The Endocrine System
Endocrine System
Function:
Regulates
Coordinates
Integrates
Works cooperatively with the nervous system
No ducts:
Reactions not immediate -last longer than N.S.
responses
Hormones
Substances secreted by cells that regulate the activity
of another tissue or organ
Most produced by glands
Some produced by clusters of cells
Some produced by neurons (neurohormones)
Hormones
 Types of Hormones
 Amino Acid Derivatives
 Simple amines, thyroxin, peptides and proteins
 Examples:
 Thyroid hormones, epinephrine and NE, insulin,
glucagon
 Most hormones this type
Hormones
 Types of hormones
 Steroid hormones
 Derived from cholesterol
 Includes gonadal hormones (sex hormones) and
adrenal hormones (cortex only)
 Examples:
 Progesterone, testosterone, cortisol, aldosterone
Hormones
 Types of hormones
 Eicosanoids
 Are paracrine hormones (local hormone = produced by
cells and released to effect cells in the same area)
 Examples:
 Prostaglandins, leukotrines
Intracellular Receptors
Receptors
On the target cell -bind hormone
Determine the effect the hormone will have on the
target cell
Binding may cause:
Change in membrane permeability or potential
Synthesis of substances such as proteins or enzymes
Activation or deactivation of enzymes
Secretion of substances
Stimulation of mitosis
Hormone Actions
Alter the activity of target cells
Decrease or increase cellular activity in target cells
Only affect cells with receptors for that hormone
Hormone action: What happens when a hormone
binds with a receptor?
1. Channels
2. 2nd messenger
3. Genes
HORMONE ACTION
Where are the receptors?
1. On the cell membrane (AA hormones)
intracellular second messenger
2. In the nucleus (steroid hormones & thyroxine)
direct gene activation
HORMONE ACTION- Second Messenger
Intracellular second messenger
Hormone
Receptor
G protein
Adenylate cyclase system
Cyclic AMP
Protein kinases
Hormone Mechanisms
Second Messengers
 Hormone binds to a
receptor on plasma
membrane
 Series of reactions initiated
within the cell
 Example:
 Cyclic AMP
Second Messengers
 Cyclic AMP (cAMP)
 Formed from ATP when a
hormone binds to receptor
 Hormone/receptor binding
 ‘G’ protein activates or inhibits
adenyl cyclase
 ATP converted to cAMP
 May activate protein kinases
 Initiates cascade of enzymes
within the cell
 Effect depends upon target cell
Second Messenger System
Second Messengers
PIP Mechanism
 PIP2 split into
diacylglycerol and IP3
 Both act as second
messengers
 IP3 triggers the release
of calcium from the ER
 Ca2+ acts as a third
messenger
 Diacylglycerol may
activate protein kinases
Second messenger system
Direct Activation of Genes
 Steroid hormones can pass through the plasma membrane
 Bind to receptors inside cell
 Hormone/receptor binding stimulates genes on the DNA to begin
protein production
Gene Activation
Hormone Regulation
Nervous System
Ultimate control of hormone mechanisms
belongs to the nervous system
Mainly hypothalamus and sympathetic nervous
system
Endocrine Gland Stimuli
Hormone Regulation
 Stimulation or inhibition of endocrine glands comes from
THREE sources:
Other hormones
Humoral stimuli
Neural stimuli
Hormone Regulation
 Hormonal Regulation (by
other Hormones)
 Hormones may stimulate or
