lecture 6 Flashcards
what does up/down regulation of a hormone mean?
cells adjust their sensitivity to hormone in response to changes in [hormone]
Up regulation of a hormone
- trying to maintain response despite low [hormone]
- increased number of receptors in response to sustained low [hormone]
Down regulation of a hormone
- decreased number of receptors in response to sustained high [hormone]
- usually involves endocytosis of membrane receptors
is up/down regulation short term or long term?
long term effects
take time to occur (endo/exosytosis, protein synthesis)
what would be a faster modulation of cell response than up/down regulation?
sensetization and desensitization
- modifying existing receptors (ie. dephosphorylation) to change their activity
- total number of receptors does not change
Tropic hormones control
secretion of another hormone
give an example of a tropic hormone release cascade
Thyrotropin releasing hormone (TRH) from the hypothlamus
–> causes release of thyrotropin (thyroid stimulating hormone; TSH) from anterior pituitary
–> causes release of thyroid hormones (T3, T4) from thyroid
synergism (hormones)
cells/tissues can be under the influence of multiple hormones at any given time
“1+1>2”
there is funtional overlap
reasons not well understood
Permissiveness (hormones)
If hormone A can’t produce its full effect without the presence of hormone B, then B is permissive for A
Functional antagonists (hormones)
hormones with opposite actions
ex. insulin vs. glucagon and growth hormone
don’t need to share receptors or signalling pathways
ligand=
a chemical molecule that binds to a receptor
agonist ligand
a ligand that binds to a receptor and enhances the receptor’s activity
antagonist ligand
a ligand that binds to a receptor and inhibits the receptor’s activity
what is the target cell response determined by?
the receptor and intracellular signalling pathways
NOT on the ligand
give an example of how an agonist can have diff effects in diff tissues
adrenaline dilates blood vessels in skeletal muscle but constricts blood vessels in intestines
Specificity (of receptors)
receptors may show preference for a particular ligand/type of ligand
what would a very specific receptor do?
bind very few ligands
what would a non-specific receptor do?
be able to bind many different ligands
competition (of receptors)
multiple ligands can compete for the same receptor active site
-the one with the higher affinity/concentration “wins”
competitive antagonist
same binding site on receptor as agonist
-can be overcome by increased [agonist]
non-competitive antagonist
different binding site on receptor (allosteric site) than agonist
- can’t be overcome by increased [agonist]
What is EC(50)?
= [agonist] producing 50% of the max response
What does % response depend on?
[agonist] and it increases with % of receptors bound to agonist
- if concentration is high enough, receptors will be saturated and the response it maximal
how do competitive antagonists affect agonist binding rate
they make it more difficult for agonist to bind and elicit a response
- max response can still be achieved with high [antagonist]
how do non-competitive antagonists affect agonist binding rate?
they change availability of binding site or irreversibly block binding site
-antagonist effect can’t be overcome by increasing [agonist]
explain a pathway of release hormones
(Thyrotropin-releasing hormone)
hypothalamic hormone (tropic)= TRH
anterior pituitary hormone (tropic)= TSH, thyroid stimulating hormone
endocrine target= thryoid gland
thryroid gland secreted T3 and T4
sensetization is also known as
phosphorylation
desensetization is also known as
dephosphorylation
what are the 3 insulin pathways?
- beta cells release insulin
- stretch receptors detect stretch in stomach
- glucose sensors in lumen (ex. small intestine) sense lumen glucose and release GLP 1
parathyroid hormone (PTH)
PTH is calcium sensing
it goes into circulation and acts on targets if they have a receptor
bone and kidney have calcium
