YouTube Transcript:
Costanzo Physiology (Chapter 9E) Endocrine Physiology: Pancreas || Study This!

hello and welcome to the next portion of
the endocrine physiology chapter going
over the endocrine pancreas of
costanzo's physiology textbook if you
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so jumping into the endocrine pancreas
remember this is different to our
exocrine pancreas which secretes
enzymes into our gi system to then break
down
our food products the endocrine pancreas
secretes hormones into the bloodstream
to mainly regulate our glucose
concentrations
so we have these areas called the islets
of langerhans
which contain the endocrine pancreas
cells
predominantly we have alpha cells beta
cells
some delta cells and then some other
cells intermixed
but the alpha cells secrete glucagon
they the cells secrete
insulin and then delta cells release
somatostatin
the other cells that aren't really
depicted in here at least pancreatic
polypeptide but there is less known
about this
actual hormone so we won't be covering
that in this chapter
so since we have this organization of
the cells and these eyelets of
langerhans
they actually have some cells to cell
communication either by gap junctions
which is just the electrical
communication between the cells or due
to the blood supply that comes in
once one cell has received its blood
supply that venous blood from that cell
actually disperses to the other cells so
they are able to communicate with one
another
and then there's also adrenergic
cholinergic and peptidogenic
neurons as well that innervate these
cells so we're going to go through
each of those major hormones insulin is
a big one
because clearly it causes a pretty
significant clinical disease and
diabetes
so starting with the synthesis and the
structure of insulin
it gets synthesized into first pre pro
insulin
from the mrna within the cell it is then
cleaved early into
pro insulin before getting shuttled away
until the endoplasmic reticulum where it
is modified to be folded
into a folded form of insulin and then
finally packaged up
into some secretory granules in the
golgi apparatus ready to be released as
actual insulin now insulin gets
regulated predominantly from
glucose but it can be thought of as a
hormone
of abundance so any abundance of
nutrients
insulin is going to be secreted to try
and store that energy in the body for
use in the future so although increased
glucose concentrations are by far the
most important stimulatory factor
increased amino acids or fatty acids
will also stimulate insulin release
in addition to glucagon which we'll talk
about in a second
cortisol which has a insulin resistant
factor
that will actually increase the
secretion of insulin just because
cortisol is going to increase our
glucose and then also increase our
insulin as well
glucose-dependent and selenotropic
peptide
gip this is a hormone that's released
from the gi system when we eat food and
this
causes an increased release of insulin
due to oral glucose
versus if we give glucose intravenously
it's all because gip comes in and
further stimulates insulin release
potassium causes the release of insulin
potassium is in our diet and this is
important because insulin helps
potassium get shuttled away into cells
so when we eat
insulin gets released to move those
potassium from the diet
into our cells vagal stimulation and
some drugs will do it so
sulfonylurea drugs increase the
secretion of insulin and these are some
treatments
for type 2 diabetes we'll get into
diabetes in a second here
and then clearly obesity there will be
abundant nutrients
with obesity so that will stimulate
increased insulin secretion
the inhibitory factors of insulin
secretion include low glucose which is
understandable fasting and exercise
because we no longer have an abundance
for nutrients we actually want to start
using those stores of energy so insulin
is going to be bad in this situation so
we inhibit the secretion there
somatostatin remember our stopping
hormone is going to stop
our insulin secretion and then some
drugs as well so getting into how
insulin gets secreted first of all the
stimuli
mainly is glucose so we're going to
focus on glucose here it enters the cell
via the glute 2 transporter which is
facilitated transfusion
going to occur when we have
hyperglycemia you know we have a high
glucose concentration outside the cell
it then gets facilitated diffusion into
the salvia glut2
it gets oxidized essentially through
glycolysis
to produce some atp to produce some
energy molecules
these energy molecules actually
ironically close the potassium channels
on the cell by closing the potassium
channels
we stop the loss of a positive ion out
of the cell
so this actually depolarizes the cell
because remember
if we wanted to repolarize a cell then
we increase the movement of potassium
out of the cell
by stopping potassium moving out of the
cell we depolarize it so that
depolarization causes an
increase in calcium influx into the cell
high intracellular calcium then results
in exocytosis of our insulin into our
bloodstream
so that is how insulin gets stimulated
to be released because of
high glucose concentrations in our blood
now that is a similar method for if we
have increased amino acids or fatty
acids etc
so once insulin is in our bloodstream it
will go to our cells and work via the
intrinsic tyrosine
kinase receptors remember these
receptors are the ones with
actual kinase enzymes as attached to the
receptor
so by the insulin binding it we get a
conformational change so then the
tyrosine kinase enzyme
will now phosphorylate proteins and
enzymes within the cell
ultimately that will produce the effects
that we'll talk about a little bit later
in the video
now once that tyrosine kinase receptor
has been bound to insulin it actually
gets
internalized and degradated by
intracellular proteases
so insulin actually down regulates its
own receptor
so now it's going to be less sensitive
to the presence of insulin
now this is becomes a problem when we
have constantly high insulin levels
such as with diabetes mellitus
specifically
type 2 which happens with obesity
because usually
with obesity you have such an abundant
