ENDOCRINE SYSTEM

Dr. DEDI ARDINATA, M.Kes

Physiology Department
Medical School of University Sumatera Utara
Comparison of Nervous and Endocrine Systems

Nervous Endocrine
hormone
messenger electrochemical
(chemical)
response milliseconds seconds to days

duration short-lived long-lived

distribution one system (several widely scattered

subsystems)

NOTE: Nervous and endocrine systems work together to coordinate and

integrate activities of body (homeostasis)
Functions of Endocrine System

1. Reproduction
2. Growth and development
3. Response to stress
4. Maintenance of fluid (water), electrolyte and
nutrient balance
5. Regulation of cellular metabolism and energy
 Organs of the Endocrine System
1. Pituitary gland
2. Hypothalamus
(neuroendocrine)
3. Pineal gland
4. Thyroid gland
5. Parathyroid
gland
6. Thymus gland
7. Adrenal gland
8. Pancreas (also
has exocrine
function)
9. Gonads (testes
or ovaries - also
have exocrine
functions)
 Hormone
Topics
Types
Modes of Action
Target cell activation
Control

Specific glands, their hormones, and disorders

Pituitary
Thyroid
Parathyroid
Adrenal
Pancreas
Thymus
Gonads (testes and ovaries)

General Adaptation Syndrome

 Hormones
chemicals
secreted by endocrine gland cells into blood
(by way of interstitial fluid)
regulate metabolic functions of other cells
(called target cells)
carried to all cells, but action is specific to cells
that have receptors for the hormone
specificity of bodys response to hormone
depends on how many cells have the
receptor (highly specific if few cells respond
[e.g., ACTH]; diffuse action if many respond
[e.g., thyroxine])
 Chemical Types of Hormones
Amino-acid based (amino acids, short or long
peptides, proteins)
e.g., insulin, growth hormone, prolactin
Steroids - lipid derivatives of cholesterol
e.g., hormones from gonads (testosterone,
estrogen)
e.g., hormones from adrenal cortex
(adrenocortical hormones)
Eicosanoids - locally-secreted, locally-acting
hormones secreted by all cell membranes
(e.g., prostaglandins, which increase blood
pressure and contribute to uterine contraction)
 Types of Changes in Target Cells
plasma membrane permeability changes
(opening of protein channels; may change
membrane potential)
activation of genes for increased protein
synthesis, including enzymes
activation or deactivation of enzymes already
present
secretion of cellular products
stimulation of cell division (mitosis)
 Mechanisms of Action
action in target cell depends on receptor
receptor may be:
in plasma membrane
second messenger mechanisms
used by most amino acid-based
hormones (water soluble)
intracellular (in cytoplasm or nucleus)
direct gene activation
used by steroids and thyroid hormones
(lipid soluble)
 Mechanisms of Action: Steroids
bind to intracellular receptors
hormone diffuses through plasma membrane
and makes its way to nucleus
> where it binds with intracellular receptor
to form hormone-receptor complex
> hormone-receptor complex interacts with
chromatin (DNA) to affect gene activity
(turn genes on or off)
> synthesis of mRNA
> synthesis of protein
Steroid Signaling
 Mechanism of Action:
Thyroid Hormone
similar to mechanism for steroid hormones
diffuses across plasma membrane
diffuses into nucleus where it interacts with
intracellular receptors to activate genes for
proteins (enzymes) involved in cellular
respiration (glycolysis)
also, binds to receptors at mitochondria to
activate genes for proteins involved in cellular
respiration (Krebs cycle and electron transport
chain)
 Mechanisms of Action:
Other Hormones
* plasma membrane receptor
used by most amino acid-based hormones
interaction of hormone with plasma membrane
receptor results in activation of second
messenger systems (cyclic AMP or PIP-
calcium)
activation of second messenger has cascade
effect resulting in:
enzyme activation, or
membrane permeability changes or
secretion
 Membrane Receptor Mechanisms:
1. Cyclic AMP (cAMP) Signaling

