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

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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

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

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