Transcription
Iron engineers, in this video we're going to continue on with our discussion about fatty acid oxidation. So if you guys already watched the first part of this video, it was specifically discussing the process of beta oxidation that was occurring in different tissue cells, like the heart, or like the muscles, or the skeletal muscles, or even the liver—many, many tissues that this could be occurring in. But what we didn't get to describe yet is how much energy is actually being produced; a little mnemonic that we're going to discuss also to remember the beta oxidative pathways and then other pathways that it can occur specifically with peroxisomes and odd chain fatty acids. Okay, let's get back here. And since we've already covered this, we don't really need to do a serious, serious in-depth topic conversation with us because we've already gone through it, so we're going to kind of fly through this really quick, guys.
So if you guys remember, we have palmitoleic acid, which is again, how many carbons? A 16-carbon fatty acid. What do we do? We converted him into palmi—let's politics—palmitoyl CoA. So what I'm going to do here is I'm going to say that we're going to have over here palmitoyl CoA. How was this reaction happening? If you remember, there was an enzyme that was doing this reaction; that enzyme was called fatty acyl CoA synthetase. So that enzyme was called fatty acyl CoA synthetase enzyme. And what was this enzyme doing? It was taking and adding a coenzyme A, but in order to do that, it cost energy. So because it costs energy, what do we have to do? We have to specifically utilize the breaking of ATP. So what did we do in that step? We took ATP and we broke it into ADP and inorganic phosphate. And whenever we did that, we utilized that energy from breaking that bond to add the coenzyme A to make palmitoyl—palmitoyl CoA.
Then we said that there was a specific transporter here, and that was called CAT1, or you remember, you can call it carnitine palmitoyl transferase one, or carnitine acyltransferase one—it's all dependent upon preference. And you guys remember that it added on a specific molecule and pulled off this coenzyme A. So if you guys remember, I'll draw the reaction here. Here's the reaction that's moving into the cell. When it moves into the cell, what does this molecule do? It adds on carnitine, but when it adds on the carnitine, what does it get rid of as a result? It gets rid of the coenzyme A, and then it gets brought in as what? Now this molecule is called fatty, or palmitoyl carnitine. So it's called palmitoyl carnitine. This palmitoyl carnitine molecule, what happens with him? Remember there was another specific type of transporter that was on the inside of the mitochondrial membrane, closer to the mitochondrial matrix, while this was on the cytosol side. This one was called CAT2, or CPT2, because remember you can call it carnitine acyltransferase type 2, or carnitine palmitoyl transferase type 2. And what does this one do? Remember that it pushes the carnitine back out to get recycled and then instead it takes and adds on a coenzyme A. So it adds on a coenzyme A. When it does that, what's the overall result of this reaction? Out of this we get palmitoyl CoA.
