YouTube Transcript:
Costanzo Physiology (Chapter 9A) Endocrine Physiology: Intro to Hormones || Study This!

hello and welcome to the start of the
endocrine physiology chapter of
costanzo's physiology textbook
in this video we're obviously going to
get started with the basics of the
endocrine
system starting off with hormone
synthesis regulation of hormone
secretion and also regulation of hormone
receptors
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description otherwise jumping straight
into it our endocrine system
works with our nervous system to
maintain homeostasis
so in order to maintain our normal
bodily functions we have our endocrine
system
that works by secreting hormones
remember hormones are secreted
from an endocrine cell typically in an
endocrine gland
to go through the blood system through
the circulation to then
go to its target cell we have three main
types of hormones
peptides made out of amino acids
steroids made out of cholesterol
and then amines which are made out of
the tyrosine
amino acid now there is this table here
a couple tables
which is an exhaustive list of every
single or the most
common endocrine hormones that we will
actually cover
at some point in this chapter or the
next chapter feel free to pause it here
if you want to
memorize these tables but we will go
through them sequentially
this figure 9.1 here is just another
figure
which shows you these hormones and where
they are secreted from so
we have all of our endocrine cells or
organs here
and their respective hormones that they
secrete so starting off with our peptide
hormone remember this is the one that's
made
out of amino acids this is created
within the cell
like any other protein so we get our dna
that gets transcribed to produce an mrna
this mrna then gets translated into
a protein molecule in this case so
there'll be a pre-pro
hormone this pre-pro hormone then gets
further modified in the endoplasmic
reticulum to become a pro
hormone packaged up in the golgi
apparatus and then
stored within a security vesicle as the
hormone itself
so this is how a peptide hormone gets
created
standard protein synthesis using
transcription and translation
from a dna molecule when it comes to the
steroid hormones these are created
from cholesterol and they are
synthesized in only specific endocrine
cells so the adrenal cortex
the gonads corpus luteum and the
placenta to produce our
main steroid hormones here cortisol
aldosterone the estradiol progesterone
and testosterone in addition to
activated
vitamin d when it comes to amine hormone
synthesis
these include our catecholamines and
thyroid hormone
and these are created from the amino
acid tyrosine so those are our three
types of hormones
when it comes to the regulation of
hormone secretion we have two types of
mechanisms here number one our neural
mechanisms which is where our nervous
system controls the release of the
hormone
this is for instance what happens with
our sympathetic nervous system acting on
the adrenal medulla to
stimulate the release of epinephrine and
norepinephrine but more commonly our
endocrine system
gets controlled via feedback mechanisms
and more typically it's a negative
feedback system because negative
feedback is able to
maintain a homeostatic mechanism at a
certain level
so if it gets too high mechanisms are
set in place to bring it back
lower and if anything goes too low then
mechanisms are in place to increase it
so negative feedback
controls itself so then there's a steady
state of a particular hormone which is
going to produce a steady state
for a particular homeostatic mechanism
whereas positive feedback
propagates itself so increased levels of
the hormone
increases the secretion of itself so
then you actually propagate the effects
of that hormone
so you can see these two examples in 9.3
here where we have the
negative feedback system on the left
positive on the right
with the negative feedback our
hypothalamus secretes a hormone which
impacts the anterior pituitary which
then stimulates a hormone release from
the particular endocrine gland
and that hormone then actually
negatively impacts the hypothalamus
and the anterior pituitary so the fact
that the hormone gets stimulated to be
secreted
from this pathway it then feeds back on
itself via long loops
to reduce the secretion of those
releasing and secreting hormones from
the hypothalamus and anterior pituitary
gland respectively we do also have a
short loop
which is where the molecule released
from the anterior pituitary gland
actually inhibits the hypothalamus
itself
and there's an ultra short loop where
the releasing hormone from the
hypothalamus
actually reduces its own secretion so
negative feedback is really just saying
if you have too much of one thing it's
going to feed back on itself
and tell either itself or somewhere
further back in the pathway to stop
secreting that releasing or secreting
hormone
whereas positive feedback as we
mentioned the hormone
