Insulin: Study with Video Lessons, Practice Problems & Examples

Insulin, a peptide hormone with 51 amino acids, plays a crucial role in regulating blood glucose levels, stimulating cell growth, and increasing lipid synthesis. It decreases blood glucose concentration by enhancing GLUT4 transporter expression and promoting glycogen synthesis. Additionally, insulin acts as a growth factor, triggering cell division through receptor tyrosine kinase (RTK) pathways. Its influence on lipid synthesis is significant, particularly after meals, highlighting its anabolic effects. Understanding these pathways is essential for grasping insulin's multifaceted role in metabolism and cellular function.

Insulin

So here we're going to briefly revisit our map of the lesson on biosignaling pathways, which is down below right here. And, of course, we know that we've been exploring this map by following the leftmost branches first, and we've already covered G protein-coupled receptors and GPCRs and all of these GPCR signaling pathways in our previous lesson videos. Recently, we've transitioned to a new branch here for the Receptor Tyrosine Kinases or the RTKs. And so here in this video, we're going to continue to talk about Receptor Tyrosine Kinases as we introduce insulin and then the insulin receptor, which is an example of a receptor tyrosine kinase. So let's get started with insulin. Alright. So here we're going to introduce insulin, which is probably a word that you've heard before in your previous biology courses. And so you may already know that insulin is really just a small protein or a small peptide for that matter, and more specifically, insulin is a small peptide with just 51 amino acid residues in it. Insulin functions as a hormone or a bio signaling molecule that can travel and affect other cells. Now, the reason that we're talking about insulin right now at this point in our lesson is because insulin is involved in classic RTK pathways or receptor Tyrosine Kinase pathways. And so as we move forward in our course, we're going to see very specific receptor Tyrosine Kinase pathways that utilize insulin. Now in our bodies, insulin signals the well-fed state or the fuel-abundant state. And so cells are capable of recognizing that, we have just eaten a meal because we are well-fed and that we have an abundance of fuel. Now when insulin is initially secreted, it's initially secreted as a zymogen called Proinsulin. Now recall from our previous lesson videos that zymogens are just the inactive precursors to active proteins or enzymes. And so initially, it's going to be secreted as the zymogen Proinsulin by pancreatic beta cells in response to eating a meal. And again, when you eat that meal, you're going to be well-fed and have an abundance of fuel. And so if we take a look at our image over here on the left-hand side, notice that at the top here we're showing you the structure of proinsulin, which is again the zymogen form of insulin. Notice that Proinsulin is a single polypeptide chain here that has one amino end and one carboxyl end, but also notice that it forms these disulfide bonds that we're labeling right here. And so, what you'll notice is that zymogens are usually activated through proteolysis or the cleavage of the protein. And so what you can see here is we are showing you the cleavage sites which are right here and there's another cleavage site over here, indicated right here. And so essentially what's being cleaved off is this blue portion of the proinsulin protein. And so when this blue portion is cleaved off, that actually creates what we have on the bottom half of our image, which is the insulin protein. Notice that the insulin protein, because of the cleavage, is actually existing as two polypeptide chains, the red one and the green one here. But in total, there are 51 total amino acids as we indicated up above. Notice that these two polypeptide chains are actually still disulfide linked together, and there's also this disulfide linkage within the same polypeptide chain up above. Now, over here on the right-hand side of our image, what you'll notice is we're showing you a diagram of someone eating a cookie, some kind of meal here, and in response to, again, eating a meal, we know that the pancreatic beta cells in our pancreas, which you can see our pancreas is right here, this yellow structure that we're zooming into here in the digestive system, and, the pancreatic beta cells here in our pancreas are going to secrete the proinsulin, or the insulin, into the bloodstream. And once insulin is in the bloodstream, it can travel to distant areas and affect cells in different areas. So insulin acts as a hormone when it's secreted into the bloodstream. And so the exact functions and biological roles that insulin has when it's secreted into the bloodstream, we'll get to talk about as we move forward in our course. But for now, this here concludes our introduction to insulin. And again, we'll be able to see insulin in very classic RTK pathways as we move forward in our course. So I'll see you guys in our next video.