inhibit the release of other
hormones
 Hypothalamus Regulates anterior pituitary
gland
 Pituitary hormones Stimulate release of
hormones from other
glands
Hormone Regulation
 Regulation by Humoral
Stimuli
 Changing ion or nutrient levels
in the blood may inhibit or
stimulate the release of
hormones
 Example:
 Low blood calcium (Ca2+)
 PTH released from the
parathyroid glands
 Ca2+ released from bone
 Increase in blood Ca2+
Hormone Regulation
 Regulation by Neural Stimuli
 Nerve impulses may stimulate
the release of hormones
 Example:
 Sympathetic neurons
stimulate release of
epinephrine and
norepinephrine from the
adrenal medulla
Feedback Mechanisms
 Negative Feedback System
 Rising hormone or ion levels
inhibit further hormone release
from the gland
 Positive Feedback System
 Rising hormone levels cause
an increase in the hormone
being secreted
Hypo or Hypersecretion
 May result in a disorder
 Examples:
 Diabetes
 Grave’s disease
 Addison’s disease
 Cushing’s disease
Major Endocrine Glands
 Pituitary Gland (Hypophysis)
 Posterior lobe
(Neurohypophysis)
 Releases 2 hormones
produced in the
hypothalamus
posterior
lobe
anterior
lobe
Posterior Pituitary Gland
Posterior Lobe
 Derived from hypothalamus
 Posterior lobe +
infundibulum =
neurohypophysis
 Neuron axons to pituitary =
hypothalamic hypophyseal
tract
hypothalamic
hypophyseal tract
Posterior Pituitary Gland
Two hormones released here
Both produced in nuclei of the
hypothalamus
Both secreted into capillaries in
posterior pituitary for distribution
to the body
Oxytocin &
ADH
Hypothalamus
 SON/PVN – produce ADH &
oxytocin
 Released from posterior
pituitary
Pituitary
 Posterior lobe:
• Pituicytes
 ADH
 Oxytocin
Posterior Pituitary Gland
 Supraoptic Nucleus
 ADH (Vasopressin)
Paraventricular
nuclei
 Stimulates increased
reabsorption of water by
kidney tubules
 Decreases urine volume
 Increases blood volume
Supraoptic
nuclei
 React to Osmoreceptors
 Paraventricular Nucleus
 Oxytocin
 Uterine contractions
 Milk release (Contraction
of mammary gland smooth
muscle
ADH &
oxytocin
Ventral Hypothalamus
Releasing and inhibiting hormones
Thru portal system
Target = anterior pituitary
Anterior Pituitary Gland
Hypophyseal Portal System
neurons in ventral
hypothalamus
primary capillary
plexus
hypophyseal
portal veins
secondary
capillary plexus
secretory cells
Anterior Pituitary Gland
Ventral
hypothalamus
 Anterior Lobe = Adenohypophysis
 Derived from roof of mouth
 Produces hormones
 Release of hormones is controlled
by hormones from neurons of the
ventral hypothalamus = releasing
or inhibiting hormones
anterior
lobe
Pituitary (Hypophysis)
 Location and relationships
 Densely packed cells (anterior)
 Anterior lobe:
 TSH
 ACTH
 FSH
 LH
 GnRH
 Growth h.
 Prolactin
 MSH
Anterior Pituitary Gland
 The following four anterior pituitary hormones are
tropic hormones
 Tropic Hormones:
TSH
ACTH
FSH
LH
Tropic Hormones
 Hormones Secreted
 Thyroid Stimulating Hormone (TSH)
 Stimulates production and release of thyroid hormones by
the thyroid gland
 Release stimulated by TRH
 Inhibited by rising blood levels of thyroid hormone
Tropic Hormones
 Hormones Secreted
 Adrenocorticotropic Hormone (ACTH or Corticotropin)
 Stimulates secretion of corticosteroid hormones (esp.