stimulates the release of additional
secreting hormones so then you get even
more
of those effects predominantly every
homeostatic mechanism every endocrine
system actually works via the negative
feedback system
there's only a couple examples of
positive feedback for example
coagulation
but when it comes to the endocrine cells
in an example given here is oxytocin
when you are about to give birth so
stretch of the cervix
causes the release of oxytocin which
then stimulates uterine contraction
and further dilation of the cervix so
then you release even more oxytocin
so this is obviously a good thing you
want that positive feedback response to
actually give birth
so there's only a few specific examples
of positive feedback in our body systems
so now talking about the regulation of
hormone receptors we have a couple
definitions here
so we have this dose response
relationship with a hormone
and its target tissue which really just
means that the magnitude of the response
is correlated to the hormone
concentration whereas our sensitivity
is just the hormone concentration that
produces a 50
of the maximal response so we can change
the sensitivity by either
increasing or decreasing the number of
the receptors
or changing the affinity of the receptor
to the hormone the affinity means how
well it's going to actually bind to that
hormone
so if we increase the number of
receptors or we increase the infinity of
the receptor to the hormone
then we increase the sensitivity of that
hormone and vice versa now changing the
number of the receptors or the affinity
of the receptors is called down or
up regulation so down regulation just
clearly means you reduce the number of
the receptors or you reduce the affinity
so you're down regulating
the amount of available receptors to
create a response
so that decreases our sensitivity and we
can do that
by decreasing the synthesis of new
receptors increasing the degradation of
existing receptors or by inactivating
the current receptors
and we will do that so then we have a
lower response
in the presence of high hormone
concentration so then we don't end up
with an exuberant response
now although these mechanisms may seem a
little boring to really understand this
is kind of the building blocks for
understanding
how our hormones function as you'll see
later on
down regulation is what happens when you
have insulin sensitivity
during type 2 diabetes so that is down
regulation we
also have up regulation which is when
you increase the number or the affinity
of the receptors
for an opposite reason as our
downregulation so we may have an
increasing synthesis of new receptors
decrease the degradation of the existing
receptors or just actually
activate our receptors so that is how we
are able to regulate
how many receptors are ready to be
influenced by
the particular hormone now we will
finish up this chapter talking about the
mechanisms of hormone action and also
secondary messengers really quickly here
now this can get very confusing if this
is the first time that you're ever
seeing this
it does take some repetition to
understand all of these types of
secondary messages but basically we have
these five main
mechanisms of hormone action the main
one is this adenylyl cyclase mechanism
so using cyclic amp
second most common is phospholipid c
mechanism
and then our steroid hormone and
tyrosine kinase
mechanism are very specific followed by
only a couple examples of the cgmp
mechanism
which is to be honest very similar to
our adenylyl cyclase
so going through each of these briefly
here all we are talking about
is how that hormone that once it binds
to its receptor
how does it cause an effect within the
cell what is it actually doing in that
cell
to produce the effect that we want so
the first example is the adenylyl
cyclase mechanism
now this is shown in figure 9.4 here
where we have the hormone attaching to
the receptor and we're going to keep
this very basic
just to cover the key points so you can
kind of understand how these secondary
messenger
systems work so the hormone comes binds
to the receptor that's sitting on the
cell membrane this receptor and that
adenylyl cyclase mechanism
is a g protein or coupled to a g protein
you'll see that it's a gs protein for
stimulatory
there are gi proteins for inhibitory
which is prevent
the next actions we are going to talk
about the stimulatory proteins
because this particular hormone is going
to cause an effect so we have the
hormone binding to the receptor and
activates the stimulatory protein which
means gtp is going to bind to it maybe
that's getting a little more complicated
but with having gtp
bound to the stimulatory g protein we
then
activate adenylyl cyclase adenylyl
cyclase is an
enzyme that's able to convert atp to
cyclic amp okay this cyclic amp is now a
secondary messenger that's going to zoom
around the cell and tell
the cell what to change so then they can
produce a new effect
so cyclic amp works by activating
protein kinases
