0:00 hello and welcome to the start of the
0:01 endocrine physiology chapter of
0:03 costanzo's physiology textbook
0:05 in this video we're obviously going to
0:07 get started with the basics of the
0:09 endocrine
0:10 system starting off with hormone
0:11 synthesis regulation of hormone
0:13 secretion and also regulation of hormone
0:15 receptors
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0:25 description otherwise jumping straight
0:26 into it our endocrine system
0:28 works with our nervous system to
0:30 maintain homeostasis
0:32 so in order to maintain our normal
0:34 bodily functions we have our endocrine
0:36 system
0:37 that works by secreting hormones
0:39 remember hormones are secreted
0:41 from an endocrine cell typically in an
0:44 endocrine gland
0:46 to go through the blood system through
0:48 the circulation to then
0:49 go to its target cell we have three main
0:52 types of hormones
0:53 peptides made out of amino acids
0:56 steroids made out of cholesterol
0:58 and then amines which are made out of
1:00 the tyrosine
1:02 amino acid now there is this table here
1:04 a couple tables
1:05 which is an exhaustive list of every
1:07 single or the most
1:08 common endocrine hormones that we will
1:11 actually cover
1:12 at some point in this chapter or the
1:14 next chapter feel free to pause it here
1:16 if you want to
1:17 memorize these tables but we will go
1:19 through them sequentially
1:21 this figure 9.1 here is just another
1:24 figure
1:24 which shows you these hormones and where
1:26 they are secreted from so
1:28 we have all of our endocrine cells or
1:30 organs here
1:31 and their respective hormones that they
1:33 secrete so starting off with our peptide
1:35 hormone remember this is the one that's
1:37 made
1:37 out of amino acids this is created
1:40 within the cell
1:41 like any other protein so we get our dna
1:44 that gets transcribed to produce an mrna
1:47 this mrna then gets translated into
1:50 a protein molecule in this case so
1:52 there'll be a pre-pro
1:54 hormone this pre-pro hormone then gets
1:57 further modified in the endoplasmic
1:59 reticulum to become a pro
2:00 hormone packaged up in the golgi
2:02 apparatus and then
2:04 stored within a security vesicle as the
2:07 hormone itself
2:08 so this is how a peptide hormone gets
2:10 created
2:11 standard protein synthesis using
2:14 transcription and translation
2:16 from a dna molecule when it comes to the
2:18 steroid hormones these are created
2:21 from cholesterol and they are
2:22 synthesized in only specific endocrine
2:25 cells so the adrenal cortex
2:27 the gonads corpus luteum and the
2:29 placenta to produce our
2:31 main steroid hormones here cortisol
2:33 aldosterone the estradiol progesterone
2:35 and testosterone in addition to
2:38 activated
2:38 vitamin d when it comes to amine hormone
2:41 synthesis
2:42 these include our catecholamines and
2:44 thyroid hormone
2:46 and these are created from the amino
2:48 acid tyrosine so those are our three
2:50 types of hormones
2:52 when it comes to the regulation of
2:53 hormone secretion we have two types of
2:55 mechanisms here number one our neural
2:57 mechanisms which is where our nervous
2:59 system controls the release of the
3:00 hormone
3:01 this is for instance what happens with
3:03 our sympathetic nervous system acting on
3:05 the adrenal medulla to
3:06 stimulate the release of epinephrine and
3:09 norepinephrine but more commonly our
3:11 endocrine system
3:12 gets controlled via feedback mechanisms
3:15 and more typically it's a negative
3:16 feedback system because negative
3:18 feedback is able to
3:19 maintain a homeostatic mechanism at a
3:22 certain level
3:23 so if it gets too high mechanisms are
3:26 set in place to bring it back
3:28 lower and if anything goes too low then
3:30 mechanisms are in place to increase it
3:32 so negative feedback
3:33 controls itself so then there's a steady
3:36 state of a particular hormone which is
3:38 going to produce a steady state
3:40 for a particular homeostatic mechanism
3:42 whereas positive feedback
3:43 propagates itself so increased levels of
3:46 the hormone
3:47 increases the secretion of itself so
3:49 then you actually propagate the effects
3:51 of that hormone
3:52 so you can see these two examples in 9.3
3:55 here where we have the
