PSL300H1 Lecture Notes - Gonadotropin, Nuclear Receptor, Catabolism

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26 Jan 2013
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Page 1 of 5
Hormone
Type
Stimulus
Released from
Target(s)
Mechanism of action
Functions to
Too much?
Too little?
insulin
peptide
high plasma
[glucose]; GLP-
1, GIP; high
plasma [AA],
parasympathetic
NS
pancreas (β cells)
most tissues in
body (not liver,
brain)
receptor Tyr kinase: (i)
Ras-MAP kinase, (ii) PI-
3 kinase/PKB
↑ glucose uptake by cells
and ↓ plasma [glucose];
promotes glycolysis;
formation of glycogen, fat,
protein
hypoglycem-
ia
hyperglycem-
ia
melatonin
amine
(W)
sleeping
(darkness)
pineal gland
(main); GI tract,
leukocytes, other
brain regions
brain and others
(behaves like peptides or
steroids)
transmit info of light-dark
cycles; immune modulation;
anti-oxidant
sleepiness
over-
alertness;
insomnia
catecholamines
(epinephrine +
NE)
amine
(Y)
sympathetic
output
adrenal medulla
(cytosol)
liver, cardiac &
skeletal muscles;
fat; intestine;
skin; kidney;
brain
(behaves like peptides)
vesicle storage & release;
G protein (both AC and
PLC pathways)
initiate fight-or-flight
response; ↑ glycogenolysis,
↓ glycogenesis
hyperglycem-
ia; skeletal
muscle
hyperactivity;
low digestion
digestive
state; reduced
alertness, etc.
parathyroid
hormone (PTH)
peptide
low plasma
[Ca2+]
parathyroid
glands (chief
cells)
bone
(osteoblasts),
kidney
calcium-sensing receptor
(G protein-coupled
pathway)
↑ plasma [Ca2+]
osteoporosis;
abnormally
high plasma
[Ca2+]
poor neural
signal
transmission
calcitriol
steroid
high PTH
activity
kidney (proximal
tubule)
kidney, intestine
intracellular receptor-
binding
↑ plasma [Ca2+]
abnormally
high plasma
[Ca2+]
low plasma
[Ca2+]; ↓
intestinal
absorption of
Ca2+
calcitonin
peptide
high plasma
[Ca2+]
thyroid gland
bone
(osteoclasts),
kidneys
unspecified (G protein-
coupled receptor
pathway)
inhibits bone resorption &
calcium reabsorption by
kidneys
abnormally
low plasma
[Ca2+]
osteoporosis
arginine
vasopressin
(AVP)/anti-
diuretic
hormone
(ADH)
peptide
high plasma
osmolarity
synthesized in
hypothalamus;
released from PP
kidney: collecting
duct
G protein pathway:
insertion of aquaporin-2
water pores into apical
membrane
↑ water reabsorption, and
ultimately ↑ b.p.
polyuria,
polydipsia;
hypertension
low b.p. may
cause
unconscious-
ness
aldosterone
steroid
high plasma
[K+],
angiotensin II
adrenal cortex
kidney: distal
tubule &
collecting duct
intracellular gene
regulation: Na+ channels
+ K+ channels + Na+/K+
ATPase
secrete K+ and reabsorb Na+
Conn’s;
polyuria;
hypertension
hypotension
renin (not a
hormone)
peptide
low blood
pressure
kidney
(juxtaglomerular
cells)
carries out
enzymatic activity
in circulation;
target substrate
angiotensinogen
n/a
leave angiotensinogen into
angiotensin I
over-
production of
angiotensin II
(see below)
angiotensin II
deficiency
(see below)
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Page 2 of 5
Hormone
Type
Stimulus
Released from
Target(s)
Mechanism of action
Functions to
Too much?
Too little?
angiotensin II
peptide
n/a
in circulation
(angiotensinogen
constitutively
released from
liver)
hypothalamus;
blood vessels;
adrenal cortex
unspecified
↑ b.p. by stimulating release
of aldosterone, eliciting
behaviour of drinking, etc.
extreme
thirst; hyper-
tension
hypotension
glucagon
peptide
low plasma
[glucose]
pancreas (α cells)
liver
G protein-coupled;
↑ plasma [glucose]; promote
glycogenolysis, lipolysis,
gluconeogenesis
hyperglycem-
ia
hypoglycem-
ia
atrial natriuretic
hormone
(ANH)
peptide
atrial stretch (↑
blood vol.)
cardiac atria
hypothalamus,
kidney, adrenal
cortex, medulla
unspecified
↓ b.p. by inhibit AVP &
aldosterone secretion
(angiotensin II antagonist),
dilation of afferent arteriole
in nephron, etc.
hypotension
hypertension
gastric
inhibitory
peptide (GIP)
peptide
glucose/FA in
intestine
small intestine
pancreatic β cells
unspecified
↑ insulin release, ↓ gastric
emptying/acid
over-
stimulation of
insulin
release
slow insulin
response to
glucose
glucagon-like
peptide-1
(GLP-1)
peptide
glucose in
intestine
small intestine
pancreatic β cells
unspecified
↑ insulin, ↓ glucagon, ↑ β
cell growth, ↓ gastric
emptying/acid, feeling of
satiety
over-
stimulation of
insulin
release
slow insulin
response to
glucose
dehydroepiand-
rosterone
(DHEA)
steroid
ACTH
(cortical), LH
(gonadal) action
adrenal cortex;
gonads
n/a
a weak androgen
women: pubic/axillary hair,
source of estrogen after
menopause; onset of puberty
in children
n/a
n/a
androstenedi-
one
steroid
ACTH
(cortical), LH
(gonadal) action
adrenal cortex;
gonads (thecal
cells)
n/a
a weak androgen
precursor of testosterone,
estradiol
n/a
n/a
adrenocorticotr
opic hormone
(ACTH)
peptide
CRH action
anterior pituitary
adrenal cortex
unspecified
stimulates adrenal cortex &
initiates
steroidogenesis/cortisol
synthesis
excess
production of
cortical
steroids
deficiency of
cortical
steroids
corticotropin-
releasing
hormone (CRH)
peptide
stress; circadian
rhythm
hypothalamus;
placenta
anterior pituitary
unspecified
stimulate ACTH release
from ant. pit.
(hypothalamic); gestation &
parturition (placental)
excess ACTH
hypoglycem-
ia; hepatitis
cortisol
steroid
ACTH action
adrenal cortex
liver, fat, muscle,
bone,
lymphocytes
unspecified
protect against
hypoglycemia; permissive
effect on epinephrine &
glucagon
Cushing’s; ↓
CRH, ACTH
release
hypoglycem-
ia
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