Speaker A
All right, engineers, in this video, we're going to talk about the pancreas, but specifically, we're going to focus on the hormone insulin.
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Speaker A
So, let's take a look here at the pancreas.
Speaker A
If you look at the pancreas, the pancreas is actually referred to as a heterocrine gland.
Speaker A
Okay, so what is it referred to as?
Speaker A
It's referred to as a heterocrine gland.
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So, what it means to be heterocrine is it's made up of two different types of tissues, right?
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One, it's just going to have this endocrine producing tissue.
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And the other one is it's going to consist of a exocrine producing tissue.
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Now, the endocrine producing tissue is actually made up of two things.
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It's actually made up of alpha cells, okay, alpha cells and beta cells.
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These are the two more significant ones.
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There is more than just alpha cells and beta cells.
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There's even delta cells and F cells and PP cells.
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There's a whole bunch of different types of cells.
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Okay, so these endocrine portion is the alpha cells and the beta cells.
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Now, the alpha cells are responsible for secreting a hormone referred to as glucagon.
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Okay, you can remember that because there's an A in glucagon and there's an A in the alpha.
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The beta cells are responsible for secreting insulin.
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Okay?
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And insulin in general, if I were to just categorize insulin as what type of hormone he is?
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He is responsible for trying to be able to bring our blood glucose levels down.
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So, he responds, so in other words, his stimulus.
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What's his stimulus?
Speaker A
His stimulus is hyperglycemia.
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And as a response to that hyperglycemia, his job is to be able to bring the blood glucose levels back down.
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Okay, so his responsibility is to be able to bring the blood glucose levels back down.
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Now, glucagon, his is the exact opposite.
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You can remember that by it's released whenever glucose is gone.
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All right, it's easy way to think about it.
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I just I think about there being a gone there, right?
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So, glucagon is released whenever your glucose is gone or whenever you have low blood glucose levels.
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So, they refer to it as hypo glycemia.
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Okay?
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Now, what's normally, uh, to kind of get an idea here?
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What's a normal blood glucose range?
Speaker A
Normally, a blood glucose range ranges from about 80 to 120 milligrams per DL.
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This is an average blood glucose level.
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Okay, so an average blood glucose levels is just going to range from about 80 to 120 milligrams per DL.
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All right, so if you're below 80 milligrams per DL.
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That's referred to as hypoglycemia.
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Whereas, if you're above 120 milligrams per DL, that's referred to as hyperglycemia.
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Okay, so again, below 80, hypoglycemia, above 120, hyperglycemia.
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And kind of an idea here is you do have a little bit of buffer here.
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You can maybe even consider about 70 milligrams still to be within the normal range.
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But generally, I'm just going to go with about 80 to 120.
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Okay?
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But it can go about to about 70.
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All right, now, the exocrine portion, we're going to talk about that in the digestive system.
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But just to highlight it, the exocrine portion is actually made up of what's called the acini.
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And this is the one that's releasing pancreatic juice, rich in digestive enzymes and bicarbonate.
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Now, the endocrine portion that we talked about with the alpha cells and the beta cells.
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If you look here, we have alpha cells and beta cells, and like I told you, there is other cells like delta cells and PP cells and F cells.
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They're actually aligned in like a cluster.
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So, imagine this cluster of cells in that area, okay?
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And it only makes up about 1% of the entire pancreas, right?
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So, 99% of it is acini.
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So, again, how much percent of it is acini?
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About 99% is acini, and about 1% of it is this structure.
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Which we call the islets of Langerhan.
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This right here is going to be the endocrine portion of the pancreas.
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Okay, it's these little clusters called the islets of Langerhan.
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Now, the islet of Langerhan, which I told you, has the alpha cells and the beta cells.
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But we're primarily in this video going to focus on insulin.
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So, which cells are we going to really be looking at?
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We're going to be looking at the beta cells.
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Okay, so now we're going to zoom in here into a beta cell.
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So, this right here, I'm zooming in on a beta cell.
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Now, beta cells, like I told you, are responsible for being able to release insulin.
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Right?
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They're responsible for releasing insulin.
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Now, with the beta cells, they're actually going to use their DNA.
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So, inside of the DNA, there's a specific gene.
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Let's say here's the gene right here.
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You know, genes, they actually undergo transcription.
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And when they undergo transcription, they get converted into mRNA.
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And then mRNA comes out here into the cytoplasm.
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And what does it do?
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It meets with a ribosome.
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So, let's say here's a ribosome right here, and here's a ribosome on the other side of it.
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Right, small and large ribosomal subunit.
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That mRNA will come in here, right?
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And it'll get read by the ribosomes, and then what, you'll synthesize a protein.
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So, out of this, there'll be a protein synthesized.
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Now, generally, what has to happen is he has to go to the rough ER.
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So, generally, he'll go to the rough ER, so let's say I just draw a generic rough ER here.
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So, it has to go to what is this structure here called the rough endoplasmic reticulum.
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And then it undergoes certain types of modifications.
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Then after that, it has to go to another structure.
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Let's say it goes to another structure, and this next structure is called the Golgi apparatus.
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So, then it goes to the Golgi.
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And in the Golgi, he gets packaged, right?
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And whenever he comes out of this, look what he comes out as.
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So, out of the Golgi, I'm now going to have this fully packaged insulin.
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Okay?
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So, now what would I have in here?
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I will have insulin.
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Now, insulin is actually made up of Now, generally, what happens is whenever you have a hormone, you start with what's called proinsulin.
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And then it undergoes specific types of cleaving processes in the rough ER, modifications, packaged and stored in these vesicles.
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So, now I have insulin in here.
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But I also have another important peptide.
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Which I should mention here.
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This other peptide is called C-peptide.
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And I'll explain that in a second.
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So, we've synthesized our insulin.
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Our insulin is sitting in these vesicles.
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So, not only there's just one vesicle, there's many, many different types of vesicles here.
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Consisting of this insulin.
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So, let's say I just draw here for the sake of it, three vesicles with insulin and C-peptide.
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So, here's insulin, here's insulin.
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And I'm just going to represent C-peptide, which is just a C here.
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So, C, C-peptide.
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Okay?
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They're in these vesicles.
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They're packaged in there.
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And they even have zinc in there, too.
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Now, look what happens.
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What did I tell you these beta cells are responding to?
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What's their stimulus?
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Their stimulus was hyperglycemia.
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So, whenever your blood glucose levels are elevated above this normal range of about 120 milligrams per DL, right?
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So, the blood glucose levels are high.
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Let's represent that then.
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Let's show here the blood glucose levels are really high.
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I'm going to represent glucose as this G here.
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Okay?
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On the pancreatic beta cell, it has these specific types of transporters.
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You see this blue transporter right here?
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This blue transporter is actually called a GLUT2 transporter.
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What the heck is GLUT2?
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GLUT2 means it's a glucose transporter type 2.
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And I know type 2 might be like, ah, who cares about that?
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It's very significant because that means that if it's a GLUT2, it's insulin independent.
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It doesn't need insulin.
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So, in other words, this glucose is going to move in here into this pancreatic beta cell.
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And if you have a lot of glucose, what does glucose undergo when it gets into the side of the cell?
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You know, it undergoes glycolysis.
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So, let's say here's glucose, he'll eventually get converted into glucose 6-phosphate, and then eventually he'll get converted into pyruvate.
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If we just keep going down here, and then eventually goes to acetyl-CoA.
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And then from acetyl-CoA, what happens?
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It goes through the Krebs cycle.
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And out of the Krebs cycle, you produce NADH's and FADH2's and all that freaking good stuff, right?
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Where do these guys go?
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Look where they go now.
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The NADH's and the FADH2's that you produce, they go to the mitochondria.
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And when they're at the mitochondria, what happens?
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They actually go through the electron transport chain, right?
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And out of the electron transport chain, what do they produce by oxidative phosphorylation?
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ATP.
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Right?
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Because that's generally what happens, glucose undergoes glycolysis, then it undergoes transition step, undergoes Krebs cycle.
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And makes these NADH's, these FADH2's, and then it gets taken to these transporters.
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Because all of this right here, pyruvate, acetyl-CoA, Krebs cycle, and even these formations of these guys.
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It's all occurring here in the mitochondria.