3:57 negative feedback system on the left
3:58 positive on the right
4:00 with the negative feedback our
4:01 hypothalamus secretes a hormone which
4:04 impacts the anterior pituitary which
4:06 then stimulates a hormone release from
4:08 the particular endocrine gland
4:10 and that hormone then actually
4:12 negatively impacts the hypothalamus
4:14 and the anterior pituitary so the fact
4:16 that the hormone gets stimulated to be
4:18 secreted
4:19 from this pathway it then feeds back on
4:22 itself via long loops
4:24 to reduce the secretion of those
4:26 releasing and secreting hormones from
4:28 the hypothalamus and anterior pituitary
4:30 gland respectively we do also have a
4:32 short loop
4:33 which is where the molecule released
4:35 from the anterior pituitary gland
4:36 actually inhibits the hypothalamus
4:38 itself
4:39 and there's an ultra short loop where
4:40 the releasing hormone from the
4:42 hypothalamus
4:43 actually reduces its own secretion so
4:46 negative feedback is really just saying
4:48 if you have too much of one thing it's
4:50 going to feed back on itself
4:52 and tell either itself or somewhere
4:54 further back in the pathway to stop
4:56 secreting that releasing or secreting
4:58 hormone
4:59 whereas positive feedback as we
5:01 mentioned the hormone
5:02 stimulates the release of additional
5:04 secreting hormones so then you get even
5:06 more
5:07 of those effects predominantly every
5:09 homeostatic mechanism every endocrine
5:12 system actually works via the negative
5:14 feedback system
5:16 there's only a couple examples of
5:17 positive feedback for example
5:19 coagulation
5:20 but when it comes to the endocrine cells
5:22 in an example given here is oxytocin
5:25 when you are about to give birth so
5:27 stretch of the cervix
5:28 causes the release of oxytocin which
5:31 then stimulates uterine contraction
5:33 and further dilation of the cervix so
5:35 then you release even more oxytocin
5:37 so this is obviously a good thing you
5:39 want that positive feedback response to
5:41 actually give birth
5:42 so there's only a few specific examples
5:44 of positive feedback in our body systems
5:46 so now talking about the regulation of
5:48 hormone receptors we have a couple
5:50 definitions here
5:51 so we have this dose response
5:53 relationship with a hormone
5:55 and its target tissue which really just
5:57 means that the magnitude of the response
5:59 is correlated to the hormone
6:01 concentration whereas our sensitivity
6:04 is just the hormone concentration that
6:06 produces a 50
6:07 of the maximal response so we can change
6:10 the sensitivity by either
6:12 increasing or decreasing the number of
6:15 the receptors
6:16 or changing the affinity of the receptor
6:18 to the hormone the affinity means how
6:20 well it's going to actually bind to that
6:22 hormone
6:23 so if we increase the number of
6:24 receptors or we increase the infinity of
6:27 the receptor to the hormone
6:29 then we increase the sensitivity of that
6:31 hormone and vice versa now changing the
6:34 number of the receptors or the affinity
6:35 of the receptors is called down or
6:37 up regulation so down regulation just
6:40 clearly means you reduce the number of
6:42 the receptors or you reduce the affinity
6:44 so you're down regulating
6:46 the amount of available receptors to
6:48 create a response
6:50 so that decreases our sensitivity and we
6:53 can do that
6:53 by decreasing the synthesis of new
6:55 receptors increasing the degradation of
6:58 existing receptors or by inactivating
7:01 the current receptors
7:02 and we will do that so then we have a
7:04 lower response
7:05 in the presence of high hormone
7:07 concentration so then we don't end up
7:09 with an exuberant response
7:11 now although these mechanisms may seem a
7:14 little boring to really understand this
7:16 is kind of the building blocks for
7:17 understanding
7:18 how our hormones function as you'll see
7:21 later on
7:22 down regulation is what happens when you
7:24 have insulin sensitivity
7:26 during type 2 diabetes so that is down
7:29 regulation we
7:30 also have up regulation which is when
7:32 you increase the number or the affinity
7:34 of the receptors
7:35 for an opposite reason as our
7:36 downregulation so we may have an
7:38 increasing synthesis of new receptors