interaction of hormone with receptor

> activates G protein (cleaves phosphate from
GTP)-> excitation
> G protein activates adenylate cyclase
> adenylate cyclase forms cAMP from ATP
> cAMP activates protein kinases
> protein kinases activate (or inhibit) other
proteins by phosphorylation
> cAMP degraded by enzyme
slightly different G protein inactivates adenylate
cyclase - associated with different hormone
receptor
Link to animation:
http://student.ccbc.cc.md.us/c_anatomy/animat/cAMP.htm
cAMP Signaling Mechanism
 Membrane Receptor Mechanisms:
2. PIP-Calcium Signaling
interaction of hormone with receptor --> activates
membrane-bound enzyme phospholipase
> phospholipase cleaves PIP2 (phosphatidyl
inositol diphosphate) into diacylglycerol (DAG)
and IP3 -- each of which acts as a second
messenger
diacylglycerol (DAG) activates protein
kinases
IP3 (inositol triphosphate) causes release of
Ca2+ into cytoplasm (from endoplasmic
reticulum or other storage areas) --> Ca2+
acts as third messenger
 PIP-Calcium Mechanism (cont)
-> Ca2+ (third messenger)
changes enzyme activity and plasma
membrane channels, or
binds to calmodulin (intracellular
regulatory protein) --> activates
enzymes
PIP-Calcium Signaling Mechanism
 Factors Affecting Target Cell
Activation
a. blood levels of hormone, which depend on:
rate of hormone release
rate of deactivation (by target cell or liver)
b. affinity of hormone for receptor
greater affinity means greater association
--> greater effect
c. number of receptors available
 Factors Affecting Target Cell Activation (cont)

c. number of receptors available

up-regulation: increase in blood level of
specific hormone (normally present at low
levels) causes cells to make more receptors
down-regulation: prolonged exposure to high
level of specific hormone --> cells remove
some receptors
-->return to normal response level
cross-regulation: influence of one hormone on
number of receptors for another hormone; e.g.,
progesterone causes uterus to make fewer
estrogen receptors; estrogen causes uterus to
make more progesterone receptors
 Hormone Removal
hormones may be:
degraded by specific enzymes within target cells;
removed from blood by kidneys (excreted in urine)
degraded by liver (excreted in urine and feces)
half-life - time for 1/2 of hormone to be removed (from
a fraction of a minute to 30 minutes)
onset - time from release to action (minutes [amino
acid-based] to days [steroids])
duration of action - how long the effects last (~20
minutes to several hours)
Control of Hormone Release

Humoral control
Neural control
Hormonal control
 Control of Hormone Release: Humoral
Hormone released in response to changing blood
levels of ion or nutrient (negative feedback)