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And then it's producing ATP.
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Why is that significant?
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You see this like a channel right here?
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This channel right here is specifically for potassium.
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So, this is a potassium channel.
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So, potassium loves to be able to move through this channel.
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So, let's say here's your potassium.
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But guess what?
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There's a little pocket here for the ATP.
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So, the ATP literally comes in here and binds.
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When ATP binds onto this channel, it closes the channel.
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So, it inhibits the channel and closes it.
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So, now this channel is closed.
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So, let's represent this channel as being closed now.
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Okay, potassium can't get out.
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If potassium can't get out, he tries to be able to escape, but he can't escape.
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What happens to these positively charged ions?
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You start accumulating a lot of potassium ions.
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Which are positively charged.
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When you accumulate a lot of positively charged ions, what happens to the cell membrane potential?
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It becomes very, very positive.
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And whenever this actually occurs, it increases and tries to bring up the the membrane potential.
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So, your positive membrane potential, right?
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Whenever this positive membrane potential occurs, that stimulates these pink channels right there.
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What are these pink channels for?
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These pink channels are for calcium.
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And calcium's going to start flooding in to this beta cell.
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Why is that important?
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Let me show you.
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You know, on top of the insulin, there's a specific protein.
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On top of the cell membrane, there's a specific protein.
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Guess what that calcium ion does?
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The calcium ions, I'm going to represent that in red here, are linking together the synapto proteins.
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It's linking together the synapto protein on the vesicle containing insulin and the synapto protein here on the membrane.
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When that happens, what happens to this actual vesicle and the cell membrane?
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They fuse.
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And whenever this fuses, it opens up into the actual blood.
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And what does it release out?
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It releases out the insulin.
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So, now what do we release out here?
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We released out here insulin.
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You'll also release out C-peptide.
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Remember, I told you, you release C-peptide.
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And for the heck of it, you also release another molecule called amylin.
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Okay?
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And this is significant in type 2 diabetes.
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I'll talk about it whenever we get there.
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But now, these molecules are going to get moved into the blood.
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Okay, so now in your bloodstream, you have insulin.
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Which is the one that we're going to focus on.
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Now, I told you, I'd give you a little brief little thing about C-peptide.
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So, let me talk real briefly about C-peptide.
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C-peptide is important because he's a good way to be able to monitor insulin levels.
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Right?
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So, because you can monitor C-peptide, it kind of gives you a decent idea of someone's insulin levels.
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So, that's what they can use C-peptide for.
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Is being a way to monitor someone's insulin levels.
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Why would that be a good monitor of insulin levels?
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Because whenever you release insulin, guess what else you release?
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C-peptide.
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And amylin is actually, if you produce too much insulin, these amylin proteins can cause amyloid deposits.
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And actually cause destruction of the beta cells.
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And that can lead to that's a usually a cause of type 2 diabetes mellitus.
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All right, so this insulin.
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What is he going to go and do now?
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That's what we want to know.
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We want to know what the heck is insulin going to do over here?
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Okay?
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So, let's see what he's going to do.
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Let's go ahead and first see what he does on the liver.
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Okay, so let's show this insulin.
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This insulin is going to come over here and it's going to bind onto a receptor.
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Now, we didn't really talk too much about this receptor.
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You probably haven't seen it too much yet.
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But it's called a tyrosine kinase receptor.
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We're not going to talk about it.
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We're not going to go over the pathway.
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It's not necessary.
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But it's a tyrosine kinase receptor.
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Okay?
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In other words, whenever insulin binds here, so let's say that I represent insulin with an I.
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Whenever insulin binds there, it stimulates specific phosphorylation of tyrosine residues.
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And the overall result is you activate this intracellular messenger called PI3K and AKT.
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And AKT is just protein kinase B, really.
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Why am I telling you this?
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When insulin does this, this enzyme is very, very important within the liver.
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Okay?
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What did I tell you was wrong with the blood?
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What was really, really high in the blood that we showed before?
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You have really, really high blood glucose levels.
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The whole goal of insulin is to bring those glucose levels down.
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So, what this actual insulin does is now, remember, I told you about the liver, right?
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You got the liver.
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You see these these blue proteins?
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It's the same ones that were on the pancreatic beta cells.
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But I was very particular about the type of GLUT receptor it was.
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It's GLUT2.
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What does that mean?
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That means that this insulin, I'm sorry, that GLUT receptor is independent of insulin.
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So, in other words, insulin doesn't control that GLUT receptor.
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Glucose can move in at its own constant rate.
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Once glucose is brought into the liver cell, that's where insulin can be of use.
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Okay?
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What insulin's going to do is it's going to convert this glucose into a specific molecule.
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It's going to take glucose and it's going to polymerize the glucose into glycogen.
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Okay?
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So, that's one thing it's going to do.
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One thing it's going to do right away is it's going to help to stimulate these PI3K and AKT.
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The protein kinase B.
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It's going to stimulate glycogenesis.
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That's one mechanism.
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You know what else it can do?
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It can take this glucose and help to be able to convert it into pyruvate.
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So, it can actually work through specific types of glycolytic enzymes.
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And takes and converts those glycolytic enzymes and makes them active to help to be able to form pyruvate.
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Through specific types of phosphatase activity.
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Okay?
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So, again, one more time.
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Insulin's binding onto the liver, activating tyrosine kinase receptors.
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Forming these intracellular messengers like AKT, protein kinase B, he's called.
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Who helps to be able to convert glucose into glycogen.
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And helps to be able to convert glucose into pyruvate.
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By activating glycolysis.
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That's one way.
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And what is that doing?
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That's yanking the glucose out of the blood and converting it into different storages.
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Because what's the end product?
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If you keep following pyruvate, he goes to acetyl-CoA, right?
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And then we know acetyl-CoA goes to the Krebs cycle, who goes to the electron transport chain.
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And produces ATP.
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So, we're going to use this to get some energy, too.
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Okay?
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All right.
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So, that's the two mechanisms.
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Let's actually outline that.
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One mechanism is forming glucose into glycogen.
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What is that called when you take glucose and convert it into glycogen?
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That is called glycogenesis.
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Okay?
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Okay, that's one mechanism.
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We also said the other mechanism was taking glucose and converting it into pyruvate.
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Which will then go through its other steps.
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What is this step here called?
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This is called glycolysis.
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Okay?
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So, that's what it's doing, it's stimulating glycolysis and glycogenesis.
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All right.
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That's what it's doing in the liver.
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Let's see what it's doing over here in the muscles.
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So, let's take this insulin and let's follow this insulin out here.
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Okay, so this insulin's going to come out to this area.
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And it's going to come and act on this receptor.
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Again, a tyrosine kinase receptor.
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Now, when it activates the tyrosine kinase receptor, I'm probably going to get on you guys' nerves.
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This is called a GLUT4 transporter.
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Why am I telling you it's GLUT4?
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Because GLUT4 is dependent upon insulin.
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So, normally, this is bringing glucose in.
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But what this insulin's going to do is it's going to activate these protein kinase B.
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This protein kinase B is going to come over here and activate this GLUT4.
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It's going to stimulate it.
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Maybe by phosphorylation reactions.
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If it stimulates GLUT4, what is that GLUT4 going to do?
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It's going to become hyperactive.
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And what was really high out here in the blood again?
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Glucose.
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So, what's glucose going to do?
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It's going to start funneling into this muscle cell.
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If it starts funneling into this muscle cell, what can the actual insulin do within that muscle cell with that glucose?
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Remember, I told you, it can take the glucose and eventually convert it into pyruvate, right?
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And then from pyruvate, where can pyruvate go?
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He can go to acetyl-CoA.
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Who goes into the Krebs cycle?
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Who goes to the electron transport chain?
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And produces ATP.
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Right?
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What is this protein kinase B?
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This whole complex from insulin doing?
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It's stimulating that glycolysis pathway.
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So, over here, what is it doing?
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One thing is it's enhancing this GLUT4 activity to bring glucose into the cell.
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So, it's enhancing this step right here.
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It's called it's increasing glucose uptake.
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Which is a fancy word for just being able to say.
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Bringing glucose into the cell.
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It's increasing the rate at which glucose is being brought into the cell.
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And it's stimulating the conversion of glucose into pyruvate.
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What's that called?
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That is called glycolysis.
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Okay?
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You know, it's not done at that, too.
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It loves to be able to do other things.
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He loves to help out.
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That's what insulin does.
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Insulin's a great helper.
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So, what insulin does is, since we already know that it does this, I'm going to get this out of the way.
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Because we're only really concerned with the pyruvate pathway.
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But it can that just understand that that pyruvate can go to acetyl-CoA and be utilized for ATP.
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Look what else it does.
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There's other transporters over here on the cell membrane.
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So, let's say here's another transporter.
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And this transporter is specific to specific types of amino acids.
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So, you know, amino acids are really, really important for making proteins, right?
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Especially within the muscle cells.
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So, you know what this actual guy does?
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He comes over here and he stimulates this red protein channel.
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What's that red protein channel?
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This is called an amino acid channel.
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Now, you know, whenever you're eating, so right when you eat, they call it the fed state, right?
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So, or the absorptive state.
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Right when you're eating, that's when your glucose levels and your amino acid levels in the blood are really, really high.
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So, what's going to be really, really high out here?
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If I were to represent it in a different color.
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Let's say I do it in brown.
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Okay, so let's say out here in the blood, you're going to have high amino acid levels in the blood.
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Why is it high?
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Because you just got done eating, right?
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So, right when you're eating, so when you're in the fed state or the absorptive state.
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Your amino acid levels within the blood are very, very high.
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Insulin takes that to his advantage.
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And he stimulates these amino acid channels.
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And helps to be able to pull these amino acids into the muscle cell.
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So, it stimulates that.
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So, what's that called whenever you're increasing the activity of these amino acid channels?
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It's stimulating amino acid uptake.
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Okay?
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Then look what else it's doing.
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He's not done.
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You know, amino acids are the building blocks, let's say I represent these dots as amino acids.
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If I take these amino acids and I string them together by making peptide bonds.
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So, now I'm going to represent those little dots as a whole component of this large, large molecule.
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Which is called a protein, right?
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So, proteins are basically the the they're actually the polymers, right?
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Because these are the monomers, amino acids are the monomers.
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So, they're the building blocks of proteins.
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What this actual insulin does through these protein kinases is it stimulates this process.
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What is this called when you're taking amino acids and converting it into proteins?
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This is called protein synthesis.
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Man, this hormone is is really, really getting around, huh?
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So, he's stimulating protein synthesis and amino acid uptake.
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He's stimulating glycolysis.
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He's stimulating glucose uptake.
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Only through the GLUT4 transporters.
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He's stimulating glycogenesis within the liver.
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He's also stimulating glycolysis within the liver.
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You know what else he can do inside of the muscle?
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He's not done.
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He can take that glucose and he can convert that glucose into glycogen.
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So, he can also stimulate this reaction here.
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And what is that called?
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That's called glycogenesis.
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Okay?
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Now, if you can think about it.
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There was high glucose levels in the blood, and I told you that there was also high amino acid levels in the blood.
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And if you really want to think about it, it also has high fatty acid levels in the blood.
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Now, technically, some of these fatty acids can also get taken up by the actual adipose tissue.
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And utilize.
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So, if I were to represent that, too, technically, these fatty acids.
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They can actually be brought into the cell.
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And insulin can actually help to stimulate some of these fatty acids.
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To be converted into triglycerides.
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Okay, so again, because you just remember, insulin is secreted whenever you're eating.
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Okay, during the absorptive state.
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So, these fatty acid levels in the blood will go down.
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The amino acid levels in the blood will go down.
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Why?
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Because insulin is stimulating the amino acid uptake.
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The glucose levels in the blood will go down.
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That's his whole effect.
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So, it's beautiful to understand that, and you can see now that whenever insulin is actually deficient.
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Or whenever it's produced in large amounts, it can cause drastic effects on the body.
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Okay, and we'll cover that in diabetes, and we'll also talk about them when we talk about insulinomas.
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All right, engineers, we covered a lot of information in this video.
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I hope it all made sense.
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I hope you guys enjoyed it.
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If you did, hit that like button.
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Hit that subscribe button.
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Speaker A
We'd love to be able to hear from you guys.