Proinsulin:

• A. Is synthesized in three parts and then assembled for storage.
• B. Is more active than insulin.
• C. Is synthesized as a single chain, folded and then cleaved into insulin.
• D. Stimulates insulin secretion.

Insulin

Alright. So here in this video, we're going to introduce insulin's 3 primary biological effects. And so after eating a large meal like this guy down below right here, insulin can actually be secreted into our blood and signal many different effects throughout our bodies. And so we're not going to talk about all of the different possible effects that insulin can have, but moving forward in our Clutch Prep Biochemistry course, we are going to talk about how insulin generates really 3 primary biological effects. And so notice down below in our table, we have each of these 3 primary biological effects listed. And as we move forward in our course, we'll talk about each of these 3 primary biological effects that insulin has in more detail. Now the first primary biological effect that insulin has is that it decreases blood glucose concentration, essentially decreasing the concentration of glucose in our blood after eating a large meal, where the glucose concentration in our blood would be really high. And so really this first effect here is probably the most well-known effect that insulin has. And again, we'll get to talk more about this effect moving forward in our course. And more specifically, we'll talk about the insulin RTK pathway that actually leads to this decreased blood glucose concentration.

Now the second primary biological effect that insulin has is that it can actually stimulate cell growth by regulating gene expression within the nucleus of a cell. And, again, moving forward in our course, we'll talk more about this particular primary biological effect, and we'll also talk about a different insulin RTK signaling pathway that leads to this stimulation of cell growth by regulating gene expression.

Now the 3rd primary biological effect that insulin has is that it increases the synthesis of very specific lipids. And later in our course when we talk about the biosynthesis and metabolism of lipids, we'll revisit this particular, primary biological effect then. But for now, this here concludes our introduction to insulin's 3 primary biological effects. And again, as we move forward in our course, we'll talk more about each of these 3. So I'll see you guys in our next video.

Which of the following is NOT a biological effect of insulin after eating a large meal?

• A. Increases the concentration of blood glucose.
• B. Regulates gene expression to activate cell growth.
• C. Stimulates the production of certain lipid molecules.
• D. Decreases the concentration of blood glucose.

Insulin

In this video, we're going to talk more details about insulin's first primary biological effect, which is that insulin decreases blood glucose concentration. And so after eating a high glucose meal, of course, the glucose concentration in our blood is going to be pretty high since, again, we just ate a high glucose meal. And so insulin's primary job or primary function, again, after eating a high glucose meal, is to help decrease that glucose concentration in the blood, which again is really high immediately after eating a high glucose meal. And so insulin can actually help to decrease glucose concentration in the blood in the following two ways that we have listed down below, number 1 and 2. And so the very first way that insulin can help to decrease glucose concentration in the blood is, that insulin will actually increase the expression of a glucose transporter called GLUT4, and GLUT4's job is to import blood glucose into cells. And of course, if you're importing blood glucose, then you're going to decrease the concentration of glucose in the blood. And so this is the first way, again, that insulin can help to decrease glucose concentration in the blood, and we'll be able to see this example down below in our image.

Now the second way that insulin can help to decrease blood glucose concentration is that insulin will actually indirectly affect cytosolic enzyme activity via biosignaling pathways, more specifically RTK or receptor tyrosine kinase biosignaling pathways. And, it will affect the cytosolic enzyme activity in such a way that it will help to convert free glucose within the cell, into glycogen. And so, of course, if we're converting free glucose into glycogen, then that's going to decrease the free glucose concentration inside of the cell, and decreasing the free glucose concentration inside of the cell is really what's going to facilitate the diffusion of blood glucose into cells. And, again, when blood glucose diffuses into cells, that is going to again decrease glucose concentration in the blood, which is again exactly what we say insulin's, effect is all about, decreasing blood glucose concentration. And so if we take a look at our image down below right here, we'll be able to visualize what we've been discussing above.