cortisol) from the adrenal cortex
 Release stimulated by CRH, fever, hypoglycemia and stress
 Inhibited by rising cortisol levels
Tropic Hormones
 Hormones Secreted
 Follicle Stimulating Hormone (FSH)
 Not present until puberty
 Stimulates gamete production and maturation in both males
and females
 Release stimulated by GnRH
 Inhibited by rising gonadal hormones
Anterior Pituitary Gland
 Hormones Secreted
 Luteinizing Hormone (LH)
 Promotes production of gonadal hormones
 Controlled by the same hormones as FSH
 Triggers ovulation in females
Non-tropic Hormones
Hormones Secreted
Growth Hormone (GH) or Somatotropin
 Produced in response to growth hormone releasing hormone
(GHRH from hypothalamus)
 Also secreted in response to hypoglycemia or decreased
blood GH or Increased amino acid levels
 Inhibited by GHIH (somatostatin from hypothalamus)
 Stimulates cell growth and division in most cells (esp. bone
and muscle)
 Mobilizes fat to conserve glucose
 Hyposecretion results in pituitary dwarfism
 Hypersecretion results in gigantism or acromegaly
Non-tropic Hormones
 Hormones Secreted
 Prolactin (PRL)
 Release
stimulated by PRH
 Inhibited
 Both
by PIH (dopamine)
are influenced by estrogen
 Stimulates
milk production by breasts
Thyroid Gland - Anatomy
The Thyroid Gland
 Two lateral lobes
 Composed of follicles
 Cuboidal follicle cells produce
thyroglobulin
 Thyroglobulin stored in lumen of follicle
 Iodine attaches
 Molecule is split into T3 and T4 (mostly T4)
 Hormones enter circulation, more T3
formed
thyroid
gland
Thyroid Gland - histology

Follicular cells
follicles
colloid
thyroglobulin
T3 – triiodothyronine
T4 – thyroxine

Parafollicular cells
Calcitonin
Thyroid Gland - hormones

Follicular cells
thyroglobulin
T3 – triiodothyronine
T4 – thyroxine
•
•
•

+ BMR (glucose oxidation)
maintains bp
tissue growth & development
Parafollicular cells
Calcitonin
•
•
decreases blood calcium
+ osteoblasts
Thyroid Gland – T3/T4 production





Follicles – colloid, follicular cells
Cells make thyroglobulin
Thyroglobulin moves into follicle
Iodine pumped into follicle
Iodine used to make subunits
• 1 OR 2 IODINE



Subunits moved into follicle cells
Subunits join to make T3 or T4
T3/T4 released from follicle cells
Thyroid Hormone Production
Thyroid Hormone
 T4 converted to T3 once in tissues
 Secreted in response to TSH
 Inhibited by rising blood thyroid hormone levels
 Effects:
 Increases metabolic rate
 Increases heat production
 Promotes protein synthesis and enhances the affect of GH
 Promotes uptake of glucose by cells
 Promotes lipid metabolism
 Speeds up actions of nervous system
Thyroid Hormone
Hyposecretion
Can result in cretinism
in children
Myxedema in adults
Hypersecretion
Grave’s Disease
Thyroglobulin
Thyroid Gland - pathology
Myxedema – adult hypothyroid
Goiter – enlarged thyroid due to lack of iodine
Cretinism – infantile hypothyroid
Grave’s disease – hyperthyroid exophthalmos
Calcitonin
parafollicular
cells
Secreted by
parafollicular or C cells
by the thyroid
Released in response
high blood calcium
Stimulates uptake of
calcium by bone
Parathyroid Glands
4 to 8 on posterior thyroid
gland
Secrete Parathyroid Hormone
(PTH)
 Secreted in response to low
blood calcium
 Stimulates bone resorption
 Released calcium enters blood
 Increases absorption of calcium
by intestines and reabsorption
by kidneys
parathyroid
glands
Parathyroid Hormone
 Hypersecretion
 Depletes calcium from bones
 Depresses nervous system
activity
 Skeletal muscle weakness
 Hyposecretion
 Over excitability of neurons
 Muscle spasms
 Convulsions
Chief cells
Adrenal (Suprarenal) Glands
Two glands--one on top of
each kidney
Outer cortex, inner medulla
adrenal gland
Cortex
Produces over 2 dozen
corticosteroids from
cholesterol
Increased hormone output in
response to ACTH or stress
cortex
medulla
Adrenal Cortex
Three Regions:
Zona Glomerulosa
 Outer region
 Production of
mineralocorticoids
(aldosterone)
 Regulation of electrolyte &
fluid balance
Aldosterone
95% of mineralocorticoids
Sodium reabsorption (and water) by kidney
tubules
Increases blood volume and pressure
Stimulated by angiotensin
 Renin secreted by kidneys
 Activates angiotensin hormones in blood
 Stimulates release of aldosterone
Inhibited by Atrial Natriuretic Factor (ANF)
 Secreted by heart cells when B.P. rises
 Blocks secretion of renin and aldosterone
Adrenal Cortex
Zona Fasciculata
 Middle region
 Secretes glucocorticoids
(cortisol)
 Cortisol
 Released in response to ACTH
 Inhibited by increased cortisol
 Promotes gluconeogenesis
(production of glucose from
non-carbohydrate sources)
 Causes a rise in B.P.