Then what do we do? We went through a series of steps, four steps, and this was the steps. Now let me give you a little mnemonic to remember all of these steps. So we're going to four steps here. Let's do that first. Let's put one, two, three, four. Okay, I like to remember this mnemonic. Let's write this one out first. One is going to be O, H, O, T. I like to remember "OH HOT." So what is "OH HOT" stand for? O stands for oxidation, H stands for hydration, O stands for another oxidation step, and then T stands for thiolysis. And if you guys remember what was happening in each one of these series of reactions, if you guys remember in the first step of the reaction we had what molecule coming into here? We had, and I'm sorry, FAD to FADH2. Now you might be saying, "Okay, well, Zack, I remember that this one had NAD+ to NADH. If they're both getting oxidized, how do I remember which one goes which, or which one goes first?" You know, there's an F in FAD and there's an F in first, so FAD is going to come first in this reaction. And then what was happening in this second step? And as a result, you guys remember from this reaction, from this reaction, you get the trans delta two enoyl CoA. Then what? Then we added in water. And when we added the water into this reaction, we got what? We got specifically beta-hydroxyacyl CoA, beta-hydroxyacyl CoA. Then what happened? He got acted on by an NAD+ to NADH to form a carbonyl. Remember that carbonyl was a ketone, so we called it beta-ketoacyl CoA, beta-ketoacyl CoA. And then what happened? And this last step, this is where that thiolase enzyme comes in. Remember the thiolase enzyme, what was he doing? He was splitting the bond between alpha and the beta carbon. When he was splitting between alpha and the beta carbon, what happened as a result? One thing is I make a new specific acyl CoA. So I make another fatty acyl CoA, but this fatty acyl CoA is going to be two carbons short. Remember how specifically what was happening here? Remember I had a 16-carbon palmitoyl—palmitoleic acid with 16 carbons. What's going to happen is I'm going to—I'm going to regenerate another fatty acyl CoA, but the problem is is that that fatty acyl CoA is no longer going to be 16 carbons; he's going to be 14 carbons. But then guess what? He'll go back into this process, and when he goes back in and gets recycled, he'll go through the same process again and break off into another 12, and then into 10, 8, 6, 4, 2, 0. Okay, you keep breaking these guys down. But what did I tell you was the most significant part of this? What was the other product here that we got that was really, really important? Acetyl CoA, acetyl CoA.
Okay, now you're probably wondering, "Okay, this was an acetyl CoA," and let's actually make that green so that we stay consistent with the CoAs here. CoA with that thiol group. You're saying, "Okay, this was an acetyl CoA and this is a fatty acyl CoA, but I only had one CoA here. This violates—" adds a color into this reaction. So this thiolase not only cleaves between alpha and the beta carbon to give you a 14-carbon fatty acyl CoA, but it also gives you an acetyl CoA. Now the question is, is what can happen with that acetyl CoA? Okay, if I keep doing that beta oxidation like we talked about before, how many acetyl CoAs would I produce from a 16-carbon fatty acid? As a result, I would produce a total of—let's take this over here. Think about it: 16 carbons, I'm breaking them into two-carbon fragments. What's 16 divided by 2? 8. So I'm producing a total of 8 acetyl CoAs. Now you guys have to come back for a second and remember the Krebs cycle. Remember in the Krebs cycle, whenever we went through the Krebs cycle, you produced a bunch of NADHs and FADH2s. Remember, for one acetyl CoA, how many NADHs did you produce, guys? You produced three NADHs, three NADHs, and then you produce one FADH2, and you also produce one ATP by substrate-level phosphorylation—four—from one acetyl CoA. You make three NADHs. If you have eight acetyl CoAs, how many NADHs would I make? I would make 24, because 8 times 3 is going to give me 24. Then if I have one FADH2 for one acetyl CoA, eight acetyl CoAs would give me eight FADH2s, and this would also give me eight ATPs.
Okay, now the next question is, this is only from that acetyl CoA. What about the NADHs and FADH2s that we generate from this part here? Okay, so this happens. You're going to undergo how many rounds of beta-oxidation? That's the key question. Remember I told you you're only undergoing seven rounds of beta-oxidation. When you undergo those seven rounds of beta-oxidation, how many FADH2s and how many NADHs am I actually going to make from this reaction? From here, I'm going to get a specific amount of NADHs, and I'm going to get a specific amount of FADH2s from this beta-oxidative pathway. Okay, so how many—how many FADH2s and how many NADHs am I going to get out of this? Okay, whatever. I told you have seven rounds of beta-oxidation, so in seven rounds of beta-oxidation, these reactions are only going to occur seven times. So I'm going to get seven of these guys and seven of these guys, so that's going to give me seven FADH2s and that's going to give me seven NADHs. Hmm, this is awesome. Okay, but here's the next thing: We can't forget about that one ATP that we used up in order to activate the fatty acid, so we'll come back to that and we'll tally it all up. Okay, so say we take a 16-carbon fatty acid. How much energy would we be able to produce? Let's tally everything up.