7:40 decrease the degradation of the existing
7:42 receptors or just actually
7:44 activate our receptors so that is how we
7:46 are able to regulate
7:48 how many receptors are ready to be
7:50 influenced by
7:51 the particular hormone now we will
7:53 finish up this chapter talking about the
7:54 mechanisms of hormone action and also
7:57 secondary messengers really quickly here
7:59 now this can get very confusing if this
8:01 is the first time that you're ever
8:02 seeing this
8:03 it does take some repetition to
8:05 understand all of these types of
8:07 secondary messages but basically we have
8:10 these five main
8:12 mechanisms of hormone action the main
8:14 one is this adenylyl cyclase mechanism
8:17 so using cyclic amp
8:19 second most common is phospholipid c
8:21 mechanism
8:22 and then our steroid hormone and
8:24 tyrosine kinase
8:26 mechanism are very specific followed by
8:28 only a couple examples of the cgmp
8:31 mechanism
8:32 which is to be honest very similar to
8:34 our adenylyl cyclase
8:36 so going through each of these briefly
8:38 here all we are talking about
8:40 is how that hormone that once it binds
8:43 to its receptor
8:44 how does it cause an effect within the
8:46 cell what is it actually doing in that
8:48 cell
8:49 to produce the effect that we want so
8:51 the first example is the adenylyl
8:53 cyclase mechanism
8:54 now this is shown in figure 9.4 here
8:56 where we have the hormone attaching to
8:58 the receptor and we're going to keep
8:59 this very basic
9:01 just to cover the key points so you can
9:02 kind of understand how these secondary
9:04 messenger
9:05 systems work so the hormone comes binds
9:08 to the receptor that's sitting on the
9:10 cell membrane this receptor and that
9:11 adenylyl cyclase mechanism
9:13 is a g protein or coupled to a g protein
9:16 you'll see that it's a gs protein for
9:18 stimulatory
9:19 there are gi proteins for inhibitory
9:22 which is prevent
9:23 the next actions we are going to talk
9:25 about the stimulatory proteins
9:27 because this particular hormone is going
9:28 to cause an effect so we have the
9:30 hormone binding to the receptor and
9:32 activates the stimulatory protein which
9:35 means gtp is going to bind to it maybe
9:37 that's getting a little more complicated
9:39 but with having gtp
9:40 bound to the stimulatory g protein we
9:43 then
9:43 activate adenylyl cyclase adenylyl
9:46 cyclase is an
9:47 enzyme that's able to convert atp to
9:50 cyclic amp okay this cyclic amp is now a
9:54 secondary messenger that's going to zoom
9:56 around the cell and tell
9:57 the cell what to change so then they can
10:00 produce a new effect
10:01 so cyclic amp works by activating
10:04 protein kinases
10:06 which then phosphorylate proteins and
10:08 then these proteins which get
10:09 phosphorylated will cause the effect in
10:12 the cell that we want
10:13 basically the majority of these hormones
10:15 here how they produce an effect in a
10:17 cell
10:17 is by altering the proteins in the cell
10:19 either phosphorylating them or creating
10:21 new proteins and those proteins
10:23 are then like our workers within our
10:25 cell to then create an effect
10:27 so the adenocyclase mechanism has the
10:30 secondary messenger of cyclic
10:31 amp to then phosphorylate proteins
10:33 through protein kinases now when we do
10:35 not want cyclic amp anymore that gets
10:38 degradated by phosphodiesterases to
10:40 become inactivated once the effect has
10:42 occurred the gtp on the g
10:44 protein gets converted into gdp and then
10:48 it becomes
10:48 inactive now if this was an inhibitory g
10:51 protein the main difference
10:53 is that instead of activating adenylyl
10:55 cyclase the enzyme
10:57 it will inhibit it so it will reduce the
10:59 amount of cyclic amp in the cell
11:01 and then therefore inhibit any of those
11:03 actions so depending on the hormone
11:05 majority of them are working via
11:07 stimulatory gene proteins but there are
11:09 the
11:10 occasional example of inhibitory g
11:12 proteins to reduce the effect in that
11:14 cell
11:15 so that is our adenocyclase mechanism
11:18 the next
11:18 more common one is our phospholipase c
11:21 mechanism which is similar we have a
11:23 g protein that is coupled to a g protein
11:25 but instead of
11:26 adenyl cyclase as our enzyme we have