And so notice over here on the left, what we have is a cell, and this is the cell's plasma membrane. But within the cell, notice that we have these vesicles, and these vesicles contain the GLUT 4 glucose transporter. But notice that when the GLUT 4 is in the vesicles like this, it's not actually being expressed. It's not able to do its job of bringing glucose into the cell, because again the glucose transporters are in vesicles, and they need to be in the membrane in order to allow glucose to come into the cell. And then also notice over here on the left-hand side, we have a relatively high glucose concentration inside of the cell. Now, of course, after eating a high glucose meal like this kid right here who's eating this cookie here packed with sugars, we know that the insulin is going to increase in our blood, and so there's going to be an increase in insulin after you eat a high glucose meal, and insulin is going to signal for these two events to take place. The first event is that it's going to signal for the increase in GLUT4 expression. And again, the second event is that it's going to signal for an increase in glycogen synthesis, converting free glucose into glycogen. And so over here on the right-hand side, what you'll notice, over here on the right-hand side is that the plasma membrane over here is now expressing the GLUT4 transporter. And so these vesicles that were over here have fused with the plasma membrane so that they can express these, again, these glucose, GLUT 4 transporters. And so this corresponds with the increase in GLUT 4 expression. And then also notice that over here on the right-hand side that the glucose, that glycogen synthesis has been increased. So now we have a relatively low glucose concentration inside of the cell because, glycogen synthesis is being increased. So you can see our glycogen structure over here. And so when we have a low glucose concentration inside of the cell, and of course after eating the high glucose meal in our blood, and notice up here is our bloodstream, we know that there's gonna be a high glucose concentration after eating a high glucose meal like a cookie. And so when we have a low glucose concentration inside of the cell and a high glucose concentration in our bloodstream, that's going to allow for glucose to diffuse down its concentration gradient, but it can only get through the membrane, through the GLUT 4 transporter here. And so you can see here that we're showing the high glucose concentration in the blood, and the glucose is able to diffuse through the GLUT 4 transporter into the cell where there's a relatively low glucose concentration since, again, glycogen synthesis is being increased. And so, ultimately, these two events right here, you can see work together to help decrease the blood glucose concentration or the glucose concentration in the blood. And really this is what we said the main effect of insulin was, that insulin is going to decrease blood glucose concentration, again, as we indicated right here. And so this here really concludes our introduction to how insulin decreases blood glucose concentration, And later in our course, we're going to talk about the exact RTK signaling pathway, that insulin is involved with, to help elicit these two effects. The increase in glucose transporter GLUT4 expression, and also the increase in glycogen synthesis, converting free glucose to glycogen. And so I'll see you guys in our next video where we can get some practice with these concepts.

What is the primary function of the peptide insulin?

• A. To stimulate transport of glucose out of the cell and into the bloodstream.
• B. To stimulate transport of proinsulin out of the pancreas and into the bloodstream.
• C. To stimulate transport of glucose out of the bloodstream and into the cell.
• D. The transport of epinephrine from the bloodstream to the cell receptor.

Insulin

In this video, we're going to talk a little bit about insulin's second primary biological effect, which is that insulin stimulates cell growth. Now, when the concentration of insulin is high, in some cases, insulin can also act as a growth factor. A growth factor is defined as a biological substance that stimulates cell growth, healing, and or differentiation. What's really important to note here is that when insulin is acting as a growth hormone or a growth factor, it's actually going to use a completely different biosignaling pathway than when insulin lowers blood glucose concentration. Later in our course, we're going to talk about two different biosignaling pathways that insulin is involved with. One of those biosignaling pathways will lead to decreased blood glucose concentration, and the other insulin pathway is going to lead to insulin stimulating cell growth, acting as a growth hormone. That's important to keep in mind as we move along in our course.

Down below here in our example, notice that we're showing you how insulin can act as a growth factor to stimulate cell growth. Notice over here on the left-hand side, we have this cell, and this cell is secreting insulin, which we're showing like this. In some cases, insulin can act as a growth factor. It will bind to the insulin receptor, which we know is a receptor tyrosine kinase, an RTK, and we'll talk more about that as we move along in our course. It's going to, of course, induce signal transduction, allowing for biosignaling, causing cell division, essentially causing a cell to multiply and divide. Again, as we move forward in our course, we'll be able to talk about the exact insulin biosignaling pathway that allows it to stimulate cell growth. But for now, this here concludes our introduction to how insulin stimulates cell growth, and I'll see you guys in our next video.

The hormone insulin can function as a(n) ________________.

• A. Secondary messenger.
• B. Adapter protein.
• C. Effector enzyme.
• D. Growth factor.