All right, so now if I add together, right here, look how many NADHs we have. We have 24 we produce from the acetyl CoA, and then we have seven NADHs that we generated from that beta-oxidative pathway. So seven plus 24 is going to be a total of 31 NADHs. So now from this, I'm going to have a total of 31 NADHs. Okay, I get eight FADH2s from the acetyl CoA from these acetyl CoAs, and then I get seven FADH2s from the beta-oxidation pathway. So seven plus eight is going to be 15. Then I get 15 FADH2s. Then you're also going to have to account for the eight ATPs that I made by substrate-level phosphorylation. So now I'm going to add in those eight ATPs now I got from substrate-level phosphorylation. But then here's the next thing: You have to subtract the ATP that you utilize in order to activate the fatty acid. So now we have to subtract one ATP from all of this whenever we get from here. We're going to have to subtract this one ATP from it. Okay, so let's put a line across here. Okay, now the next question is, one NADH is going to be specifically three ATPs. So if I take this and I multiply this by three, because that's how many ATPs I'll get, so what is 31 times 3? That's going to give me—it's going to give me how many? It's going to give me specifically 93 ATPs. So this is going to be 3 times 1, 3; 3 times 3 is 9. I'm going to get 93 ATPs from those 31 NADHs. Then 15 FADH2s. If you remember, FADH2 gives you two ATPs. So again, what's 15 times 2? That's going to get me how many? 30 ATPs. Okay, so now I'm going to have 30 ATPs here. Plus, don't forget about the eight ATPs that I got by substrate-level phosphorylation. So now I have 93 plus 30 plus 8. So if we take all of that and sum that up, what's 93 plus 30 plus 8? So 93 plus 30 plus 8; 3 plus 8 is going to be 11, carry that one over; 9 plus 1 is going to be 10; 10 plus 3 is going to be 131. So that's going to give me how many? 131 ATPs, but then as how much we get, we'll say gross. All right, but then don't forget to subtract the ATP that it required in order to—what is this for?—activate the fatty acid. So in order to activate the fatty acid, so now you have to subtract that one ATP. So now what is completely left over as a result for your net gain? Your net gain of ATP from this process is going to be how much? 130 ATPs. That is absolutely insane, to make 130 ATPs from this actual 16-carbon fatty acid, which is palmitate—palmitate CoA. That's why they say that specifically fats are such a high-concentrated source of energy because they can produce significantly large amounts of ATP.
Okay, so from that we were able to calculate how much ATP we generated from the 16-carbon fatty acid. We did a little quick review of the beta-oxidative pathway. Now what we're going to do is we're going to come over here, and we're going to look at another pathway, which is going to be oxidizing specifically odd-chain fatty acids. Okay, so now we understand specifically how much ATP that we totally produce. And again, here's the thing, guys: Certain textbooks and certain literature will say that the NADH actually accounts for not exactly 3; it's like 2.5. And they'll also say that FADH2 actually doesn't account for 2; it's actually 1.5. Now if I'm just rounding it to 3 and I'm rounding this FADH2 to 2, then I'll get 130 ATP by rounding it. But if we were to be really particularly, because some of you guys might get into your textbook and say, "Oh, is AK, that doesn't make any sense," well, just in case you look in your textbook, if I were to do this: 31 times 2.5, so I'm making here red, if I made this 2.5, and then I made this one, instead of making it 3, I made it 1.5, then actually after I subtract everything, my overall total will keep this one here as the rounded. Will keep this one here as the rounded, but I'll write down below it: If you were to utilize those values of 2.5 and 1.5, you're actually going to get 108 ATP. Okay. Okay, so just in case you guys are looking into your literature, you might see 108 ATP from this actual reaction here, accounting for the 2.5 instead of 3 and the 1.5 instead of 2. And then again, if you actually have to subtract this ATP, you're also going to have to get about 107 ATP because you're going to subtract it from that point there. Okay, so now that we've done that, now what we're going to do is we're going to take and look at these odd-chain fatty acids and how they're being oxidized because they're a little bit different.
Odd-chain fatty acids, obviously, you know, odd-chain just means that it's not, you know, 2, 4, 6, 8, 10, 12. These ones could be, instead of like 16, it could be a 15-carbon fatty acid. So let's say I have a 15-carbon fatty acid here. If I have a 15-carbon fatty acid and I bring this 15-carbon fatty acid into the actual mitochondria, and then as a result I take this 15-carbon fatty acid through rounds of beta-oxidation, and when I go through this process of beta-oxidation, I give off a three-carbon group at the end of it, and that three-carbon group that I form is called propionyl CoA. Now here's the thing: Most of them were going into what when you were undergoing the beta-oxidative process? Most of them were producing acetyl CoA; most of them were being produced into this. But what happens is is whenever you're breaking one of those actual last bonds, you're giving rid of this acetyl CoA and a propionyl CoA. That propionyl CoA is going to have to go through a different process to be utilized for energy. So what happens is the propionyl CoA is actually going to be acted on by a special enzyme. This process is going to require ATP, so actually going to have to utilize ATP in this process. And the reason I'm going to have to utilize ATP, okay, is I'm going to have to do some type of special mechanism. We're going to add another carbon into this guy. So this is—I'm going to—what I'm going to do is I'm going to take this propionyl CoA, and I'm going to add another carbon into it. So in order for me to do that, I have to have a special enzyme that can do that process. Usually enzymes that are adding carbon dioxides or carbons in are going to be called carboxylases. So this enzyme is called propionyl CoA carboxylase. Now what's interesting about this enzyme is this enzyme, not only is he catalyzing this step in adding a carbon in the form of usually the CO2, so usually going to add a carbon in the form of CO2, this enzyme, he's stimulating this step right; he also consists of a very important vitamin called biotin. So this is one of our complex B vitamins, and it's very, very necessary in order for this enzyme to function. So the propionyl CoA carboxylase is going to be doing what? It's going to be adding in a carbon and breaking this ATP into the ADP and inorganic phosphate, and there's also going to be some bicarb that can go into this reaction also. So I can even put that if I need to. I'll put bicarbonate actually going into this reaction also. Usually that's the form of how we're actually adding the CO2 is we're actually adding in the form of the bicarb. Now this propionyl CoA, when it reacts with the bicarbonate, ATP to give you ADP and inorganic phosphate in the presence of this enzyme, propionyl CoA carboxylase, which needs biotin to be present, what it's going to do is it's going to convert this propionyl CoA into methylmalonyl CoA. It's going to break it into—it's called methylmalonyl CoA. And usually there's two different forms; technically there's a D form, and then what will happen is that methylmalonyl coenzyme A mutation reaction where it'll get converted into the L form. So there is two different forms of the methylmalonyl-CoA: one in the D form, one in the L form. Not really relevant here. What is relevant is this next step. I'm going to take this methylmalonyl CoA, and I'm going to feed it into a specific step of the Krebs cycle, and you guys have probably seen this Krebs cycle intermediate before, I would assume. The enzymes catalyzing this step is very, very dependent upon vitamin B12, but this enzyme is called methylmalonyl coenzyme A—methylmalonyl CoA mutase enzyme. And this enzyme, what he's going to be doing is he's going to shuffle around the structure to be able to produce a very important molecule, and this molecule that he'll be producing is called succinyl CoA. And I already told you guys that this guy is a Krebs cycle intermediate. So what can happen with that succinyl CoA? I can technically take this succinyl CoA, and I can convert him into two different things. One is I can convert him eventually into oxaloacetate. And if you guys remember anything about oxaloacetate, remember he can be hidden in the form of malate. And when he's hidden in the form of malate, he can get shuffled out here. So here's our—let's say this is the form of malate. Remember that malate can get converted back into oxaloacetate. And then what can happen with that oxaloacetate? If you guys remember, there's a special enzyme called PEPCK, and PEPCK was converting the oxaloacetate into phosphoenolpyruvate. And then what can happen? He can eventually go up to make glucose. And if he eventually goes up to make glucose, what is that called when I took a non-carbohydrate source and turned it into glucose? This is called gluconeogenesis. So this can lead to gluconeogenesis. Okay, so now we have gluconeogenesis occurring here, which is coming from these odd-chain fatty acids, right? So this 15-carbon—or let me put here right next to it, what is this again? This is an odd-chain fatty acid. This reaction is producing acetyl CoA molecules, but as a result, it's producing a three-carbon fragment called propionyl CoA. Propionyl CoA is being acted on by propionyl CoA carboxylase, which needs biotin; it's adding in bicarbonate for that extra carbon that's going to be adding in, and this reaction requires ATP. It produces methylmalonyl-CoA, which can shuffle between the D form—dextro rotary—into the L form—levo rotary—form. Not significant in this process, but it is acted on by a mutase enzyme, a methylmalonyl CoA mutase enzyme. Okay, so now in order for this to happen, we require vitamin B12. So B12 is very, very important for this reaction to occur. Another thing that can happen with this succinyl CoA is, you know that you can continue throughout the Krebs cycle. So if he continues throughout the Krebs cycle, what's another such significant function of this guy? So technically he can go to form ATP; he can go into forming ATP, right, because you can continue to go through the Krebs cycle and be utilized to make NADH and FADH2, take those to the electron transport chain and make ATP. One more interesting function of this guy: He can also be utilized to make porphyrins, specifically porphyrins—porphyrins and...
Heme groups and the team, and porphyrins are important. Because, where have you heard the word team or porphyrin molecules before? Team clothing! So this isn't—and this actually can help to make what molecule? Hemoglobin. So you guys can realize how significant this process is. Any breakdown in this process of succinylcholine being able to make more porphyrins, which is consistent with in hemoglobin structure, it causes detrimental effects on the body. One of them you probably heard of is called pernicious anemia, which is the lack of, by a vitamin B12, usually due to the lack of a protein produced by our stomach called intrinsic factor. Okay, so this is one of the ways that we can deal with these odd-chain fatty acids. So the ultimate result of odd-chain fatty acid oxidation is what? I can eventually make succinyl CoA. What are the destinations of succinyl CoA? One is, I can make glucose through gluconeogenesis. The second one is, I could actually continue throughout the Krebs cycle and produce ATP. And then the other one is, I could take it and actually use it as a precursor to make heme groups and porphyrins, which is necessary for hemoglobin. And again, remember that this step here, to do that, convert the methylmalonic acid into succinyl CoA requires vitamin B12.
Okay. Now the last thing that we're going to do is we're going to talk about the metabolism of these fats within peroxisomes. Okay, so let's come over here now. So this structure is specifically a peroxisome. This is a peroxisome. Now peroxisomes play a very, very tiny role, but they do have—they do nonetheless—they are important within the fatty acid oxidation, but they're not as significant as compared to the amount of fatty acid oxidation that's occurring within the mitochondria. Now the steps in this peroxisome are almost exactly identical; there's just one step that really differs significantly, and that's the one that we'll talk about. It's actually the first step of beta-oxidation. So let's go straight to that step. But what—here's something that's got to realize—this peroxisomes, and they do have transporters to bring specific types of fatty acids into this structure, which is kind of interesting. But again, this is important that these do have transporters on the peroxisome to bring the fatty acids in. So let's say that I bring these fatty acids in. So let's say I put fatty acids, but specifically this should be what it should technically be—this fatty acids that I'm going to have here, I should have a CoA on them, right? But they're going to come in fatty acyl CoA in. Once we have this fatty acyl CoA, and what's going to happen, you're just going to undergo the similar steps of beta-oxidation, but with the exception of one specific step in the first step. If you guys remember—remember we had FAD, and FAD was reacting with this fatty acyl CoA and picking up the hydride ions, and when it was picking up the hydride ions it was being converted into FADH2. And then, if you remember, FADH2 generally, and the actual mitochondria, will take those electrons to the electron transport chain to be utilized for energy. In the peroxisomes it's something different; they actually take oxygen, okay, plus water and react that with the FADH2. And what's happening is the FADH2 has those electrons, right? He's going to react with those guys and regenerate the FAD. As a result of when this oxygen and water gain those electrons, they get converted into a new molecule which is called H2O2, which is called hydrogen peroxide. So this molecule is called hydrogen peroxide. Hydrogen peroxide is extremely—you know, it can be extremely dangerous on our body, and the reason why is because it can act like a free radical and it can cause a lot of damage to our DNA and proteins and cause a lot of oxidative damage. So what happens is inside of these peroxisomes they have special enzymes to deal with that hydrogen peroxide. So say I take this hydrogen peroxide, I bring it down here. What happens is, is I take this H2O2, this hydrogen peroxide, and I'm going to have a special enzyme. This enzyme is called catalase. So let's add here an enzyme, and this enzyme is called catalase. And what this catalase enzyme is going to do is it's going to work your specific reaction to break up the hydrogen peroxide and convert it back into oxygen and water. So I'm going to take this hydrogen peroxide and convert it back into oxygen and water. And then what will happen? They'll go back in, remove that—if they remove the electrons off the FADH2 and convert back into hydrogen peroxide. That's the whole purpose, and that's because peroxisomes do generate a lot of hydrogen peroxide for certain types of cellular functions. But this is the main significant difference is that within the first step of fatty acid oxidation inside of the peroxisome, the real difference is instead whenever they generate these FADH2s in the peroxisomes, they don't have an electron transport chain; they take and drop it onto oxygen and H2O to make hydrogen peroxide, which can perform certain cellular functions within inside of the body. But to prevent this from causing excessive damage to ourselves, because it can act like a free radical, what happens? We take that hydrogen peroxide and we react it with catalase. When we react it with a catalase enzyme, that converts it back into oxygen and water.
Okay. Now last thing I want to talk about, guys, in this video, I want to talk about certain types of disorders in which certain enzymes within the body are not functioning correctly. The most common one that I want to talk about that is extremely dangerous is actually called medium-chain acyl-CoA dehydrogenase deficiency. We actually refer to it as MCAD deficiency. And what happens in MCAD deficiency is that they're obviously not having an enzyme called what? Medium-chain acyl-CoA dehydrogenase. There will be a CoA dehydrogenase enzyme is very, very important within inside of this pathway. If they're lacking this enzyme, think about what can happen inside of the body. So let's come over here to this actual pathway over here. Imagine we're lacking a specific enzyme in this pathway, specifically right around this point—this acyl-CoA dehydrogenase. If we're lacking that, then we can't generate this trans-Delta-2-enoyl, and we can't carry out the rest of the beta-oxidative processes. So what happens is these fatty acyl CoAs are building up, and they start building up and building up and building up within the liver. As these fatty acyl CoAs build up in the liver, they cause extreme damage of the body, right? So what's some of the signs of someone who has MCAD? One is, they're going to have lipid accumulation. So they're going to have high lipid