parathyroid glands:
detects low blood Ca2+
PTH raises blood
Ca2

thyroid (parafollicular
cells) detect high blood
Ca2+-->calcitonin--
>decrease blood Ca2+
 Control of Hormone Release:
Humoral
Other examples:
pancreas:
beta cells detect high blood glucose
insulin decreases blood glucose
alpha cells detect low blood glucose
glucagon raises blood glucose
zona glomerulosa (of adrenal cortex)
detects low blood Na+ or high blood K+
aldosteronetthy, K+
 Control of Hormone Release:
Neural
Hormone released in response to nerve impulse
preganglionic impulses from
fibers of hypothalamus
sympathetic result in release of
division oxytocin or ADH
stimulate release from posterior
of catecholamines pituitary
(epinephrine,
norepinephrine)
from adrenal
medulla
 Control of Hormone Release:
Hormonal
Hormone produced by one endocrine gland (or
hypothalamus) affects secretion of hormone by
another endocrine gland
hypothalamus acts as overall coordinator
releases regulatory hormones (releasing
hormones or inhibitory hormones) affects
anterior pituitary
anterior pituitary, when stimulated, secretes
hormones that affect other glands (e.g., TSH
[thyroid stimulating hormone] stimulates release
of thyroid hormones from thyroid gland)
 Hormonal Control: Role of Hypothalamus
Releasing hormones from hypothalamus
stimulate secretion from anterior pituitary
Inhibitory hormones from hypothalamus
inhibit secretion by anterior pituitary
Impulses from hypothalamus cause release
of hormones from posterior pituitary
 Hormone Control - Misc.
nervous system can override normal endocrine
control
e.g., in fight-or-flight response, sympathetic
impulses result in release of epinephrine and
norepinephrine from adrenal medulla -->
increases blood glucose levels to maintain fuel
supply during stress or exertion (overrules effect
of insulin on blood glucose level)
 Organs of the Endocrine System and
Their Products
The following major
glands will be covered
one at a time with their
products:
1. Pituitary gland /
Hypothalamus
2. Thyroid gland
3. Parathyroid gland
4. Adrenal gland
5. Pancreas (also has
exocrine function)
6. Gonadal hormones
(ovaries and testes)
7. Thymus
 1. Pituitary Gland (Hypophysis)
located in sella turcica of sphenoid bone (in cranial
cavity), inferior to hypothalamus
consists of two lobes:
A. neurohypophysis (~ posterior pituitary)
attached to hypothalamus by infundibulum
contains axons and axon terminals of
neurosecretory cells whose cell bodies are in
hypothalamic nuclei
B. adenohypophysis (~ anterior pituitary)
consists of glandular epithelium

http://www.usc.edu/hsc/dental/ghisto/end/c_1.html
Pituitary Development

From roof of mouth

http://
calloso.med.mun.ca/~tscott/hea
d/pit.htm
A. Neurohypophysis (Posterior Pituitary)
consists of nerve fibers (axons of neurosecretory
cells with cell bodies in hypothalamus) and
pituicytes (glial cells that support nerve fibers)
acts primarily as a storage and releasing area for
hormones actually made in hypothalamic nuclei
hormones released in response to impulses from
hypothalamus (neural control)
hormones are short amino acid chains (peptides)
oxytocin
antidiuretic hormone (ADH or vasopressin)
 A. Neurohypophysis : Oxytocin (OT)
action, in pregnant or nursing women:
stimulates contraction of smooth muscle of
uterine wall during labor and delivery
stimulates ejection of milk in lactating mothers
action, in men and non-pregnant women, may be
involved in sexual arousal and orgasm
 A. Neurohypophysis : Oxytocin (OT)
control:
during labor/delivery, positive feedback:
stretching of uterus/cervix --> sensory
impulses to hypothalamus --> increased
secretion of OT --> increased contraction
suckling: sucking of infant on breast -->
sensory to hypothalamus --> oxytocin release
--> release of milk
 A. Neurohypophysis:
Antidiuretic Hormone (ADH)
action: antidiuretic hormone (ADH) directly
affects blood pressure - acts as powerful
vasoconstrictor --> increases blood pressure
(hence name vasopressin)
* action: affects water balance (indirect affect
on blood pressure) - acts on tubules of kidney
to increase reabsorption of water less
water lost in urine
 A. Neurohypophysis: ADH
disorders:
hyposecretion due to damage of
hypothalamic nucleus or neurohypophysis--
> diabetes insipidus - excessive urine
production (polyuria) and thirst
hypersecretion --> SIADH (syndrome of
inappropriate ADH secretion) - water
retention, headache, cerebral edema,
weight gain, hypoosmolarity
 Antidiuretic Hormone (ADH): Control
neural control: increased electrolyte (NaCl)
concentration --> affects (supraoptic) nucleus in
hypothalamus --> impulse to neurohypophysis -->
release of ADH --> increased water reabsorption
--> decrease in electrolyte concentration
other stimuli: pain, low BP, morphine,
barbiturates, nicotine, aldosterone (hormone from
adrenal cortex - hormonal control)
inhibition: alcohol (results in more urine
production and, potentially, dehydration)
diuretic drugs - some act to supress ADH
secretion; used to treat hypertension and
congestive heart failure
B. Adenohypophysis (Anterior Pituitary)
linked to hypothalamus via hypophyseal
portal system (capillary networks and small
veins)
carries regulatory hormones from
hypothalamus to pituitary
releasing hormones stimulate secretion
of pituitary hormones
inhibitory hormones inhibit secretion
consists of epithelial cells
all hormones produced are proteins
* tropic hormones - affect some endocrine
glands or provide maintenance oversight for
other organs
B. Adenohypophysis : Growth Hormone (GH)
highest levels during evening and sleep
action: stimulates increased rate of protein synthesis
leading to cell growth and division
bones and skeletal muscle respond more than
other body cells
action: stimulates use of fat as energy source and
decreases rate of glucose uptake and glucose
metabolism (diabetogenic effect spares glucose)
control:
release stimulated by GHRH (growth hormone
releasing hormone) from hypothalamus
inhibited by GHIH (from hypothalamus) and
somatomedins (produced by liver under GH
stimulation)
Growth Hormone (GH): Disorders
Disorders:
hypersecretion
gigantism (in children)
up to 8 tall, normal body proportions
acromegaly (after epiphyseal plates close)
enlargement of extremities and face,
thickening of soft tissue
hyposecretion
pituitary dwarfism - in children, up to 4 tall
progeria - premature aging, atrophy of
body tissues
 B. Adenohypophysis: Prolactin (PRL)
action:
* stimulates milk production in mammary
glands;
helps stimulate development of mammary
glands (along with other hormones);
in males, may help regulate testosterone
production
control:
stimulation: PRH (prolactin-releasing
hormone from hypothalamus), high
estrogens, breast-feeding
inhibition: PIH (hypothalamus), stimulated
by rising PRL levels, low estrogen
 B. Adenohypophysis : Prolactin (PRL)

