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RHSC 3072
ENDOCRINE SYSTEM
d) AUTOCRINE:
– Hormone released feeds-back on the cell of
origin, again without entering blood
circulation.
Major endocrine glands in the body
HORMONE-TARGET CELL
SPECIFICITY
• Only target cells, or cells that have specific
receptors, will respond to the hormone’s
presence.
– The strength of this response will depend on:
• Blood levels of the hormone
• The relative numbers of receptors for that hormone
on or in the target cells
• The affinity (or strength of interactions) of the
hormone and the receptor.
HALF-LIFE, ONSET, and DURATION
of HORMONE ACTIVITY
P ro te in O H + ATP P ro te in O P O + ADP
O
Pi H 2O
P ro te in P h o s p h a ta s e
outside
A G-protein that is
part of a pathway GPCR plasma
membrane
that stimulates
Adenylate Cyclase cytosol
AC
is called Gs & its GDP GTP
subunit Gs. GTP GDP ATP cAMP + PP i
outside
GPCR plasma
The complex membrane
outside
GPCR plasma
membrane
outside
GPCR plasma
membrane
outside
GPCR plasma
membrane
– Net result: Amino acids are shunted to protein synthesis and glucose
is shunted to metabolism.
– Net result: Both glucose AND amino acids are shunted to metabolism.
Pathophysiology of abnormal GH
secretion:
• Hyposecretion:
• Pre-adolescents:
– Decreased GH secretion (or sensitivity) results in slow
growth and delayed onset of sexual maturation.
These children also tend to be slightly chubby.
• Post-adolescents:
– Generally, no serious problems are associated with
hyposecretion of GH in mature individuals. However,
in very severe cases there can be progeria (rapid and
premature aging).
Hypersecretion:
• Pre-adolescents: (before closure of
epiphyseal plates)
• Increased cAMP
• Increased [Ca2+]i
• Main target for ADH are the cells in the kidney which reabsorb
water (will be covered in detail in the section on renal
physiology).
• Symptoms:
• Symptoms:
– A short disproportionate body, a thick tongue
and neck, and mental retardation.
– The condition is preventable by thyroid
hormone replacement therapy. However, once
developmental abnormalities and mental
retardation appear, they are not reversible.
Hyperthyroidism:
• The most common form of hyperthyroidism is Grave's disease,
believed to be an autoimmune disease.
• The immune system produces antibodies that mimic TSH, which bind
to TSH receptors and permanently switch them on, resulting in
continuous release of thyroid hormones.
– skeleton
– kidneys
– intestine
PTH stimulates the following on
these target organs:
• Osteoclasts (bone absorbing cells) are stimulated to digest
bone and release ionic calcium and phosphates to the blood.
• Results in hypercalcemia
• Each gland is
structurally and
functionally two
endocrine glands in
one.
• The inner adrenal
medulla is made up
of nervous tissue and
acts as part of the
sympathetic nervous
system. The outer
adrenal cortex forms
the bulk (about 80%)
of the gland. Each of
these regions
produces its own set
of hormones.
Adrenal Medulla:
• It is made up of chromaffin cells which secrete the catecholamines
epinephrine (E) (adrenaline) and norepinephrine (NE)
(noradrenaline) into the blood.
• In most cases the two hormones have very similar effects on their
target organs. However, E is the more potent stimulator of the heart
rate and strength of contraction, and metabolic activities, such as
breakdown of glycogen and release of glucose).
• Glucocorticoids:
– Secretion of glucagon from the alpha cells is induced by, most importantly, low
blood sugar levels but also by high amino acid levels in the blood (e.g.
following a protein-rich meal). Rising blood sugar concentration and
somatostatin from the delta cells inhibit glucagon release.
Insulin:
• Insulin is a 51 amino acid protein consisting of two polypeptide
chains linked by disulfide bonds. It is synthesized as part of a larger
molecule called proinsulin and packed into secretory vesicles where
its middle portion is excised by enzymes to produce functional
hormone, just before insulin is released from the beta cell.
• In general, insulin: