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BIOL 3324 Human Physiology - BIOL3324_lecture23_1116
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00:01 All right, y'all, let's It looks like it's working.
00:04 great. Sorry about being late. know like I said, someone,
00:08 fine, it's not fine. You paid for an hour and 20 minutes
00:12 me, you're getting an hour and minutes of me. It's like,
00:16 . All right, today, what doing is we're doing the endocrine system
00:19 it's really not the whole endocrine Really. What we're covering here are
00:23 hormones or the end. Yeah, . The hormones of metabolism. That's
00:27 it boils down to. And so we'll do is we're gonna look at
00:31 and Glucagon, we'll move through the cortex. We'll deal with growth
00:35 We're gonna talk about calcium regulation, hormone. So we're kind of jumping
00:40 over the place. But ultimately, big picture is these are the hormones
00:44 govern metabolism. All right. So starting point here is gonna be the
00:50 . We already talked about the pancreas terms of its exac function and creating
00:54 low zymogen and other fun little And so what we're doing now is
00:58 moving into the pancreatic islets or the of Langerhans and here, this is
01:03 we're producing the insulin and the Glucagon a couple of other fun things.
01:07 , here's somatostatin again. It just showing up over and over again,
01:12 produced in a whole bunch of different . Um There's also something in here
01:15 pancreatic polypeptide. I don't even know it does. It's just mentioned in
01:18 book and I don't think the book talks about what it does. It's
01:21 things are being produced there. And one day we'll find out it's the
01:25 most important hormone in your body and it, we all explode or something
01:29 that. So, um it's just . Um So what I have up
01:35 , as I say that the pancreatic are richly perfused and richly innervated.
01:40 so what does that mean? It that there's lots of blood vessels,
01:43 a lots of nerves. And so we're doing is we are supplying that
01:48 with a lot of blood so that can release its materials into the bloodstream
01:53 then have an effect on the rest the body. All right. So
01:58 were pictures that you see in the and really there's there while, while
02:03 information there is incredibly overwhelming, we're make this as simple as possible.
02:08 is where I hope this will make lot of sense. So first
02:12 we got insulin and Glucagon, they paired uh hormone set, one is
02:16 gas one is a break. So you do whenever you have anything like
02:20 you ask the question is all what does one of these do?
02:24 if one of them is the then the opposite or the other one
02:27 just the opposite. So it makes really, really simple. So what
02:31 gonna do is we're gonna focus in insulin and then just say Glucagon does
02:34 opposite and I'm gonna show you the or two cases where Glucagon doesn't do
02:38 opposite because it would kill you if did. All right. So that's
02:42 idea. So, first off, do we make insulin? Well,
02:46 gonna be first, it's made in beta cells. So, Glucagon is
02:50 cells, uh uh insulin is beta . And so the things that stimulate
02:55 production of insulin include all your little , glucose and galactose and some
03:01 for example, the presence of amino , especially these two arginine and
03:08 And then there's a weak stimulator in of fructose. And the reason I
03:12 this out was being when I was reading your textbook about this, I
03:15 like, well, that explains exactly high fructose corn syrup is so terrible
03:20 you, right? You've heard right? Why? Because you get
03:25 this sugar circulating in your body and body doesn't know what to do with
03:29 because it's not up regulating the insulin make it happen. And So it
03:32 a while for that fructose to be into something that then causes insulin to
03:38 up. So you actually end up more sugars in your body, which
03:43 what results in the problems. Like two diabetes, et cetera, et
03:48 , et cetera. All right. I just point that out because everyone
03:52 , oh, if you're hungry, eat an apple. You know,
03:54 apples are good for you and they , but too much fructose is not
03:59 for you. OK? Just pointing out. Hm. Too much of
04:06 good thing. There you go. right, in terms of neuro
04:10 we know sympathetic versus parasympathetic. So in really things without looking at all
04:14 stuff, which system is activated while eating parasympathetic or sympathetic parasympathetic. So
04:21 is the dominating activator of insulin Well, what is sympathetic, doing
04:26 , sympathetic is actually stimulating the alpha and it does so better than it
04:33 the beta adrenergic. And that is causes the inhibition of insulin release.
04:38 difference with the acetylcholine is gonna be from the vagus nerve. And remember
04:42 vagus is also promoting through acetylcholine, activation of digestion activation of absorption.
04:49 this other fun stuff that we saw in the stomach and in the small
04:53 . So we just kind of lump in there with parasympathetic choline keeps it
04:58 . All right, in terms of things, humeral, these are what
05:04 the hormones? And we've only talked one of them, we talked about
05:08 , right. That's going to stimulate production of insulin. And then I
05:13 mentioned these two because they're in those popular drugs right now. Um,
05:18 , now I'm forgetting the, Ozim will gov and the third one
05:23 Monja. Those are the three big right now. And all three of
05:28 are responsible for up regulating G IP up regulates G LP and G
05:36 So what they're doing is they're cause use, these are, these are
05:41 diabetic drugs. They're used for type diabetes. And what they do is
05:46 amplify or override the body's normal response sugars in the blood by basically down
05:53 . So it's a negative feedback loop we're not gonna get into. But
05:57 idea is, is like, I'm ignore the negative feedback loop and I'm
06:01 pump out the G IP and I'm pump out the G LP which causes
06:05 to be flooded into the body. I start mobilizing all that sugar.
06:09 on top of that, what I'm do is I'm gonna slow down the
06:12 of digestion. That's how they work essence. And so you become full
06:17 you don't want to eat. And then that's gonna drop your blood sugar
06:21 down. So that's how we control diabetes. All right. Second thing
06:26 we can do, we can have in the digestive tract. And
06:29 that's how these two things are actually activated as food shows up in the
06:34 tract. That's where you get that response. So you get the insulin
06:39 from the beta cells there. All . The idea is, hey,
06:45 coming, let's get ready to start it, moving it into the cells
06:50 will normally pick this stuff up. this is a really, really old
06:53 showing you how do we regulate the cells. And so we have all
06:59 things that are positively regulating and one that's negative regulating here is really,
07:03 simple, right? So the idea I increase my hormones, I have
07:08 in parasympathetic stimulation. My blood glucose go up and my blood amino acid
07:14 go up. All those are positive of insulin production, sympathetic activity says
07:20 , no, no, you suppress . So that's where the, where
07:24 do that. And so as a , insulin levels climb and what does
07:28 do? Well, in very generic , it brings down the blood
07:31 fatty acid amino acids levels and it protein synthesis and increases fuel storage.