which then phosphorylate proteins and
then these proteins which get
phosphorylated will cause the effect in
the cell that we want
basically the majority of these hormones
here how they produce an effect in a
cell
is by altering the proteins in the cell
either phosphorylating them or creating
new proteins and those proteins
are then like our workers within our
cell to then create an effect
so the adenocyclase mechanism has the
secondary messenger of cyclic
amp to then phosphorylate proteins
through protein kinases now when we do
not want cyclic amp anymore that gets
degradated by phosphodiesterases to
become inactivated once the effect has
occurred the gtp on the g
protein gets converted into gdp and then
it becomes
inactive now if this was an inhibitory g
protein the main difference
is that instead of activating adenylyl
cyclase the enzyme
it will inhibit it so it will reduce the
amount of cyclic amp in the cell
and then therefore inhibit any of those
actions so depending on the hormone
majority of them are working via
stimulatory gene proteins but there are
the
occasional example of inhibitory g
proteins to reduce the effect in that
cell
so that is our adenocyclase mechanism
the next
more common one is our phospholipase c
mechanism which is similar we have a
g protein that is coupled to a g protein
but instead of
adenyl cyclase as our enzyme we have
phospholipase c
so this just catalyzes a different
reaction so it turns pip2
into ip3 and diacyl glycerol now ip3
actually
causes calcium release within our cell
so from the endoplasmic and sarcoplasmic
reticulum
so that increased calcium can have an
effect within the cell but also with the
increased calcium and this dial glycerol
we then activate our protein kinases to
then phosphorylate our proteins and have
our physiological actions
so this is just a slightly different
mechanism with different secondary
messengers where we're working
predominantly through the increase of
calcium within the cell now when it
comes to the
guano cyclase mechanism that i said was
similar to our adenylyl cyclase just
think that you're replacing everything
with a g so instead of adenyl cyclase
you have guanocyclase instead of cyclic
amp
you have cyclic gmp but it works very
similarly to that first mechanism that
we talked about with adenyl cyclase
this is just how amp and nitric oxide
works now that brings us to
these kinase mechanisms so tyrosine
kinases or tyrosine kinase associated
receptors
these guys work by having the enzyme
that's going to cause the effect within
the cell
by changing the proteins or what have
you on the cell itself
so we don't have a quote-unquote
secondary messenger it's all
happening at the receptor itself so for
our receptor tyrosine kinases
our hormonal just binds to these
receptors this is how insulin works
and the tyrosine kinase effectively gets
activated and then we'll catalyze
a reaction to then cause an effect
within the cell
so that may be breaking down a protein
activating a protein
phosphorylating a protein etc now the
tyrosine kinase associated with
receptors these are slightly different
because it does not have tyrosine kinase
activity itself it's just
associated with them via what's called
the janus
kinase pathway you may see this later on
and more in depth which is just probably
getting a little bit more complicated
for this textbook but
effectively it's a jack pathway or
just another kinase so this kinase then
causes downstream effects
on something called an stit or stat so
you'll see this being the jack stat
pathway
stats are signal transducers and
activators of transcription
basically that's going to actually cause
transcription of mrnas on our dna to
then create
new proteins and then our last hormone
mechanism that we're going to talk about
is our steroid and thyroid hormone
mechanism now this one is different to
the others because these hormones
actually
enter the cell so they can diffuse
across the cell because they're lipid
soluble and then they
directly bind to the dna and by binding
to the dna
they are then able to transcribe their
own
mrna that they want that then gets
translated to create new proteins
so instead of activating the proteins
within the cell
the steroid and thyroid hormones
actually increase the production of the
proteins that they want within the cell
by binding to the dna itself now the
main difference between
these guys and the peptide hormones that
bind to a receptor on the cell membrane
is that our steroid and thyroid hormones
actually
act much slower over many hours rather
than having a rapid response like the
ones that bind to a receptor on the cell
so they're slightly slower create a more
gradual effect by actually producing new
proteins
rather than just activating the proteins
that already within the cell so that
will be it for today's video
i hope you enjoyed it next we are going
to cover the hypothalamic pituitary
system feel free to drop a comment
otherwise we'll see you in the next one