Disorders
hyperprolactinemia = hypersecretion due to
adenohypophyseal tumors; results in
galactorrhea, lack of menses and infertility in
women, impotence in men
 B. Adenohypophysis:
Thyroid-Stimulating Hormone (TSH)
TSH = thyrotropin
action:
stimulates secretion of hormones from
thyroid gland (T4 and T3); also stimulates
development of thyroid in youth
control:
release stimulated by TRH (thyroid
releasing hormone from hypothalamus)
inhibited by rising levels of thyroid
hormones and by GHIH
 B. Adenohypophysis:
Adrenocorticotropic hormone (ACTH)
ACTH=corticotropin
action: stimulates release of hormones from
adrenal cortex
control:
release stimulated by CRH (corticotropin-
releasing hormone from hypothalamus)
release inhibited by rising levels of
glucocorticoids from adrenal cortex
 B. Adenohypophysis:
Gonadotropins
regulate activity and secretion by gonads
(testes in males; ovaries in females)
control:
stimulated by GnRH (gonadotropin-
releasing hormone from hypothalamus)
release of GnRH is inhibited by rising
levels of estrogens, progestins and
androgens (testosterone)
two important hormones
FSH
LH
 Gonadotropins:
Follicle-Stimulating Hormone (FSH)
action:
females (ovaries) - stimulates development
of ovarian follicles and estrogen production
males (testes) - stimulates sperm
production and development
inhibited by inhibin and testosterone from
testes (feedback to hypothalamus and
anterior pituitary) and estrogen, progesterone
and inhibin from ovaries (feedback to anterior
pituitary)
 Gonadotropins:
Luteinizing Hormone (LH)
LH=lutropin
action:
females (ovaries) - induces ovulation;
stimulates secretion of estrogens and
progestins (e.g., progesterone)
males (testes) - stimulates production of
androgens (e.g., testosterone )
inhibited by estrogen, progesterone and
inhibin form ovaries (feedback to anterior
pituitary) and by inhibin and testosterone from
testes (feedback to hypothalamus and anterior
pituitary)
 2. Thyroid Gland
located anteriorly in cervical region, just
inferior to thyroid cartilage; two lobes
connected by thin isthmus
largest purely endocrine gland in body
consists of follicles (cuboidal or simple
squamous epithelium) filled with colloid
(combination of protein [thyroglobulin]
containing amino acid tyrosine [building block
of thyroid hormones])
parafollicular cells produce calcitonin