07:39 right. So what we're doing here insulin is a way to get the
07:44 out of the blood and into the that are gonna use them. All
07:48 . So what does Glucagon do the ? All right. Now, in
07:55 terms, this is what's going on carbohydrates. This is what's going on
07:59 the amino acids. This is what's on with the fatty acids. First
08:02 carbohydrates, we are going to move glucose in the most cells. We're
08:07 stimulate glycogenesis in skeletal muscle and We don't wanna have free glucose just
08:12 around. What do we want to with it? Store it up for
08:15 rainy day. There you go. . All right, we're going to
08:19 glycogen lysis. So we're saying, , hey, lots of sugar,
08:24 it this direct direction. Don't move out. And then the other thing
08:28 we're gonna do is we're not going make new glucose from all the amino
08:31 that we have. So, the again is I've got the fuel,
08:36 putting it away. So you can a postabsorptive state. That's when I've
08:41 food and I'm absorbing materials. I'm the glucose into cells for storage in
08:46 form of glycogen. And I'm not mobilize glycogen or make new glucose because
08:51 have plenty. All right, with to the lipids, I'm gonna push
08:56 acids into adipose tissue. All I'm also going to increase the transport
09:01 glucose into adipose tissue. Why would do sugar into my fat? What
09:07 I do with sugars? I can them all up, right. And
09:13 I can make long fatty acid chains then I store up all my sugars
09:16 the form of fats. It's a , very efficient method of storing up
09:21 . All right. So, Glycogen an efficient method to store up energy
09:27 the short term fats are an efficient of storing up energy for the long
09:34 . Ok. That's why ice cream immediately turn into Glycogen for your skeletal
09:41 to use. That's why you store over here and other places in your
09:47 . OK. O other things, going to promote uh triglyceride synthesis,
09:55 makes sense and we're gonna inhibit break down of fats. Finally,
10:00 acids. What are we doing Well, we're going to promote the
10:03 of amino acids into the cells. cells are gonna use those amino acids
10:07 make proteins. And what we're gonna is we're going to stop protein
10:13 In other words, don't free up amino acids, don't make more amino
10:16 . We don't need to do So we're just gonna walk through the
10:19 cells of importance here. Given that framework in which we're doing stuff we're
10:25 about storing things away. So what the liver do again? Look at
10:28 those fun steps that you guys have at least once in your life.
10:31 you remember doing that bio chemistry? they make you memorize all the
10:35 Yeah. So sorry, you'll never that ever. All right. Except
10:41 the exam over and over again whenever take a biochemistry class. All
10:45 So liver promoting glycogen synthesis promote uh have here promoting glycolysis. And I
10:54 remember why I say that. But idea here is I am trying,
10:58 it's glycolysis, not gly glycogenolysis. , that's the thing I gotta catch
11:04 . You see all the evil do you guys remember all the evil
11:07 glycogenolysis, glycogenesis, gluconeogenesis, They're all the evil GS because it's
11:14 easy to get them confused, So this is a ag this is
11:19 . So what am I doing? promoting glycolysis. So, if I'm
11:22 glycolysis, what am I telling that to do? Make well pirate rate
11:29 . But what's the end result? , the far end energy A TP
11:33 what we're shooting for. So what I'm telling you is I'm telling
11:36 cells get active and start working. giving you fuel, use it.
11:41 in the liver, I'm actually promoting process. All right. So I'm
11:47 store up the fats again. This all in the liver, right?
11:51 then what am I doing? I'm protein synthesis. I'm hitting protein
11:56 OK. In terms of muscle, we go again, glucose uptake glycogen
12:04 , promoting glycolysis. Said it glycolysis. Man, this is just
12:10 of those days. I was up in my office, why I was
12:14 . I'm sitting there. I have 616 petitions. I had to sign
12:18 have proven a sign and stuff like . And I'm like, oh I
12:21 just get all these done right before . And I'm like getting closer,
12:24 can do it. I can do . I can do it. And
12:25 why my brain is turned off. I apologize, proving and disproving
12:32 All right. But again, it's the same thing promoting glycolysis, moving
12:37 down the pathway, promoting protein So, insulin is important for the
12:42 . So they can do their Finally, in terms of adipose tissue
12:46 . So I can make prva, I can convert them into fatty
12:49 Take those fatty acids, make And I'm also gonna pro promote the
12:54 of lipoprotein lipase. All right. , when I wouldn't, I can
12:58 this, I was like, oh , I can't even remember what this
13:00 does. Let me show you what does. Remember we have Chylomicron floating
13:04 in the blood. I wanna get Chylomicron and what it's carrying inside the
13:08 . But the problem is that Chylomicron too big to move from the blood
13:11 the interstitial space to the cell. what do I need to do?
13:15 to break apart that Chylomicron? So we're doing is we're sending a signal
13:21 the adipose cells to the cells of capillary to introduce the lipase to its
13:29 . And what does that lipase Recognize that Chylomicron says break down and
13:34 starts pulling out the triglycerides and the materials that, that Chylomicron is carrying
13:39 that it can be transported across the walls into the cells for storage.
13:46 its purpose. So look at the name lipoprotein lipase lipoprotein. It's attacking
13:52 Chylomicron. Ok. Oh, Now we get to Glucagon. So
14:00 really new in all those, any those tissues basically move glucose in store
14:04 up either as glycogen activate glycolysis so we can get en energy freely
14:10 whatever's left over, stored away, either as a fat or as
14:15 Yeah. So when is high? , you're, you're really, you
14:24 to think of it in terms of dealing with synthesis, but all of
14:28 pathways require some degree of A So what you're doing is you are
14:32 burning through this material so that you make the A TP available,
14:37 It's not like a, which one first? It's like a both and
14:41 right. All right. With I like this picture because you
14:45 you know, really, when we of these, these molecules, we
14:48 , OK, they're peptides and they made and they're released and they're
14:50 they're actually larger structures, right? they, they are uh these pre
14:57 hormones as they were and then they're . And I like like how you
15:01 here. So one pathway in the cells, what am I getting?
15:05 getting Glucagon. But if I go the intestinal cells, what am I
15:09 G LP? One? So I'm different things by breaking this pre pro
15:15 down and they do very different Glucagon does the opposite of what insulin
15:21 . All right. So we're gonna it up in the vesicles. And
15:24 when you are, um when the sugar levels go down, what's gonna
15:30 is is that we're going to release Glucagon. So glucose being present in
15:36 blood literally inhibits the cells from releasing . And so when those levels get
15:41 , that's when it's like, oh . Now I'm gonna start releasing
15:45 Now we're gonna just jump into just one in the liver. All
15:49 So I'm just gonna walk through them tell me if you can see the
15:52 here, right? So antagonize the of insulin. OK. We know
15:56 . So we're going to see a glycogen break, net gluco genesis and
16:02 gonna see a net oxidation of What's missing proteins? Why do I
16:09 want to break down proteins? I barely hear you. It's not that
16:16 don't need amino acids. What Think about starvation. All right.
16:20 mean, this is, this is biology, one stuff, right?
16:22 , we've learned like your body goes a process during starvation to first break
16:28 , you know your sugars and then goes to fats and then when you
16:32 in starvation mode, presuming you have water, what does it go after
16:36 ? Proteins, structural proteins, the that are responsible for keeping you
16:41 right. So that's like a last , right? And so notice here
16:46 glucagon is not doing is it's not after the structural proteins. We're not
16:51 worry about the presence of amino Why? Because I can make um
16:58 , this is gluconeogenesis but the idea that I can make amino acids available
17:04 me. I can create amino acids than the essentials. So I'm not
17:08 to jeopardize my cells by destroying them so I can have free amino acids
17:15 . It's only as a last resort that happens. All right. So
17:19 is just showing you the gas pedal the brake thing as we're going
17:22 So what happens when blood glucose levels ? I'm gonna promote insulin production.
17:27 gonna drop down glucagon levels until blood gets back to normal. But then
17:31 my blood glucose levels drop below then what happens is the gluco levels
17:36 and that causes inhibition of insulin production things return back to normal. So
17:41 you're doing here is you're playing kind on a seesaw and so your body
17:44 kind of going back and forth all time between the dominance of insulin and
17:49 dominance of glucose. So insulin Guam straightforward, things are going to cells
17:58 insulin is available, things are released cells when Glucagon is available. That's
18:02 it boils down to. No. what remember what we said is that
18:10 is being made, but it's being up. It's really, it's
18:14 So you can think of being constitutive and same thing with insulin, it's
18:18 made. It's how it's being That becomes important. Right.
18:25 there's our first metabolic hormone pair. what we're doing is we're shifting gears
18:30 moving to a structure. We haven't talked about all that much. It's
18:33 ignored for the most part in physiology because we're just kind of like,
18:38 , yeah. Well, that's way there. This is the adrenal
18:41 All right. And if you don't where the adrenal gland, do you
18:45 where your kidney is? All Kidney sit here and then if you
18:48 your kidney and look at a it looks like a bean and then
18:52 take a dollop of whipped cream and it on top of the bean.
18:54 an adrenal gland. All right, can see it there. It's like
18:58 , it's a dollop of whipped You can see it right. And
19:01 what we have here is structurally, adrenal gland has two basic regions.
19:06 has the outer cortex and the inner , we talked about the medulla when
19:11 talked about the autonomic nervous system, was where those autonomic neurons of sympathetic
19:16 traveled in. That's a pre ganglionic . And the medulla is a former
19:22 of the sympathetic system. And instead having neurons that leap out of it
19:27 we have these cells that are there produce norepinephrine and epinephrine. We're not
19:32 in those today. All right. , not interested in the catecholamines.
19:36 , we wanna go to that cortex in the cortex, we have three
19:41 regions and I'm not gonna ask you identify them. So we have the
19:44 , the Pascua and the reticularis. each of these regions are responsible for
19:50 steroids, but each region produces its specific steroid. All right. So
19:56 outer glom glomerulosa is responsible for the corticoid. What are the mineral
20:03 Well, the one that we've learned already is aldosterone. So do we
20:06 to talk about al aldosterone anymore? do you think? Do we need
20:10 talk about it? We do. . So remember aldosterone is responsible for
20:16 water salt balance. And so how it regulate water salt balance? I
20:24 want to talk about I lost or not on my list today. It's
20:29 . All right. It's sodium. . Remember the sodium potassium pumps,
20:34 put them into the system that pumps in the body allows us to release
20:38 or sorry. Flip that around sodium into the body. Potassium is released
20:41 removed. So, sodium goes in follows. We are now raising blood
20:47 . All right, we have the . Glucocorticoids are gonna be down here
20:51 the fasula. All right. So is gluco, what do the glucocorticoids
20:56 by? Well, we're representing them the hormone cortisol. All right.
21:00 the primary one. And there's some , but we're not gonna worry about
21:03 . All right. That's the one gonna talk about here in just a
21:07 . And then the third type is makes me so excited sometimes is the
21:13 . The reticularis produces androgens in particular we're gonna focus on which is D
21:20 , which is a very, very , horrible word di hydro epi
21:25 So the hea is much, much . All right. But you have
21:30 here also, Anderson and ion, uh another hormone that gets converted into
21:35 other stuff. But the androgens testosterones the easy way to think about
21:39 Ok. So we're gonna focus first cortisol and then we're gonna jump in
21:44 look at those um uh sex All right. The androgens here.
21:49 right. So the purpose of cortisol our body is to be released in
21:56 to stress. And what we see we see a diurnal pattern of cortisol
22:02 . So your highest levels of cortisol at the end of the day,
22:05 lowest levels of cortisol are in the . Now, let's think about your
22:09 . Do you have stressful things going all day long? Yeah.
22:13 food, fighting for food, listening my lectures, finding a parking
22:20 right. Just the normal daily stresses a person's life. And so you
22:24 imagine over the course of the you're accumulating stress. And so what
22:28 you doing? You're responding to it releasing cortisols. So you start off
22:34 during the day and over the course the day, it gets higher and
22:37 and higher and higher. And then go to sleep and then you don't
22:40 at night because reasons and then you back down and then it starts all
22:44 again. So you can imagine we this daily pattern of cortisol production.
22:49 right. Now, the way that regulated how we create this pattern is
22:54 the hypothalamic hypothesis pathway, specifically through corticotropic releasing hormone, adrenal corticotropic hormone
23:03 . So that's the crh ac th . Now, what do we
23:08 This is just a negative feedback This is stuff we've already learned about
23:11 we talked about the pituitary. So hypothalamus releases crh acts on the pituitary
23:17 which, which releases ac th ac goes down to the adrenal cortex and
23:22 the production of cortisol. And then cortisol and a negative feedback loop goes
23:28 to the other two and negatively regulates in addition to what it does in
23:33 of regulating or responding to stress. right. Now, it's a steroid
23:38 it binds to its own specific receptor we call that receptor, the Glucocorticoid
23:44 . I've abbreviated it. Gr because how we abbreviate it everywhere. All
23:48 . So that's what it is just Glucocorticoid receptor. Ok. Now,
23:54 are its effects? Well, generally , when we're dealing with stress,
23:59 we wanna do is we wanna mobilize so that our cells can respond to
24:04 stresses appropriately. So, really what is, it's a metabolic hormone,
24:11 ? So it has this metabolic it acts on the liver. And
24:14 is it doing? It's promoting gluco . So what is gluco neogenesis making
24:19 from amino acids? So I'm making available right in the muscle. What
24:24 it doing? It's promoting uh oh , breaking down proteins, making amino
24:33 available. So what can I do them? I can now have amino
24:36 to make glucose from what am I in adipose tissue? Uh Well,
24:42 releasing that triglyceride and converting it and it down into the free fatty acids
24:49 glycerol. So I can make free acids available for fuel and the glycerol
24:55 for gluco neogenesis. I can make . So do you see the pattern
24:59 ? What am I doing? I making energy available so that the cell
25:03 respond? All right, and not in positive ways. All right.
25:09 , here's the thing when you think stress, you think about this was
25:14 to me, right? Like, I've got a test tomorrow. So
25:19 alas, right? That's that is we think of stress, but that's
25:23 what stress really is. Stress is state of living. Ok. So
25:28 give you an example of stress is not eating for a week because food
25:33 unavailable to you. Right. Sleeping the street because you have no
25:38 That would be stressful. Right. . Because it's a constant state and
25:43 body is desperate for this need of to sustain you and keep you alive
25:49 the laboratory. The way that we stress is in a couple of different
25:53 . So I'm just gonna tell you horrible things we do to rats.
25:57 , so one thing we can do we can take rats, put them
25:59 their cages and put the cages in rooms, four degrees or minus 20
26:03 whatever and see how they do. you agree that being cold all the
26:07 is kind of stressful? Yeah. know, especially if you're from down
26:10 . It's like, you know, than a day and it's like,
26:13 , I'm done, I'm, I'm to move. Let's, let's get
26:16 to summer. Right. Another thing we can do is we can take
26:20 and put them in little tiny And when I say bathtubs, I
26:23 , take their cage, fill it water and then they have to swim
26:27 for the rest of their lives. . So, what do they do
26:30 they're tired? They just tuck their underneath them and they kind of float
26:33 they're a little bit more buoyant than are. Right. But imagine not
26:37 able to touch the bottom of a pool and you can't hold on to
26:41 sides of the swimming pool. in essence, you are now swimming
26:45 hours a day. That would be example of how we induce stress in
26:49 . Third thing that we can do , that is a common thing.
26:52 I mean, again, these are like the common ones. Another one
26:55 we disrupt their sleep wake cycle, ? So normal mice and rats have
27:02 are, are nocturnal. And so they do in the laboratories is they
27:07 a 1212, uh hour day. 12 hour light, 12 hour
27:12 So what you can do is you create a 24 hour light day or
27:15 can create an 18 hour light you never give them extra dark because
27:19 be just happy and fine. What do is you give them the opposite
27:23 what they like and that's where the comes from. Right. Imagine it
27:28 light all the time. And you're familiar, like, because we're changing
27:33 right now. You know, like you live like north of the Mason
27:38 , it's getting dark, not at o'clock, it's getting dark at 430
27:43 the afternoon and then it's not getting until about seven in the morning.
27:49 . That's stressful. Right. This why we're happy. You've heard this
27:54 changes in latitudes, changes in People are grumpy in New York.
28:01 for those who live are coming from York. I apologize. People are
28:04 in New York because they just have daytime. We're happy down here because
28:08 bright all the time and it's, is a constant for us for the
28:12 part. Anyway, I digress. , what we're dealing with are those
28:18 of stresses that when we talk about , that's what we're talking about.
28:22 just, oh, no test right? That can be a stressful
28:28 . It's just not a state of right now. What's it doing?
28:33 to see if this sounds like this sense right? In the bone,
28:36 gonna fear with osteogenesis. So when feeling uh affecting osteogenesis, are you
28:43 bigger and bigger and bigger now in G I tract, you're interfering with
28:48 absorption, which is going to interfere bone production. Right? Third
28:54 it is an it interferes or doesn't , it promotes anti inflammatory activity.
29:00 this sound like you're trying to deal uh sickness and death? Yeah.
29:05 . And then lastly, in the , we're gonna see behavioral modifications.
29:09 you seen people who are stressful, behave and act in manners that are
29:16 with nor societal norms. How's Notice how I said that very scientifically
29:23 with societal norms? All right. essence, what we're seeing here is
29:29 we are responding to the stress to ourselves alive, but it has an
29:34 external to just keeping the cells Right. So people under stress are
29:42 in their growth. I mean, time. Right. That's an example
29:47 . All right. There's behavioral modifications fight and stuff. Yeah. Go
29:55 . Whatever is available. The question what, what proteins would be broken
30:02 the muscle? It's, it's, very non-specific, right. So,
30:06 enzymes are just looking for a cleavage . Yeah. Um, let's
30:12 what else did I have here about ? I didn't. Oh, anti
30:17 . Notice, would you say that finals week is kind of stressful?
30:21 mean, does it fall into the because, I mean, are you
30:24 less sleep? Are you eating Yeah. So you can see that's
30:28 of like this is now kind of lifestyle. Have you noticed that around
30:31 ? That not just the winter but even in the spring ones,
30:34 kind of get sick? All So do you see what's, what's
30:38 on here? Is cortisol levels are through the roof or relatively speaking and
30:45 body is responding in that way. , all right. So that's
30:51 But notice it is a metabolic Yeah. Mhm. Is it
31:00 Well, so that again, that's on the body. So again,
31:04 , you, you could throw it that category of excessive ideas.
31:08 um I'm sure this is something that done is put mice on continuous treadmills
31:13 just see what happens. I bet levels go through the roof again.
31:18 don't know. I never did cortisol . These are just things that I'm
31:21 with. You know, when you your medical ethics course in graduate
31:25 these are the things. Do not these to animals type things.
31:32 Well, no, it's, it's putting priority over living over,
31:37 , the minutiae. So it doesn't that you're sick as long as you're
31:42 because it can deal with the sick if you can get past your life
31:46 . Right. But if it's keeping un sick, but you're dead,
31:49 know, that's, do you, you see the balance there?
31:51 I know that's really facetious how I that, but that's, that's kind
31:54 what it's doing. It's, it's changing priority. It's saying I
31:59 stop this if this occurs. So don't I just stop this? Make
32:04 this doesn't happen. And I can deal with this later and then,
32:08 your body does this all the even during pregnancy, primarily, I'm
32:12 gonna use pregnancy as an example. primarily the woman, the mother's body
32:17 responsible for providing those nutrients for the . And so that's where it's presenting
32:21 of its energy is saying you go . But if there is AAA stressor
32:27 results in causing harm to the the mother's body will switch how it's
32:32 the energy and focus it towards the because great. You kept the baby
32:37 , but the mother is dead, the fetus is alive, but the
32:39 is dead. And that doesn't help fetus because it will die anyway.
32:42 the idea is live to reproduce another is, is kind of the philosophy
32:48 . All right. And again, far a field. But it's just
32:51 of the example of how the body particular priorities in order to ensure the
32:58 of the, of the organism. ? If that makes sense. All
33:06 , there's a lot about sex hormones the adrenal glands. Typically, when
33:09 f about focus on the sex we're gonna go right to the gonads
33:12 deal with the testes and the And we're gonna do that when we
33:15 into the reproductive systems. But your system is initially entirely dependent upon the
33:24 of your adrenal glands. All your puberty begins with a stage called
33:30 Archy. And Adren Archy is simply your, uh your uh pituitary gland
33:35 releasing the hormones that act not on uh ovaries and testes, but instead
33:43 on the adrenal glands to start producing steroids, which promote the growth of
33:50 gonads. And that's where you start that, that, that process.
33:54 right. So the adrenal glands are the, the starting point for all
33:58 the stuff when we think about sex . All right. Now, one
34:04 I would, I, I would you because when we think about sex
34:08 , we usually think, ok, are testosterone, females are estrogen and
34:12 and we're happy and we're good. I've already showed you the chart of
34:15 everything is kind of made, but don't need to memorize that.
34:18 But the truth is, is I, what I'm trying to get
34:20 here is that men produce progesterone. just doesn't stick around that long.
34:25 know, women produce androgens and they don't stick around that long because they're
34:30 step in a longer pathway to get the hormone of interest, right?
34:35 what we try not to do is , hey, your sex hormone is
34:38 to you. The only exception to rule is those hormones which are produced
34:42 the placenta. All right, and not gonna get there um today.
34:47 right. But there are, there hormones that are produced by the placenta
34:50 are unique to the female. All . Now, the thing about the
34:54 sex hormones that there's not a lot them and they are very limited in
34:59 functionality. So they're not particularly All right. So the hormone I'm
35:05 about here right now today is D it is a type of androgen and
35:14 not particularly powerful. I'm gonna use for an example. We're just gonna
35:18 scales. All right. So if the male, you have d hea
35:22 gonna give the power of DH a unit, whatever, whatever that strength
35:27 . Ok, androgen strength, we'll call it androgen strength. It has
35:30 power of one testosterone in the male a power of say 100. So
35:36 shows you when males start producing testosterone A is such a non factor that
35:42 not even considered. And the funny is, is d hea is not
35:47 , or, or testosterone is not the most powerful uh sex steroid in
35:52 , it's five DH T which is dihydrotestosterone. And that's about five times
35:58 10 times more powerful than testosterone. so usually testosterone is converted into that
36:04 it starts doing its stuff. All . So DH A, not a
36:10 deal in males but in females, have two androgens, you're dealing with
36:15 A and uh the uh andros in which is gonna be converted into
36:21 So we don't really worry about Anderson ion DH A is the androgen of
36:25 , of the female body for the part. And so it has a
36:30 and so here is the majority of function, it plays the androgen role
36:34 the female. So we're talking about and pubic hair, for example,
36:38 , the pubertal growth spurt that women through. And also it's been evidence
36:44 it plays a role in but is the most important role in the female
36:48 drive. The biggest role in the sex drive. Surprisingly is estrogen shocking
36:53 , right. Shocking. You'll, see why it's not shocking when we
36:58 the female reproductive system. Now, weird thing about D hea is that
37:02 not activated through the same mechanisms as and estrogen are in the gonads.
37:10 uses the ac th or crh ac axis just like cortisol does,
37:17 So when you have a tumor, example, right. I'm gonna do
37:23 . It's gonna be a, a tumor. All right. So here
37:28 going to produce tons and tons of th in the, in my little
37:33 model. So, as a result producing a lot of ac th I'm
37:37 produce a lot of d hea which gonna cause a little bit of masculinization
37:42 a female body. Ok. what testosterone would do what it would
37:49 fade back to the hypothalamus to affect releasing hormone. All right. And
37:56 expect something downstream of ac th would back to the hypothalamus and affect
38:02 it does not do that. So the hea is because it's a
38:06 it feeds back to the sex steroid . So it affects just like
38:13 What estrogen affects, it'll affect FSH llh production through goo trippin releasing
38:18 It will down regulate estrogen production in , it will down regulate testosterone production
38:24 males. And so what ends up is, is you can imagine in
38:28 woman who has a pituitary tumor, adrenal cortic adrenal, corticotropic hormone
38:34 you'll see masculinization of that female. right, because it's down regulating all
38:40 estrogen stuff. Now, I'm not fun of grandmothers here, but I
38:46 you to think about what your grandmother like. Ok. Is her body
38:51 male than female ish? I if it's a young grandmother that's gonna
38:57 a different question. But is she boxy or is she more hourglass
39:04 Right. Is she growing a little of that hair going on on that
39:10 again, this is an age So the older you get, you
39:12 imagine it's gonna be more so, I have a 96 year old grandmother
39:16 is still boxy even though she's like as a rail, you know,
39:20 she has that super chin of you know that, you know,
39:24 plucks that but can't get them. right. So why does that
39:28 Right. Well, after menopause estrogen drop and so now d hea has
39:36 broader effect. And so you start the masculinization of the female form.
39:41 right. So instead of having that shape, right? What you end
39:45 with is more of a boxy You start seeing hers, which is
39:50 the growth, the the male pattern of hair growth. And I'm not
39:54 like beard, you're not walking going check this bad boy out and
39:58 in a mu mustache contest. But start seeing more of that thicker,
40:03 hair that's typically associated with prepubescent boys pubescent boys. Right. So,
40:12 about the sex hormones. That's all want to talk about with D
40:15 So we kind of get that one hea sex steroids starts everything up.
40:20 weird stuff. When you get There we go. Thyroid. All
40:29 . I apologize about the stuff about thyroid. All right. There's a
40:33 of stuff I think that are in textbooks on thyroid that exist in textbooks
40:37 it was one of the first ones first organs and first hormones described.
40:42 they got so excited about it that put into the textbooks and then as
40:45 learn more and more about the they never took the stuff out.
40:49 right. And you'll see what I'm here in just a moment.
40:52 So your thyroid gland is kind of shaped or bow tie shaped, sits
40:58 near the trachea. So that's kind what it looks like. And if
41:01 take a slice through it, you'll that it's basically a bunch of little
41:04 bubbles. All right. What we follicles. And so the follicles are
41:09 by or are, are bounded by cells and it's the follicular cells that
41:15 interested in. But on the inside have this goo, this colloid and
41:20 where we're gonna be storing up the until we're ready to go with
41:24 All right. So, the follicular produce colloid. That's what the purplish
41:29 color here is supposed to represent. it's here where you're gonna have a
41:34 called thyroglobulin. Thyroglobulin is the molecule we're gonna use to build thyroid hormone
41:42 . So, this is like the hormone factory. All right. And
41:47 surrounding in uh like they're trying to you like here and stuff specifically
41:53 Those are C cells or para follicular . We're gonna talk about them.
41:57 the end of class, the C are real simple because C stands for
42:04 . All right. That's what they . That's where they're found. But
42:07 para follicular pera next to the They're not part of the follicles.
42:12 right. So, thyroid hormone, we're gonna do is we're gonna get
42:16 and what we're gonna do is we're add iodine to the tyrosine and once
42:20 get it iodized, then what we're do is we're gonna add some other
42:23 to it. So, what we here is so you can see here's
42:27 tire. It doesn't show you a one, but you'd have a tyro
42:30 you're gonna iodize it and then you another tied and you attach it to
42:34 . All right. And so we're kind of go through the steps here
42:37 because it's fun to say and, I'll show you just a second.
42:41 we end up with like two All right. So we have T
42:44 and T four, T three is trio, triiodothyronine and T four is
42:51 uh uh tetra. Thank you. was like stuck on Quad. I'm
42:55 , there's no Q in there. stuck tetra odore or thyroxine is,
43:00 is known name. All right. so both of these are released in
43:05 , into the uh blood, but T three is more powerful than the
43:10 four, but most of your thyroid is T four. So it needs
43:14 be converted into the more active form it passes through the body, primarily
43:18 and the kidney. But we just to them collectively as thyroid hormone.
43:22 , there's two molecules that are thyroid . All right. And so they're
43:26 around in the blood by a binding . Um they um are uh fat
43:34 . They don't like to hang out . So that's why you need to
43:36 the binder. They pass through a membrane just fine and then they act
43:41 the thyroid hormone receptor, which is be localized inside the cell. All
43:45 . So they behave like a Now, there is a long process
43:52 producing it. This is the type stuff I've talked about where it's
43:55 I do not understand why they include . We don't talk about how we
43:58 any other hormone, but this one have to talk about. And so
44:03 gonna keep it really, really You can see here here's the
44:06 you bind up the different tyrosine to , you add iodine to them.
44:11 so you end up with two different of this iodized tyrosine. One that
44:16 11 that has two. OK. the one that has one we call
44:21 , I odo tyro, the one has two, we call it
44:25 I odo Tyrine see the complicatedness of . So we abbreviate because saying those
44:30 is really long. So we end with a mitt or you end up
44:32 a dit. All right. And what you're gonna do is you're gonna
44:36 a mitt and a dit and you make T three, you can take
44:38 dit and a dit and you can , make a T four, but
44:41 can't get a mitt and a mi there's no such thing. So you
44:46 me to do that again. A a dit equals T three di di
44:49 T four. But there is no plus mit. It's very Doctor
44:55 All right. But ultimately, you're just creating these chains. So
44:59 can see here that right there, T four, you can see the
45:02 , there's two dits right. Here's T three, there's a dit and
45:06 a mitt. But if you there are no mid mits,
45:14 So you keep it in storage, hold it on to that thyroglobulin.
45:19 right. And so when your body thyroid hormone, what's gonna happen is
45:24 thyroid cell, that follicular cell comes , pinches off a portion of the
45:29 and then it starts cleaving off uh, potential, uh, thyroid
45:36 . So you'll end up with some threes. You'll end up with some
45:38 fours. You might end up with mitt, you might end up with
45:41 dit, you might end up with basic thyro attached to the thyroglobulin.
45:45 there's stuff that you'll recycle. So things you'll recycle would be the
45:49 the mitt and the dits because they're ready. And then the other
45:53 you just send off into the blood they bind up to the thyroglobulin and
45:56 they move not thyroglobulin, thyroid binding , thyroid hormone binding globulin, excuse
46:02 . And then they just uh travel and get to where they need to
46:05 to do their thing. So, do they do? Why do,
46:09 do we have to go through all stuff? I'm not gonna ask you
46:12 and dits. I just, it's to say. All right, what
46:16 they do? Well, thyroid hormone the hormone that is responsible for regulating
46:24 basal metabolic rate. Let's put it ways that are really, really easy
46:29 understand. Do you have that friend can eat anything and never gain
46:32 In fact, they just go through , losing weight all the time.
46:36 then you look at like a, a brownie across the room and you
46:39 gain £10. Ok. So I there's an exaggeration there. But the
46:45 is, is, yeah, the who can lose weight simply by existing
46:49 a high, high basal metabolic right? And so what thyroid hormone
46:54 is it tunes your basal metabolic it increases your oxygen, oxygen consumption
47:00 en energy expenditures. The quest for of us is to increase our basal
47:07 rate, right? That is like make everybody happy. Then you could
47:10 ice cream and never have to worry gaining a pound fistfuls of Doritos.
47:17 ever bad happens. Life would be . I actually had a friend like
47:21 . He was, he was my friend. I mentioned he could literally
47:24 anything and he lost weight. We go to dinner together and it would
47:29 like food after food, after food he'd be like, I'm still hungry
47:34 I'm sitting there going, yeah. thyroid hormone, but there is a
47:44 to increasing your metabolic rate. Are efficient engines? We are you sh
47:51 , we are not efficient engines. about all the energy that's in glucose
47:54 gets lost to heat production. People high metabolic rates are horrible people to
48:00 next to because they're like little tiny and they just produce heat all the
48:06 . So that is the by product the increased metabolic rate. Now it
48:12 some other effects. Uh it's sympathomimetic growth hormone secretion. And again,
48:18 are you seeing here? This is metabolic hormone, right? The idea
48:22 is I am burning through fuel. so if I'm gonna burn f through
48:28 , I need to have fuel made to me. And I'm gonna help
48:32 this happen by acting with these other . All right. So that's what
48:36 saying is being sympathomimetic, it's gonna responsiveness to catecholamines. When are,
48:42 do we do the catecholamines? And pi sympathetic, parasympathetic, sympathetic,
48:49 ? When I'm talking about growth when you think growth hormone, what
48:52 you think of? No, not sympathetic. I mean, what
48:56 you think when you hear the word hormone, what should be the first
48:59 that comes out of your mouth? ? Right. So you can,
49:05 see how these two things would go , right? If I'm increasing my
49:09 activity, what am I doing? promoting cells to go through this process
49:15 growth. That's why they work They promote a whole bunch of other
49:19 together. And we're gonna kind of through this list. How is it
49:22 hypothalamic pituitary pathway? Right. same sort of thing. Hypothalamus,
49:27 , releasing hormone causes the production of thyroid or sorry, uh thyroid stimulating
49:34 which causes the release of T t four, t three T
49:39 Back up to the pituitary, back to the hypothalamus. Now, I'm
49:44 pause here for a second before I to the growth if you're having trouble
49:48 the stuff that we're talking about here is the easiest way ever to
49:54 hormones table. Ok. One side the table, you put your
50:03 where is it made? How is regulated? What does it cause?
50:07 or what is the result of Right. Where does it act?
50:11 make yourself a simple table and you're find out your list of hormones is
50:15 very long and they're actually pretty easy you have the gas and pedal stuff
50:20 they're being regulated through this anterior or hypothalamic anterior tu anterior pituitary pathway.
50:27 , I am just struggling with that . So, so far, so
50:33 . All these are metabolic, So it, it's kind of making
50:37 simple along those lines here. We in growth. All right. So
50:45 hormone, you do need it for . It is essential for growth,
50:49 ? But it's not wholly responsible for growth. All right. So there
50:54 some factors here that play a role your growth. If your mother is
50:59 and your father is tiny, you going to be tiny. Odds are
51:04 your favor that tininess is in your . OK? That's it's, that's
51:10 . OK? We know that you be a homozygous. Um uh Let
51:17 out here, recessive. Thank you . I was just, I'm just
51:21 on words, right? Homozygous, , right? That could happen.
51:25 the odds are not in your Right. Adequate diet matters.
51:31 this goes back to the cortisol I'm just gonna give you an
51:35 So, um, I think I've you, I have, uh,
51:37 , two sets of twins of you know, as Children. So
51:41 wife who is a twin, her , who's not, her twin had
51:47 . Ok. Right. And and one of them is an absolutely
51:53 eater, like refuses to eat anything than like spaghettio's. It has for
51:59 now 12 years old. Right. the twins, this is a perfect
52:03 of this. So one of the , the good eater is now about
52:08 ft 10. He's playing basketball. he's as tall as I am as
52:12 12 year old. I mean, gonna be like 6 ft eight.
52:16 mean, he's a monster, But his sibling, his twin is
52:23 this tall. All right. So want you to see it. All
52:26 . It's a perfect example of good versus terrible diet. So, diet
52:32 , chronic disease, stressful conditions. , what would happen? Cortisol would
52:36 , uh uh uh better to keep alive than to keep you tall.
52:41 . Don't need that hair would rather you alive. Let the hair fall
52:45 , that sort of thing. And normal levels of other growth influencing
52:50 This includes thyroid hormone, insulin as as your sex hormones. All
52:55 And so we'll see that So this just a simple graph showing you
53:01 your growth pattern over your life. we have the postnatal growth spurt.
53:07 we're not even doing the stuff right? Pre birth, right?
53:11 remember how, how big are you you start life, single cell?
53:16 you're like like that, right? then when you're born, how big
53:20 you like that big? Right? we stretch you out, but you're
53:26 in ac shape. So you seem but you're about 18 inches,
53:31 And then, so you start off r roughly around 18 inches. And
53:35 look what happens. What have you two year olds and three year
53:39 How big they are? Oh, goodness. They grow so fast.
53:44 have a picture of me holding my son when he was born, his
53:48 was the size of an orange, ? Much bigger than that. I
53:52 think it would have been a fun , right? So I'm sitting there
53:57 his hand like this big and he, he extends this whole thing
54:01 then I have pictures of him like to here when he's two years
54:04 right? It's normal. So that's first growth spurt. So we have
54:08 fetal growth spurt that fetal growth That's genetics and environmental factors. But
54:14 the materials coming from the placenta you're . Now, your growth hormone is
54:18 is playing a role, but it is dependent upon your nutrition as well
54:22 your genetic factors and then puberty comes and smacks you with the growth
54:27 So now it's not just growth We're talking about the androgens as well
54:30 your nutrition, your genetics. All . So all these have a role
54:36 your growth but growth hormone notice is all along. Now, growth
54:43 there are lots of different types of hormone. All right. So the
54:48 we talk about, the one we're to is the one that's called
54:51 it's produced in the anterior pituitary by specific cells called the somatotroph. So
54:57 you hear somatotroph, somatomedin, it's referring to growth hormone. All
55:03 . But you do not need to this list. But look, we
55:06 a placental variant. We have the lactogen, we have prolactin, they're
55:11 related to each other. All And we already know what does prolactin
55:16 promotes milk production, right. no, it doesn't have a role
55:21 growth. It plays a different right. So, typically this is
55:27 , a protein that's made first. the precursor and then we chop it
55:31 . So we store it up until need it. It's regulated through the
55:36 pituitary pathway. So, g hr from the hypothalamus, anterior pituitary,
55:42 the GH it goes on and acts the liver and at the liver,
55:48 it's gonna do is gonna produce IGF , I'm gonna come back. All
55:52 . So IGF one is the downstream that growth hormone does its business
55:59 So, g growth hormone isn't doing work. IGF one is for the
56:03 part. All right. So, , we've mentioned this a couple of
56:10 . Somatostatin is the negative regulator of hormone. So, in some
56:15 you'll see reference to Ghih growth hormone hormone. Those books were written before
56:23 Mein or somatostatin was discovered to be hormone. So they knew something was
56:30 . They just don't know what it . That's this one. All
56:35 Ghrelin. Have you ever heard of molecule? It's the appetite hormone.
56:40 right. It stimulates the production of hormone. It also stimulates your
56:48 So this is just another hormone of stomach. Just one of millions.
56:54 right, we're not even covering all them. So, growth hormone,
56:59 releasing hormone acts on the pituitary cause production of growth hormone. Growth hormone
57:05 on the liver cause of production igf , there is an IGF two,
57:09 we're gonna ignore that one because it weird and is on as far as
57:13 know it's only in the reproductive but it exists. All right.
57:18 what does growth hormone do? one, it increases insulin resistance.
57:26 right. It has an anti-insulin Ok. What is insulin doing?
57:33 causes uh energy to be stored. , growth hormone is saying,
57:38 no, no, I don't want to store stuff. I want you
57:41 mobilize it. I want all the to get their, get their fuel
57:45 that they can do their things. that's its job. All right.
57:50 we're gonna promote lipolysis. We're gonna gluco neogenesis. All right.
57:55 we're gonna go back to puberty. remember puberty? Do you remember those
57:58 days? Do you remember your, , you and all your friends were
58:01 little tubby? A little bit. . It was that prepubertal fat,
58:05 know, little girls, they were and they're kind of chunky and then
58:09 go away for the summer, they back, they have boobs and an
58:12 figure. And you're just like, all the guys are still stuck in
58:15 , right? So we're just uh, I've told you about my
58:19 , uh, who is now a surgeon, but he was a
58:24 He, you know, he, , he was, he was
58:27 bright red hair and I mean, was not more of a cartoon of
58:31 person than could possibly imagine so perfectly . Right. And I mean,
58:38 waddled. I mean, the whole you pushed him over, I guarantee
58:40 he'd roll right. He went away the summer. You know, this
58:45 again, after all the girls had through puberty said now it's his
58:47 He goes away and he comes back I'm, uh, and he's,
58:51 at this event and he's all, , Doctor Wayne, because that's what
58:55 called me. Right. Hey, Wayne, and I looked up and
58:58 like, who are you? I know who he was because he had
59:01 every bit of his baby fat. . I mean, and he now
59:06 the carrot figure and he actually you know, the whole,
59:12 six pack, I mean, the nine yards and he, all he
59:15 was went to summer's camp and it fat camp because I went to the
59:18 summer camp that he did. You , it just puberty hit him and
59:23 was just like, boom, I'm now and it was a different
59:26 So, and I still remember the anyway. So, so what it's
59:34 that's mobilizing that fuel so that this can happen. All right. And
59:39 we have these words up there which mean horrible, horrible things, especially
59:43 you're taking a class in cell biology on oncology. So, hyperplasia
59:49 and um a hypertrophy, these are things in puberty. These are not
59:54 things when you're talking about somebody's right? Like late in life.
60:00 would be bad. So, What does that mean? Right.
60:05 the cells are rapidly dividing and ok, outside of their normal
60:11 which is what puberty is. I , you're literally the best way to
60:14 puberty is that you guys are well, we are all not just
60:18 , I'm just further away from it that we are caterpillars and then our
60:23 is completely and totally remodeled. The is, is that we don't actually
60:27 a cocoon around us that includes your , right? And so again,
60:34 , I'm gonna make things grow So I get lots more cells and
60:38 the hypertrophy is I make bigger So those are the two things that
60:43 going on there. And that's what hormone is promoting other hormones that are
60:48 in this include thyroid hormone. It's glucocorticoids, it inhibits growth. All
60:55 . So, cortisol inhibits growth. not shocking. We've already talked about
60:59 . Ok. The sex steroids, fly or mosquito, great um
61:06 These are promoting growth, estrogens, growth. But wait a second.
61:13 Wayne, I, I went through . I'm a woman and I have
61:17 estrogen. You said the A T is low. Yes. But think
61:21 , I, I mean, I've you, I've got the twins,
61:24 . We've talked about the weird twins over at the cousins. Let's talk
61:27 my weird twins. All right. got uh a boy and a
61:32 right? My daughter went through puberty , right? Because that's what girls
61:38 . So here they are, they're small puberty hits. She grows
61:42 right? That's the D hea but estrogen causes the epithelial plates in her
61:47 bones to close. She stops My son hadn't hit puberty yet,
61:52 he's growing at his nice little constant and then puberty happens and he doesn't
61:59 the estrogen to cause the epiphyseal plates close so quickly. So he's gonna
62:03 growing for a little while. He'll end up being about this. Tall
62:05 my guess. Right. So they're in high school now. She's
62:11 He's still ongoing. It's an ongoing in our family. I'm always gonna
62:16 short. Sorry, mother's kinda Your grandmother's kinda short, your other
62:23 kinda short, sorry about the So the question is when do plate
62:31 happen? Um they can happen as as 16 and they can happen as
62:36 as 25 right? So I play didn't play, I was uh an
62:46 um advisor for an athletic program. was uh so we had the football
62:51 and I was basically there to make that they studied and answer their questions
62:55 they needed them, which they never questions because they never studied.
62:59 but anyway, I was in the once, you know, so this
63:02 like right after, after college and was in the elevator with three of
63:06 freshman players, one was 6 ft was 6 ft six and the other
63:10 was 71, right? So I among Giants. So here I
63:16 I'm looking, you know, in elevator. So all I see are
63:19 up there, the guy that was had not stopped growing. I don't
63:24 what his final height was, but was not 71, I think he
63:27 like 74 or something like that, know. So that's not uncommon.
63:34 right. So some of you are growing is what my point is.
63:39 right. Insulin. Um They're structurally to the somatomedin. We don't use
63:46 uh all that much when we talk it. So it's abbreviation is IGFIGF
63:50 insulin like growth factor. So it like insulin. And so the likelihood
63:56 that the somatomedin are capable of binding the IGF one receptor and causing some
64:01 the effects that IGF one does. , insulin may have a growth
64:06 And then when you think about individual and stuff like that, all those
64:10 growth factors that we're not gonna bother play a role in their growth.
64:14 so what regulates them is entirely different they're not dependent upon the somatomedin for
64:19 EGF or uh whatever else I have there, I have nerve growth
64:24 but all the different growth factors that . So growth isn't just growth
64:29 there's a lot of different things But when we talk about growth
64:34 one of its primary functions is growth down the last one. Yeah,
64:43 the course of this class, we've calcium a lot. Have you noticed
64:47 calcium shows up over and over and and over again. Like just think
64:52 muscles, calcium plays a role in contraction it plays an important role in
64:58 heart contracting and smooth muscle contraction. it also plays an important role in
65:04 signaling, doesn't it? And it an important role in how nerves
65:09 So, calcium is a big deal the body. All right, we
65:14 even talk about the bones and the being, you know, primarily calcium
65:19 . So it plays an important role too. So we regulate calcium because
65:24 such a significant molecule. But the is, is the amount of calcium
65:28 is actually under the control of reg is reg under regulatory control is actually
65:32 small. And the reason for that because of where that calcium is actually
65:37 . So I have a list up , most of your calcium is in
65:39 bone and teeth, the remaining I mean, just look at that
65:42 , 99% of the calcium is sequester where you can't get to it.
65:47 right. It's like, it's like you have in the bank and a
65:51 fund, you're not allowed to touch , right. So that's the
65:55 the grand majority. And then you calcium that's found in soft tissues that
66:00 be your muscles and cells and And then that means about 0.1% of
66:04 the calcium is in circulation and half is unbound or is, is bound
66:10 . So you can't use it or a uh access it. So when
66:13 talking about calcium regulation. We're talking , uh, 0.05% of the calcium
66:19 your body is what's actually being So this is why it's so important
66:23 it's such a small portion that if muck with that, it will have
66:28 ramifications because it interferes with all the stuff. All right. So,
66:33 that small bit is important for all other bits. Now, that picture
66:41 , sorry, this picture there and one previous are good ways to kind
66:46 think about this system in calcium So, what we're talking about here
66:50 regulating the amount of calcium in circulation any given time. All right,
66:57 we're gonna do is we're gonna deal the kidney. We're gonna be dealing
67:00 the intestines and we're gonna be dealing the bone. These three are the
67:04 players in regulating calcium production. if calcium is in plasma, what's
67:11 of the places calcium can do? you like? Is it likely that
67:18 could pee it out if it's in , if it's in your plasma?
67:24 . So that's one thing. Do eat food that has calcium in
67:29 Yeah. So we want to regulate we move calcium from the digestive tract
67:33 the body, we want to regulate calcium is pulled from the renal system
67:39 into the body or just let it . Right. And then the last
67:43 we're gonna regulate it is, can move things or not, can
67:47 But do we need to move calcium of the bones or do we need
67:50 put calcium away to the bones? those are the three things that we're
67:54 of regulating here. All right. so we're gonna balance around this plasma
68:00 . So if pla plasma calcium levels too low, I can pull it
68:05 from the digestive tract, I can it in from the kidney or I
68:08 pull it in from the bones. if my calcium levels get too
68:12 I'm not gonna bother bringing in from digestive tract. I'm gonna let myself
68:16 it out and oh by the I'm gonna put that excess into the
68:21 so I can make stronger bones. that's, that's the access through which
68:24 doing it. The two hormones are the insulin, the glucagon. All
68:28 , they're petals. All right. the way that I remember this,
68:31 the two hormones are parathyroid hormone, ? Which you're gonna be made in
68:36 C cell or not in the C . It's gonna be made in the
68:40 , excuse me, which are two structures that sit four little structures that
68:44 on the four wings of the So if you think of your little
68:47 , each of the two wings on top and the two on the bottom
68:51 a little dot on the back of . That's the para uh thyroid
68:55 there's four of them. And then have calcitonin, which is gonna be
68:58 in the C cells inside the All right. Now, how do
69:02 remember which one does? Which, one is gonna move calcium to the
69:05 and which is gonna move calcium out the blood? All right. So
69:09 my dumb thing. Ready for my thing. Calcitonin the bones. All
69:15 . So it's calcitonin, whereas calcium going into the bones. All
69:20 So that's how I remember it. can confuse yourself using our cal calcitonin
69:25 or something like that. Just calcitonin . All right. So what it's
69:29 is it's gonna promote calcium moving into bones. That means it's trying to
69:33 calcium out of the plasma. That parathyroid hormone is putting calcium into the
69:39 . All right, if you have better way to remember it, make
69:43 work and then come tell me. I can teach you guys something
69:46 All right. So this is the hormone. All right, when you
69:52 low plasma calcium levels. So the calcium levels drop. What I'm gonna
69:56 is I'm going to signal to the to increase osteoclasts activity. Osteoclast clasts
70:03 the cells that break down bones. right. So they start breaking down
70:07 bones that releases the calcium from the . All right. So we move
70:13 there. So calcium is coming from bones into the blood. Second
70:17 we're gonna go, we're gonna go the kidney and say, hey,
70:19 know what, um, instead of that calcium will go out into the
70:22 , I want you to bring that into the system. So I'm gonna
70:25 the calcium, but calcium doesn't just around as a free ion. It
70:30 a partner likes phosphates, calcium right? So what we do,
70:35 when we're breaking down bones, you're both calcium and phosphate. We're gonna
70:38 the phosphate go. But we're gonna on and sequester the calcium. So
70:42 reabsorbing or absorbing the calcium to put back in the body. Third thing
70:46 gonna do is we're gonna act on small and tested and here, what
70:50 gonna do is really, this is secondary mechanism through calcitriol. Calcitriol is
70:55 fancy word for vitamin D. So I do is I up regulate the
70:59 of calcitriol. Calcitriol acts on the intestine. And really what it's doing
71:05 I remember correctly is it's uh increasing factor production which allows you to bring
71:10 in. Don't write that down intrinsic just in case I'm wrong.
71:16 So that's how parathyroid works, acts all three tissues. All right.
71:24 , I've done all this. I calcium in. I'm uh reabsorbing
71:28 I'm breaking down bone, my calcium start rising too high in the
71:32 So what do I wanna do? ? I wanna do the opposite
71:37 OK. Here I'm gonna act on of the systems and I'm gonna ignore
71:42 third one. So I bone, going to inhibit osteoclast activity, quit
71:47 down the bones. All right, gonna promote, on the other
71:52 I'm gonna promote bone production. basically, the Osteoblast rebuilding just
71:56 you know, your bones are actually , uh roughly five times a
72:02 I mean, by weight by You know, it's not actually you're
72:05 rebuilding your entire skeleton, but that's active your bones are. It's a
72:10 active system, right? So I'm to stop the osteoclast activity and I'm
72:16 promote the osteoblast activity. And the thing I'm gonna do is I'm gonna
72:20 reabsorbing. I'm just gonna let the flow out of the body just like
72:23 I have too much sodium in my , do I bother reabsorbing it?
72:26 , I just let it go. right. So that's the same sort
72:29 thing. And then we have one missing small intestine. I don't need
72:34 tell my small intestine to stop absorbing because what I'm doing is I'm
72:39 I'm activating a system to cause the intestine to absorb calcium. It's not
72:43 constitutive activity. So, all I do is just stop doing it.
72:48 right. So I'm not bothering with . I just let the calcium
72:51 So, you know, if you're there consuming that calcium, you're just
72:55 have chalky poop if you need um, map to kind of show
73:03 this feedback loop. So this is level you're trying to keep. This
73:06 what calcitonin is doing this down That is what parathyroid hormone is
73:12 All right. My last little slide the day so that we can almost
73:17 done. Yeah, we do meet Tuesday. I'm sorry. Huh?
73:22 week I know. Well, we three more lectures to go. We
73:26 get them in. Somehow I could to your house and have Thanksgiving with
73:30 . Give you a personal lecture. , no, I don't wanna do
73:32 . Ok. All right. Last is just the Calci trial. All
73:36 . So what is vitamin D? , vitamin D is your body taking
73:41 in the skin and through uh activation UV, light converts it into this
73:47 this molecule. It's a precursor, not the active form. So that
73:51 be the inactive form. And then you do is you go through the
73:55 um or sorry, there's the inactive of right there. So you go
73:59 the uh go into the kidney that in the cala trial and now you
74:03 do the activity. And so it the thing that it promotes the reabsorption
74:08 the kidney. So you can see is the signaling molecule. So this
74:12 why vitamin D three is important, ? It facilitates the reabsorption by the
74:18 . It promotes intestinal absorption shouldn't be should be absorption and it promotes uh
74:25 mobilization via the osteoclasts. So, trial gets thrown into the mix because
74:32 the one that's doing most of the . Does that make sense?
74:36 parathyroid hormone is activating calcitriol production so your calcitriol can promote all that
74:43 And then when calcitonin comes up, basically says stop doing the parathyroid work
74:47 all the other stuff just kind of down. That's it, guys.
74:57 we come back, all reproduction all time, I'm gonna try really hard
75:05 make some of you turn bright That's, that's my goal.
75:10 all right, you guys have a
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