Insulin

So recall from our previous lesson videos that Insulin's third primary biological effect is that Insulin increases lipid synthesis and so insulin actually has a large effect on lipid synthesis. And in this video, we're pretty much going to leave it at that and that's because later in our course in a completely different chapter, we're going to talk a lot more details about how insulin increases lipid synthesis. But for now, if we take a look at our image, notice on the left-hand side we have this character who seems pretty healthy and, pretty fit. And he's eating this meal here and of course, we know that eating a meal is going to lead to the increase in insulin. And, of course, here what we're saying is that insulin has a large effect on lipid synthesis and it will increase lipid synthesis and so over here what we can see is that lipid synthesis has been increased and our character seems much more lipid-packed. But again this is really where we're going to leave it at and later in our course, we'll get to talk more details about this idea right here. And so, I'll see you all in our next video.

What is the effect of insulin on lipid fatty acid synthesis?

• A. It activates regulatory proteins that inhibit synthesis of fatty acids.
• B. It increases the synthesis of fatty acids resulting in higher amounts of fat storage.
• C. In causes fatty acids degradation by liposomes.
• D. It decreases fat storage by converting fatty acids to energy.
• E. None of the above.

Which of the following is NOT an effect of insulin?

• A. It increases the rate of fatty-acid synthesis and storage.
• B. It decreases the concentration of blood glucose.
• C. It stimulates cell growth and division.
• D. In stimulates the release of proinsulin from the pancreas.

Here’s what students ask on this topic:

What is insulin and what are its primary functions?

Insulin is a peptide hormone composed of 51 amino acids, produced by the pancreatic beta cells. Its primary functions include regulating blood glucose levels, stimulating cell growth, and increasing lipid synthesis. Insulin decreases blood glucose concentration by enhancing the expression of the GLUT4 transporter, which imports glucose into cells, and by promoting glycogen synthesis, converting free glucose into glycogen. Additionally, insulin acts as a growth factor, triggering cell division through receptor tyrosine kinase (RTK) pathways. Its influence on lipid synthesis is significant, particularly after meals, highlighting its anabolic effects. Understanding these pathways is essential for grasping insulin's multifaceted role in metabolism and cellular function.

How does insulin decrease blood glucose concentration?

Insulin decreases blood glucose concentration through two main mechanisms. First, it increases the expression of the GLUT4 transporter on cell membranes, which facilitates the import of glucose from the blood into cells. Second, insulin promotes glycogen synthesis by activating cytosolic enzymes via receptor tyrosine kinase (RTK) pathways. This process converts free glucose within the cell into glycogen, reducing the intracellular glucose concentration and promoting further glucose uptake from the blood. These combined actions effectively lower blood glucose levels after a high-glucose meal.

What role does insulin play in lipid synthesis?

Insulin plays a significant role in lipid synthesis, particularly after meals. When insulin levels rise, it stimulates the synthesis of specific lipids by activating various biosignaling pathways. This anabolic effect helps store energy in the form of fats, which can be utilized later when the body requires it. The detailed mechanisms of how insulin increases lipid synthesis are covered in more advanced biochemistry courses, but it is essential to understand that insulin's influence on lipid metabolism is crucial for maintaining energy balance and overall metabolic health.

How does insulin stimulate cell growth?

Insulin stimulates cell growth by acting as a growth factor, which is a biological substance that promotes cell growth, healing, and differentiation. When insulin binds to its receptor, a receptor tyrosine kinase (RTK), it triggers a biosignaling pathway that leads to cell division and proliferation. This pathway is distinct from the one that lowers blood glucose levels. By regulating gene expression within the nucleus, insulin can promote cellular growth and multiplication, which is vital for tissue development and repair.

What is the relationship between insulin and receptor tyrosine kinases (RTKs)?

Insulin interacts with receptor tyrosine kinases (RTKs) to exert its biological effects. The insulin receptor itself is a type of RTK. When insulin binds to its receptor, it activates the RTK, initiating a cascade of intracellular signaling events. These events lead to various outcomes, such as decreased blood glucose concentration, increased lipid synthesis, and stimulated cell growth. The RTK pathways are crucial for transmitting the insulin signal from the cell surface to the interior, ensuring that the appropriate cellular responses are carried out.