http://www.usc.edu/hsc/dental/ghisto/end/c_26.html
 2. Thyroid Gland: T4 and T3
hormones based on amino acid tyrosine (differ
in number of iodine ions)
thyroxine (tetraiodothyronine [T4]) and
triiodothyronine (T3)
T3 is 10x more active, but less common (T4
accounts for about 90% of all thyroid
hormone)
much T4 converted to T3 by liver, kidneys,
some other tissues
 2. Thyroid Gland: T4 and T3
affect metabolic rate of every cell in the body,
except brain, spleen, testes, uterus and
thyroid gland
affect other activities within these organs
and glands
readily cross membranes (diffuse through
plasma membrane to bind to mitochondrial
receptors and receptors in nucleus)
2. Thyroid Gland
 T4 and T3: Actions
increase synthesis of enzymes involved in
cellular respiration --> increase basal
metabolic rate
increases glucose oxidation --> ATP
synthesis
increases ATP synthesis in cytoplasm
and by mitochondria
results in increased heat production
(calorigenic effect)
work with GH to promote normal tissue growth
and development, especially important to
growth/development of CNS, skeletal and
reproductive systems
 T4 and T3: Control
release stimulated by TSH (thyroid-
stimulating hormone from adenohypophysis)
release of TSH stimulated by TRH from
hypothalamus
release of TRH is stimulated by cold,
pregnancy, low thyroxine
release inhibited by GHIH, high glucocorticoid
levels, high sex hormone levels, high iodine
 Hypothyroidism
too little thyroid hormone (thyroid gland defect, inadequate
TSH, TRH, or iodine)
Hashimotos thyroid autoimmune disorder in which
thyroid is attacked and function decreases
myxedema - low BMR, constipation, puffy eyes, edema,
lethargy, mental sluggishness
endemic goiter - enlargement of thyroid gland usually
due to lack of sufficient iodine
cretinism - genetic deficiency of thyroid gland or lack of
dietary iodine during development resulting in mental
retardation, disproportionate growth, short body with
thick tongue and neck
treatment - reversed by iodine supplements or hormone
replacement therapy
 Hyperthyroidism
too much thyroid hormone (thyrotoxicosis)
Graves disease - autoimmune disease in which
abnormal antibodies similar to TSH mimic its
function and continuously stimulate release of
thyroid hormones; results in high BMR, sweating,
rapid heart rate, weight loss, restlessness, mood
shifts, fatigues easily, limited energy; also toxic
goiter
exophthalmos - protrusion of eyeballs, fibrous
tissue become edematous (swollen)
treatments - removal of thyroid gland or irradiation
patient must be on synthetic thyroid hormone the
rest of his/her life
 2. Thyroid Gland: Calcitonin (CT)
polypeptide produced by parafollicular cells
actions: decreases blood calcium levels by:
stimulating osteoblasts (Ca2+ uptake and
incorporation into bone)
inhibiting osteoclast activities (osteoclasts break
down bone matrix releasing calcium)
control: responds directly to blood calcium levels
very rapid effect
probably more important during childhood when it
stimulates bone growth
important because at high blood Ca2+, membranes
become less permeable to Na+
 3. Parathyroid Glands
2 paired structures on posterior of thyroid gland
oxyphyil cells - function unknown
chief cells secrete parathyroid hormone (PTH;
protein)
actions: increases blood Ca2+ by:
stimulating osteoclast activity (which break
down bone matrix) while inhibiting osteoblasts
(which form bone matrix)
stimulating increased reabsorption of Ca2+ by
kidney
indirectly stimulating increased absorption of
Ca2+ by small intestine by causing secretion of
calcitrol form kidneys
3. Parathyroid Glands
 Hyperparathyroidism

rare; caused by parathyroid gland tumor

results in hypercalcemia (excess Ca2+
levels in blood) --> depression of nervous
system (because of effect on sodium
permeability), abnormal reflexes, skeletal
muscle weakness, nausea, vomiting,
kidney stones, calcium deposits in soft
tissues; bones become soft
 Hypoparathyroidism