11:30 phospholipase c
11:31 so this just catalyzes a different
11:34 reaction so it turns pip2
11:36 into ip3 and diacyl glycerol now ip3
11:40 actually
11:41 causes calcium release within our cell
11:43 so from the endoplasmic and sarcoplasmic
11:45 reticulum
11:46 so that increased calcium can have an
11:48 effect within the cell but also with the
11:50 increased calcium and this dial glycerol
11:53 we then activate our protein kinases to
11:55 then phosphorylate our proteins and have
11:57 our physiological actions
11:59 so this is just a slightly different
12:00 mechanism with different secondary
12:02 messengers where we're working
12:04 predominantly through the increase of
12:06 calcium within the cell now when it
12:07 comes to the
12:08 guano cyclase mechanism that i said was
12:11 similar to our adenylyl cyclase just
12:13 think that you're replacing everything
12:15 with a g so instead of adenyl cyclase
12:18 you have guanocyclase instead of cyclic
12:20 amp
12:21 you have cyclic gmp but it works very
12:24 similarly to that first mechanism that
12:26 we talked about with adenyl cyclase
12:28 this is just how amp and nitric oxide
12:30 works now that brings us to
12:32 these kinase mechanisms so tyrosine
12:35 kinases or tyrosine kinase associated
12:37 receptors
12:38 these guys work by having the enzyme
12:41 that's going to cause the effect within
12:43 the cell
12:44 by changing the proteins or what have
12:46 you on the cell itself
12:48 so we don't have a quote-unquote
12:49 secondary messenger it's all
12:51 happening at the receptor itself so for
12:54 our receptor tyrosine kinases
12:56 our hormonal just binds to these
12:58 receptors this is how insulin works
13:00 and the tyrosine kinase effectively gets
13:03 activated and then we'll catalyze
13:05 a reaction to then cause an effect
13:07 within the cell
13:08 so that may be breaking down a protein
13:11 activating a protein
13:12 phosphorylating a protein etc now the
13:14 tyrosine kinase associated with
13:16 receptors these are slightly different
13:18 because it does not have tyrosine kinase
13:20 activity itself it's just
13:21 associated with them via what's called
13:24 the janus
13:25 kinase pathway you may see this later on
13:27 and more in depth which is just probably
13:28 getting a little bit more complicated
13:30 for this textbook but
13:31 effectively it's a jack pathway or
13:34 just another kinase so this kinase then
13:38 causes downstream effects
13:39 on something called an stit or stat so
13:42 you'll see this being the jack stat
13:43 pathway
13:44 stats are signal transducers and
13:46 activators of transcription
13:48 basically that's going to actually cause
13:50 transcription of mrnas on our dna to
13:52 then create
13:53 new proteins and then our last hormone
13:55 mechanism that we're going to talk about
13:57 is our steroid and thyroid hormone
13:59 mechanism now this one is different to
14:00 the others because these hormones
14:02 actually
14:03 enter the cell so they can diffuse
14:05 across the cell because they're lipid
14:06 soluble and then they
14:07 directly bind to the dna and by binding
14:11 to the dna
14:12 they are then able to transcribe their
14:15 own
14:15 mrna that they want that then gets
14:17 translated to create new proteins
14:20 so instead of activating the proteins
14:22 within the cell
14:23 the steroid and thyroid hormones
14:25 actually increase the production of the
14:27 proteins that they want within the cell
14:29 by binding to the dna itself now the
14:31 main difference between
14:32 these guys and the peptide hormones that
14:35 bind to a receptor on the cell membrane
14:38 is that our steroid and thyroid hormones
14:41 actually
14:41 act much slower over many hours rather
14:44 than having a rapid response like the
14:46 ones that bind to a receptor on the cell
14:49 so they're slightly slower create a more
14:51 gradual effect by actually producing new
14:53 proteins
14:54 rather than just activating the proteins
14:56 that already within the cell so that
14:57 will be it for today's video
14:59 i hope you enjoyed it next we are going
15:01 to cover the hypothalamic pituitary
15:04 system feel free to drop a comment
15:05 otherwise we'll see you in the next one
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