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

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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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forget to give it a like and subscribe

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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

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

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