trauma to or removal of parathyroid

gland
results in hypocalcemia (low blood Ca2+)
--> neurons become too excitable -->
muscle tetany --> spasms/cramps -->
respiratory paralysis --> death
 4. Adrenal Glands
located in abdominal cavity against back wall
(retroperitoneal), superior to kidney
surrounded by connective tissue capsule
two regions:
cortex - outer region, glandular, three zones
zona glomerulosa - outer zone
zona fasciculata - middle zone
zona reticularis - inner zone
medulla - inner region,
modified neural tissue
(develops from same tissue
in embryo as ganglionic
[postganglionic] neurons of
sympathetic division)
 4. Adrenal Gland Development

http://sprojects.mmi.mcgill.ca/embryology/ug/Adrenal_Stuff/Normal/zones.html
4. Adrenal Gland: Regions and Zones
 Adrenal Cortex: Zona Glomerulosa
produces steroid hormones based on
cholesterol
mineralocorticoids - ion (and water) balance
main hormone is aldosterone
action:
* stimulates reabsorption of Na+ and
secretion of K+ from kidney, sweat glands,
salivary glands, pancreas
secondarily, increases water reabsorption
in kidney (water follows Na+)
 Adrenal Cortex: Zona Glomerulosa
control:
aldosterone release
stimulated by:
high K+, low Na+
angiotensin II (result
of renin-angiotensin
pathway stimulated
by low blood
pressure),
ACTH (when under
severe stress)
inhibited by low K+,
high Na+
Adrenal Cortex: Zona Glomerulosa
Disorders:
aldosteronism = hypersecretion (adrenal
tumor)
increased water and Na+ reabsorption -->
hypertension, edema;
loss of K+ --> disruption of neural and
muscle function
Adrenal Cortex: Zona Glomerulosa
Disorders:
Addisons Disease = hyposecretion
glucocorticoids and mineralocorticoids
results in decreased Na+ and water
reabsorption, increased blood K+ --> low
blood volume --> hypotension, dehydration;
changes in membrane potentials -->
disruption in neural and muscular function
also decreased cortisol secretion by zona
fasciculata --> decreased blood glucose
levels (especially during prolonged stress)
 Adrenal Cortex: Zona Fasciculata
glucocorticoids - effects on glucose metabolism
main hormone is cortisol (hydrocortisone)
actions:
maintains blood glucose levels, especially in
times of stress, by:
promoting gluconeogenesis (making new
glucose in liver) and use of alternative
fuels by other cells (saves glucose for the
brain)
anti-inflammatory decrease immune
response
* can be used clinically to treat allergic reactions
(e.g., poison ivy), rheumatoid arthritis
 Adrenal Cortex: Zona Fasciculata
Control
stimulated by ACTH
inhibited by cortisol (inhibits secretion of CRH
from hypothalamus)
blood levels peak in the morning

Disorders:
Addisons Disease
- hyposecretion of glucocorticoids and
mineralocorticoids
 Zona Fasciculata: Cushings Disease
hypersecretion of glucocorticoids
caused by hypersecretion of ACTH due to tumor in
ZF, pituitary, lungs, kidneys, or pancreas
suppresses glucose metabolism resulting in
hyperglycemia (elevated glucose= steroid
diabetes),
stimulates lipid metabolism (weight loss),
loss of muscle and bone mass,
buffalo neck and moon face (fat
redistribution),
anti-inflammatory effects (mask infection)
water and salt retention (effect of aldosterone
hypersecretion --> water retention -->
hypertension)
 Adrenal Cortex: Zona Reticularis
gonadocorticoids
most are androgens (male sex hormones) -
converted to testosterone; small amounts of
estrogens
actions: may contribute to onset of puberty (levels
rise between 7 and 13 years of age; exact function
compared to hormones from ovaries or testes
unclear)
control: stimulated by ACTH
 Adrenal Cortex: Zona Reticularis
hypersecretion results in:

masculinization and masculine pattern of hair

distribution in females
in males - rapid maturation of reproductive

organs, secondary sex characteristics;

hypersecretion of estrogens causes feminization

and gynecomastia (enlarged breasts)

 Adrenal Medulla
chromaffin cells (modified neurons - arise from
same embryonic tissue as postganglionic
neurons of sympathetic division)
catecholamines - epinephrine (~80%), norepi
(NE)
control: secretion stimulated by preganglionic
fibers of sympathetic nerves during flight-or-
fight response
 Adrenal Medulla
actions:
epinephrine (more potent) - increases HR
(beta receptors), bronchodilation (in lungs),
increased blood glucose (breakdown of
glycogen in liver and skeletal muscle, and
breakdown of adipose tissue)
NE - peripheral vasoconstriction -->
increased BP
 5. Pancreas

has both exocrine (acini secrete digestive

enzymes) and endocrine function (islets of
Langerhans)
control: responds to blood glucose levels
(humoral)
hormones are polypeptides (proteins)
 5. Pancreas
major cell types
alpha cells secrete glucagon
beta cells secrete insulin
delta cells secrete somatostatin (which inhibits
insulin and glucagon secretion, and decrease
fat absorption in intestines)
F cells regulate exocrine function of pancreas
(secrete pancreatic polypeptide)
 5. Pancreas: Glucagon
actions: hyperglycemic (increases blood
glucose)
stimulates formation and release of glucose
from liver (main target)
glycogenolysis - breakdown of glycogen
(storage form of glucose)
gluconeogenesis - formation of glucose
from noncarbohydrate molecules (e.g.,
amino acids, glycerol, lactic acid)
stimulates glycogenolysis in skeletal muscle
stimulates triglyceride breakdown in adipose
tissue (fat mobilization)
 5. Pancreas: Glucagon
control:
secreted in response to low blood sugar,
rising amino acid levels in blood
inhibited by increased blood glucose and
by somatostatin
 5. Pancreas: Insulin
actions: hypoglycemic (lowers blood glucose)
increases transport of glucose into muscle
and fat cells (NOTE: does not increase
uptake by brain, liver, or kidney)
inhibits breakdown of glycogen and
formation of glucose from amino acids or
fatty acids (inhibits glycogenolysis and
gluconeogenesis)
promotes formation of glycogen (liver,
skeletal muscles), protein synthesis
(muscle), and fat synthesis and storage
(adipose)
 5. Pancreas: Insulin (Control)
stimulated by:
increased blood glucose
increased blood amino
acid and fatty acid levels
parasympathetic impulses
hyperglycemic hormones
(GH, glucagon,
epinephrine, thyroxine,
glucocorticoids) indirectly
result in insulin secretion
by increasing blood
glucose levels
inhibited by:
low blood glucose and by
somatostatin
sympathetic impulses
 5. Pancreas: Insulin - Disorders: Diabetes
Mellitus (DM)
hyposecretion (or hypoactivity) of insulin
body cells not stimulated to take up glucose
hyperglycemia (excess blood glucose)
very high glucose --> nausea --> fight-or-flight
response --> secretion of hyperglycemic hormones
(epi, NE [adrenal medulla], glucocorticoids [adrenal
cortex]) --> stimulates gluconeogenesis, lipolysis,
glycogenolysis --> adds to already high glucose
not all sugar reabsorbed from urine --> glucose lost
in urine (glucosuria) --> increased water loss -->
excessive urine production (polyuria) and
excessive thirst (polydipsia)
 5. Pancreas: Insulin - Diabetes Mellitus
cells use fats as energy source (due to poor
glucose uptake)
hyperglycemic hormones stimulate fat
mobilization --> fats in blood (lipidemia) -->
increase in lipid metabolites in blood (ketone
bodies, which are strong organic acids) -->
decrease blood pH (ketoacidosis) and ketone
bodies in urine (ketonuria)
decreased blood pH --> severe depression of
nervous system --> deep breathing --> diabetic
coma --> death
polyphagia (excessive hunger) - final sign, due to
use of fats and proteins as energy sources
 Type I Diabetes mellitus
also called insulin-dependent diabetes
(IDDM; formerly juvenile onset diabetes)
onset is sudden, usually before age 15
may be due to autoimmune attack of proteins
in beta cells (see A Closer Look, p. 640-641)
result is lack of insulin activity
lipidemia (high blood lipid content) and
increased cholesterol lead to long-term
vascular problems (arteriosclerosis, strokes,
heart attacks, renal shutdown, gangrene,
blindness)
treated with insulin injections or pancreatic
islet transplant (newer technique)
 Type II Diabetes Mellitus
non-insulin-dependent (NIDDM; formerly
mature-onset diabetes)
usually starts after age 40
insulin levels are normal or elevated, but
peripheral tissue become less sensitive to it
25-30% of Americans carry gene that
predisposes them to NIDDM, more likely in
over-weight people (~90% of cases)
adipose cells secrete tumor necrosis factor
alpha that depresses production of protein
needed for glucose uptake
often controllable with diet and exercise
 Hyperinsulinism
excess of insulin (usually from injection of
excess)
causes hypoglycemia --> secretion of
hyperglycemic hormones (to raise blood
glucose) - low glucose to brain --> anxiety,
nervousness, tremors, weakness -->
eventually, disorientation, convulsions, death
due to insulin shock
treated by providing sugar source
 6. Gonadal Hormones
Female - ovaries
produce/secrete estrogens
and progesterone
estrogens alone -->
development and
maintenance of ovaries,
uterus, secondary sex
characteristics
estrogens with
progesterone --> breast
development, uterine http://www.lab.anhb.uwa.edu.au/mb1
cycle 40/CorePages/FemaleRepro/femalerep
ro.htm#Follicles
 6. Gonadal Hormones
Male - testes
produce androgens (testosterone) -->
development and maintenance of male
reproductive system and secondary sex
characteristics; sperm production, protein
synthesis
inhibin - inhibits release of FSH and LH