accumulation, mainly in the tissues of the liver. This is usually going to be in the liver, but it can occur in different cells, but one of the dangerous ones is lipid accumulation in the liver. And again, what is this for? This is for MCAD deficiency. Okay, that's one dangerous thing. The next dangerous thing is they have hypoglycemia. These individuals also have hypoglycemia because it throws off other reactions in the body due to this MCAD deficiency. And you know what can happen whenever you have severe hypoglycemia and lipid accumulation in the liver? It can cause extreme vomiting. So some of the signs of these people is that they're going to have signs of vomiting; they're going to be extremely sleepy, very, very sleepy, and they can get so bad to where it can actually put them into a coma. Okay, that's one. Another one that I want to mention is over here with the peroxisomes. Now with the peroxisome, remember I told you these are—these transporters are responsible for bringing certain types of fatty acids into this actual peroxisome. There is a condition in which there is a deficiency within those transporters. If you have a deficiency in these transporters, can you bring the fatty acid in? No. And so the lipids start actually accumulating in the blood. And whenever the—what is this actual condition called? This condition is called X-linked adrenoleukodystrophy. Now, as you can tell, it's X-linked. What does that mean? It's more common in boys, usually. It's a common—more common in boys before the age of 10. So it's more common in boys before the age of 10 years old. Now what happens with these people? Well, one thing I told you, they don't have the transporters to bring the fatty acids in. Not only does that can happen—that they can't bring the fatty acid in and undergo beta-oxidation—but what can happen is that these actual fats can start building up in the blood. So as these fatty acids—so some of the actual signs of this person is that they're going to have high fatty acids in the blood—hyperlipidemia. When there's high fatty acid levels in the blood, this can cause disastrous effects on the body. Some of the effects that it can actually cause, and cause of visual disturbances, it can actually cause visual disturbances; it can also cause significant behavioral disturbances; and it can also cause coma and even significant death. And obviously, if untreated, it can lead to death. Now another thing that you can actually derive from this name—look at this name—that can actually can come from them which you can explain some of the neurological problems. You hear the word adrenal; leuco—leuco means white. So there's white matter within the actual central nervous system. In this condition, there is actually not going to be as heavily myelination. So you know the white matter is actually myelinated axons, and actually in adrenoleukodystrophy, they're actually not having myelination of their axons, which can cause significant damage. Another one is adrenal—their adrenal gland is also going to be damaged because the adrenal gland being damaged, that also can affect a lot of hormones being produced from that organ. So there's actually two—adrenoleukodystrophy, which can occur in boys below the ten years old, or MCAD deficiency. Oh, one other thing with MCAD deficiency, let's come back over here for a second because they have high lipid accumulation, right? And they're lacking a specific enzyme that can actually break down these fatty acids. You want to avoid this person from ever having to have to utilize or break down fatty acids. So what is the treatment for these people? Usually one of the treatments is that you try to give them a high-carb diet—put them on a high-carb diet to avoid and stay away from fats. If you put them on a high-carb diet, which avoids taking in the fats, that's going to help to prevent this breakdown of fats. The next thing that can also—you want to do is you're going to want to specifically be able to actually have decreasing time intervals between eating, and that's going to help with this process also. Last but not least, there is one last disorder—we're not going to spend a lot of time—but there is a condition which you can't make these peroxisomes, and whenever you're not making these peroxisomes, it can cause multiple disastrous effects on the body, not just with relates to fatty acid oxidation, but other different types of conditions. And this—whenever you're not able to make these peroxisomes functionally—it's called Zellweger syndrome. Okay, high-yield. So in this video we covered a lot of information. We went over just basically a review of the beta-oxidation pathway, in the activation, the transport. We went over the energy tally with respect to just rounding—I remember I rounded it within this video to give us a simpler idea of how much ATP, but if you did take into consideration the 2.5 and the 1.5, it would give you a little bit of a different answer, around 108. We talked about specifically the actual oxidation of odd-chain fatty acids with relationship to succinyl CoA and how that can be utilized in certain processes. And we talked about the fatty acid oxidation, how it differs in peroxisomes, as well as MCAD deficiency, X-linked adrenoleukodystrophy, as well as Zellweger syndrome. Iron engineers, I hope all of this made sense. I hope you guys enjoyed it. I really, really hope it helped, guys. Iron engineers, until next time.