 Anti-inflammatory if given in
higher doses
Cortisol
Hypersecretion
Cushing’s Syndrome
Depressed bone and cartilage formation
Depressed inflammatory response and immune
system
Edema, hypertension, loss of muscle and bone,
‘moon face’
Hyposecretion
Addison’s disease
Drop in blood plasma volume
Inability to cope with stress or regulate blood sugar
levels
Increased skin pigmentation
Adrenal Cortex
Zona Reticularis
Inner region
Produces
glucocorticoids &
gonadocorticoids
(androgens and
estrogen)
ADRENAL MEDULLA
Chromaffin Cells
Secrete epinephrine and
norepinephrine
(Catecholamines)
Release stimulated by
sympathetic neurons
Prolongs the fight or
flight response
The Pancreas
Mixed endocrine and
exocrine function
Acinar Cells
 Secrete digestive
enzymes into small
intestine
Islets of Langerhans
 Contain alpha cells
 Glucagon
 Contain beta cells
 Insulin
Pancreas
 endocrine and exocrine
 Islets of Langerhans
 Cell Types:
Alpha
Beta
Delta
Glucagon
Insulin
Somatostatin
Increases blood sugar
PP
Pancreatic
Polypeptide
Regulates exocrine function
Inhibits bile release
Decreases blood sugar
Inhibit glucagon/insulin release
Inhibit digestive tract activity
Insulin
 Stimulated by high blood
sugar
 Inhibited by decrease in
blood sugar or somatostatin
(GHIH)
 Lowers blood sugar
 Enhances glucose transport
into cells (esp. muscle)
 Stimulates glycogen
formation
 Promotes conversion of
glucose to fat
 Stimulates protein
synthesis in muscle
Islet of Langerhans
Glucagon
 Released in response to low
blood sugar
 Mobilizes fatty acids, glucose
and amino acids from storage
 Promotes release of fat from
adipose tissue
 Promotes:
 Gluconeogenesis (production
of glucose from non-carb.
sources)
 Glycogenolysis (breakdown of
glycogen into glucose)
 Raises blood sugar levels
Diabetes
 Diabetes Insipidus
 Caused by ADH deficiency
 Large quantities of urine
 Dehydration
 No blood sugar accumulation
 Diabetes Mellitus
 Results from Hyposecretion of insulin or hypoactivity of insulin
Diabetes
Diabetes Mellitus
Two types:
 Type 1 (Juvenile Onset)
 Usually before age 20
 Decreased amount of beta cells in pancreas
 Possibly autoimmune cause
 Long term vascular and neural problems
 Type 2 (Adult Onset)
 Insulin is produced but receptors are resistant to it
 Family tendencies
 Influenced by weight, diet and exercise
Diabetes
Lack of insulin or response to it
Inability of glucose to enter body cells
High blood sugar
Fat stores are mobilized for fuel
Blood sugar and fatty acid levels rise higher
Ketone bodies build up from breakdown of fatty acids
Ketosis or acidosis results (lowered blood pH)
Crisis, coma or death
Diabetes
Symptoms
Polyuria
 Large urine output
Polydipsia
 Excessive thirst
Polyphagia
 Excessive hunger caused by the inability to use glucose as
an energy source
The Pineal Gland
Secretes melatonin
May affect responses to
light cycles
May inhibit gonad activity
in humans until puberty
“brain sand”
The Thymus Gland
Shrinks with age
Produces thymopoietin and
thymosin
Aids in development of the
immune response
(development of Tlymphocytes)
THE GONADS
Produce gametes and reproductive hormones
Testosterone in males
 Maturation of reproductive organs
 Secondary sex characteristics
 Sex drive
Estrogens and progesterone in females
 Estrogens cause maturation of reproductive organs and
appearance of secondary sex characteristics
 With progesterone, promote breast development and cyclic
changes in uterine lining