitus Type II (“insulin at the door, but the door doesn’t
open”)
• Usually in adults over the age of 40
• Accounts for about 90% of diabetes
• May be due to an insulin deficiency but more commonly results
from reduced responsiveness in target cells because of changes in
insulin receptors
• Treated with diet and exercise
• May require greater supplements of insulin as disease progresses
 monitoring of blood glucose increases
○ Homeostasis of blood glucose levels (90mg/100mL)
 Rising blood glucose levels (eg. After eating carbohydrate-rich meal)
• Blood sugar levels elevate
• ß cells of the pancreas activate and release insulin into the blood
• insulin causes:
 uptake of glucose from blood is enhanced in most blood
cells (greater permeability)
 liver takes up glucose and stores it as glycogen
 conversion of glucose to fat (adipose tissue)
• blood glucose levels decline – stimulus for insulin release
diminishes (negative feedback)
 Declining blood glucose levels (eg. Skipping a meal)
• Low blood sugar levels
• ɑ cells of pancreas activate and release glucagon into blood
targeting the liver
• liver breaks down glycogen stores and releases glucose to the
blood
• blood glucose levels increase – stimulus for glucagon release
diminishes (negative feedback)
Insulin (ß cell): glucose  glycogen
Glucagon (ɑ cell): glycogen  glucose
 – STS (Science, Technology, and Society)
○ Endocrine disrupters/modulators
 May cause rare form of cervical cancer, lowering of sperm count, possible
due to the rising concentrations of estrogen mimics in the environments
 Endocrine disrupters have structures similar to real hormones
• Sources:
 Breakdown products of pesticides
 PCBs
 Dioxins
 Chemicals found in epoxy lining of tin cans
 Plastics used for storing food
 Dental sealants
 Fungicide found in fruit
 Endocrine disrupters give a signal stronger than the body’s hormone at the
wrong time or gives a weaker signal at the wrong time
– Hormones
○ Steroids (lipid-based)
 Thought to move into the nucleus because they are permeable through the
phospholipids bilayer of a cell membrane (“like dissolves like”)
○ Peptide (protein based)
 Remain on the membrane surface (less permeable) and increases or
activates a second messenger which may be inositol triphosphate or
cAMP.

Source Hormone Type Function

Hypothalamus Antidiuretic Protein Promotes reabsorption of water in
via posterior Hormone (ADH) kidneys and sweat glands; constricts
pituitary arterioles
Oxytocin Protein In females, stimulates contraction of
uterine muscles during childbirth, milk
ejection, and maternal behaviours
In males, causes sperm ejection
Anterior Thyroid-Stimulating Glycoprotein Stimulates thyroid to release thyroxine
Pituitary Hormone (TSH)
Growth Hormone Protein Stimulates growth, protein synthesis,
(somatotropin) and fat metabolism; inhibits sugar
metabolism
Adrenocorticotropic Protein Stimulates adrenal cortex to release
Hormone (ACTH) hormones, especially glucocorticoids
Thyroid Thryoxine (T4) Modified Increases metabolic rate of most body
amino acid cells, increases body temperature;
regulates growth and development
Calcitonin Protein Inhibits release of calcium from bones
Triiodothyonine (T3) Modified Increases metabolism; regulates growth
amino acid
Parathyroid Parathormone Protein Stimulates release of calcium form
bone; promotes absorption of calcium
by intestines; promotes reabsorption of
calcium from kidneys
Adrenal Adrenalin and Modified Increase lvels of sugar and fatty acids in
Medulla noradrenalin amino acids blood; increase metabolic rate; increase
rate and force of contractions of the
heart; constricts some blood vessels
Adrenal Glucocorticoids Steroid Increase blood sugary; regulate sugar,
Cortex (cortisol) lipid, and fat metabolism; anti-
flammatory effects
Aldosterone Steroid Increases reabsorption of salt in kidney
Testosterone Steroid Causes masculinisation of body
features, growth
Pancreas Insulin Protein Decreases blood glucose levels by
increasing uptake of glucose into cells
and converting glucose to glycogen,
especially in liver; regulates fat
metabolism
Glucagon Protein Converts glycogen to glucose, thereby
raising blood glucose level