nutrients within your bloodstream you
typically are always hyperglycemic
then that's going to constantly cause
the secretion of insulin
the receptors get down regulated so now
you no longer respond to insulin
and you effectively have no useful
insulin in your body and that is when
you get diabetes mellitus
now the actions of insulin is next now
once again
this is a hormone of abundance so it's
going to function to try and shut all
away
all of our nutrients inside our body for
use at a later date
so it's able to decrease our blood
glucose concentration by
increasing the glucose transport into
cells using
the glute for transporters and increases
the production of those transporters
it promotes the formation of glycogen in
the liver and muscle remember glycogen
is just a big polymer of glucose that
stores that glucose away
it also inhibits the breakdown of
glycogen and also inhibits the formation
of new glucose via gluconeogenesis
which creates glucose basically from
amino acids
it reduces the blood fatty acid and
ketoacid concentration and stimulates
all that fat in the bloodstream to
actually get deposited
in your fatty tissue and inhibits your
lipolysis
it decreases your amino acid
concentration by increasing the uptake
by tissues and
increasing your protein synthesis and
also
promotes the uptake of potassium into
your cells remember we talked about that
you have high potassium in your diet so
insulin at the same time getting
secreted but the glucose is going to
help shuttle away all that extra
potassium into your cells
so if you have an abnormality in your
insulin you essentially end up with
diabetes mellitus
diabetes mellitus just means sugary
urine and the reason behind the sugary
urine
is because you have high blood glucose
concentrations
now that's either because of type 1
diabetes mellitus which means you are
not producing enough insulin
and that usually occurs due to an
autoimmune destruction
of your beta cells so you no longer
produce insulin
or type 2 diabetes which is insulin
resistance
and that may occur due to a constant
hyperglycemia state
this is the one that's typically
associated with obesity
due to just having so much glucose in
the bloodstream there are some
other causes for insulin resistance but
let's get into too much detail for this
particular chapter so with diabetes
since we have
ineffective insulin either due to a low
concentration
or low receptor numbers we are going to
have
increased glucose within our bloodstream
that's unable to get into our cells
so that increased glucose in our
bloodstream is going to make us pee more
because that's going to be
over the threshold for our kidneys being
able to reabsorb it so you end up with
more glucose and your urine which has an
osmotic effect to drag water with it so
you become polyuric
subsequently polydipsic as well you'll
also end up being hyperkalemic because
your potassium can't get into your cells
you start to break down your proteins
because you don't have that stimulus to
get your amino acids into your cells and
start to
produce your proteins you also increase
the amount of fatty acid and keto acids
in your bloodstream because you have
reduced
that hormone that tells that fatty acids
to get into your
fat cells and store away so that can
result in an issue actually called
diabetic ketoacidosis which is more of
an
emergency because you have so many of
these acids in your bloodstream you get
this metabolic acidosis that you have to
treat
emergently now the treatment for type 1
diabetes
is obviously going to be giving insulin
if you're able to give insulin
you essentially solve the problem of not
being able to produce it
when it comes to type 2 diabetes that's
slightly different that is non-insulin
dependent the problem is not
essentially related to insulin quantity
is related to the fact that your insulin
receptors have been down regulated
so the best way to treat this is trying
to reduce your blood glucose
concentrations
from diet restriction weight reduction
and then also some drugs that help
to try to promote some insulin secretion
but also
increase our sensitivity of insulin at
our target cells
so type 2 diabetes slightly different
where there's more of an environmental
component
into the treatment now glucagon is the
complete
opposite of insulin so it is the hormone
of starvation
and that is really to remember from our
alpha cells and it's trying to maintain
normal glucose concentrations so it's
going to be secreted for the opposite
reasons of insulin whenever we have low
sugar
within our bloodstream so low glucose
concentrations
it will also interestingly be stimulated
if we ingest
protein but this will be reduced if we
have
glucose simultaneously being secreted so
if we have high glucose high amino acids
we won't have an increased glucagon
because that'll be an issue
because that'll try to increase the
glucose even further so essentially
glucagon
is trying to increase or maintain normal
glucose concentrations
when we are hypoglycemic so it's able to
break down glycogen
via glycogenolysis it's also able to
reproduce
new glucose via gluconeogenesis from our
amino acids it's also able to increase
the breakdown
of our fat tissue via lipolysis to
increase the amount of available energy
and then also help to produce more
glucose
so everything is centered around
increasing our glucose
concentrations and then the last hormone
that we'll talk about
is somatostatin remember this is the
stopping hormone we talked about this
with growth hormone we talked about this
with our gastrointestinal hormones here
it's
once again showing its face but this
time being secreted from the delta cells
of the pancreas to actually reduce the
stimulation for secretion
for glucagon and insulin it's having
this protective effect so we don't get
an
overwhelming response of insulin or
glucagon whenever they get secreted
so it's kind of dampening their response
to a stimuli so this is all that we're
going to cover for today
going over the pancreas join us for the
next video we're going to go over the
regulation of calcium and phosphorus to
finish up this chapter
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