http://www.usc.edu/hsc/dental/ghisto/rep/c_72.html
 7. Thymus
located in mediastinum
function:
active during childhood and before puberty,
after puberty gradually decreases in size and
becomes fibrous (involution)
secretes thymosin (thymic extract containing
several complementary hormones)
action: promotes development and maturation of
lymphocytes
* gradual decrease in size and secretory abilities
make the elderly more susceptible to disease
 General Adaptation Syndrome
(GAS)
stress response
stress = any condition that threatens to alter
homeostasis
same general response to a variety of stress
major endocrine player is adrenal gland
(medulla and cortex)
three phases:
alarm
resistance
exhaustion
 GAS: Alarm Phase
immediate response to stress
mobilization of energy sources
sympathetic division activated results
in release of epinephrine, NE from
adrenal medulla
 GAS: Alarm Phase
direct neural and epinephrine effects:
increased heart rate
dilation of pupils
changes in circulation (more to skeletal &
cardiac muscle, less to gut)
increased respiration
increased energy use by cells
increased blood glucose
decreased digestion and urine production
increased perspiration
 GAS: Resistance Phase
when stress is present more than a few hours, able
to cope for weeks to a few months
secretion of renin from kidney --> renin-angiotensin
pathway --> aldosterone secretion --> increased
Na+ reabsorption --> increased water retention
secretion of ACTH from pituitary
increased aldosterone secretion
* increased glucocorticoid secretion --> increased
blood glucose, conservation of glucose by
muscle, lipids and proteins mobilized as
alternative energy sources
secretion of glucose conservation hormones
(growth hormone, thyroid hormone, epi) -->
conservation of glucose and use of alternatives
 GAS: Exhaustion Phase
prolonged stress (more than a few months)
homeostatic breakdown due to:
mineral (electrolyte) imbalances
depletion of glucocorticoids
exhaustion of lipid reserves (especially with
starvation)
structural or functional damage to organs
Adrenal Gland Role in GAS

Fig. 17.15, p. 635