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Glycolysis, Glycogeneses
In this episode, we delve into the intricacies of glycolysis and glycogenesis, exploring the biochemical pathways that convert glucose into energy. The discussion covers key processes, including ATP i...
Glycolysis, Glycogeneses
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Interactive Transcript
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Hello, so this is the first audio that I'm gonna do and I'm just gonna go over my notes.
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It will be really rough because this is my first time going over these notes and it is for a chapter that I am still trying to completely finalize and explain to myself better.
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So it's gonna get better but it's okay. I'm gonna start with a hard really really hard biochemistry chapter about the Kybra hydrate metabolism.
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So first I'm going to explain the things that I have learned through the read in the Kaplan book and looking at Crash Course and Khan Academy videos.
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So glycolysis is two ATP's you need to invest first before you can get a result. So you invest two ATP's into start glycolysis.
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And then as a return investment for ATP's are produced so that means a total of two ATP gain and you get two pyruvate, two NADH and that NADH is used to make sure that you are not used to.
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So glycolysis does not need O2 and it is an aerobic.
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Just so you know what all of this is and why we even have glycolysis is because we want to convert glucose into energy.
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And in order for us to unlock glucose and break it into energy we're gonna need to go through three steps which is the first one is glycolysis, second one is curb cycle and first one is the electron transfer chain.
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Energy the energy pretty much the money of the cell is ATP.
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It is the currency of the cell. It is why we have mitochondria and like the purpose of the mitochondria is to help us with unlocking the energy from the cells such as glucose.
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So each glucose molecule gives us 38 ATP and I'm just gonna dive into how we get that 38.
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So as I said first we do glycolysis the anaerobic process and it gives us the 280P and it also gives us 280P total and which is actually for ATP but we say to just because we are not gonna count the two ATP's we put in in the beginning as an investment.
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And then it also gives us 2Pi-revates and 2NEDH.
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This occurs in the cytoplasm.
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Then we move on to the curb cycle.
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So from the curb cycle where it is a continuation it happens in the inner mitochondrial membrane so the really curvy one kind of looks like a wrinkled membrane inside of the outer mitochondrial membrane.
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So across that membrane the two pyruvates from glycolysis gets turned into 2 ATP plus NED plus 4NEDH and 4FADH.
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Another way to really talk about it is something important to say is pyruvates let's imagine it as three molecules, three little pieces.
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So one of those pieces gets oxidized and breaks off so that carbon gets oxidized and it becomes CO2 and what we're left with from that pyruvates molecule isn't a Cetyl-CoA.
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Cetyl-CoA is very important and I'm gonna talk a lot more about it.
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So a Cetyl-CoA then gets converted into ATP and CO2 as well.
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And NAD plus is just a depronated version of NADH and NAD plus and NADH consistently throughout these mechanisms we are either input in NADH and then it gets depronated to a lock energy or the opposite happens.
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It just depends on what happens for each step of the cycle.
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And so for one pyruvates it gives us three NADH and one FADH.
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So this is things to talk about in the curbsicle. Also the curbsicle is aerobic.
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If we are doing glycolysis and we cannot do an aerobic process after we will not be going into the curbsicle and say we'll be going into fermentation and a different type of anaerobic cycle that I'll talk more about as well.
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So now as a result as I said through the curbsicle we have the two ATP's and four NADH and four FADH.
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So now we are ready to move on to something else that is going to happen in the inner mitochondria membrane. This is actually quite fascinating.
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I watch an animation online on YouTube about the energy, how it gets, how we unlock energy from the protonation and the phosphorylation and how that energy is then used in the electron transfer chain is just very mind blowing.
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So a very simplified way to describe it. Imagine three, so three IN gates and when we have these NADH or FADH they are losing their proton and that proton is traveling through the gates outside of the inner mitochondrial membrane.
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And when it travels, when it is traveling out, it is unlocking energy and every time it jumps a level to seek a more favored level, energy level, it is energy being released.
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And these electrons, because of that these electrons release enough energy that all these three work pretty much give that energy to ATP synthase.
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ATP synthase is the gate that forces these electrons or protons, something I need to look at whether it's electrons or protons, I think it's protons.
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I'm pretty sure it's protons against the ion gradient and it also then gives us ATP by phosphorylation, the original ATP that did not have that third phosphate.
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So at the end what we have is we have multiple ACP molecules that were created in the inner mitochondrial membrane through this very interesting and very impressive electron transfer chain that through the protonation we get energy that energy then gives us a protonation, it gives us energy for ATP synthase.
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So we work through electron transfer chain, it is so impressive that we get 34 ATP through it. So 34 ATP plus the 4 ATP that we made in the curves, like in the two from the curves I called the two from glycolysis, that's a total of 38 ATP and that's how one glucose molecule gets converted into that.
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I am explaining this through looking at the board that I made, so for me this is a note for me, it's just would be helpful for me to look at this can that I made of the board and it's going to be in my excel sheet or in my notes.
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Okay, so this is the through the board, now I'm going to go and dive into my notes through the can academy book. So it is chapter 9, Carbohydrates Metabolism.
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Okay. All right, so what I see here is first there are two transporters for glucose transporters.
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We have the glutes 2 and we have glutes 4. So glutes 2 captures the excess glucose primarily for storage and it is a low affinity transporter in the hippocytes and pancreatic cells.
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Hippocytes, hippocytes I believe are cells within our liver and pancreatic cells that's self explanatory, it's pancreas.
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So yes, well after a meal the blood travels through the hepatic portal vein from the intestine and it is rich in glucose and as I said that glutes 2 captures the excess glucose and uses it for storage.
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So when the glucose concentration drops below the KM much of the remainder bypasses the liver and enters a peripheral circulation, the remainder glucose.
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So KM is the concentration of a substrate when an enzyme is active half of its maximum velocity so Vmax. So the lower the KM the higher the enzymes affinity for the substrate.
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All right, so in other words the liver will pick up excess glucose and storage preferentially after a meal and when the glucose levels are high the BILOILIT cells of the pancreas and glute 2 as well as the glycolytic enzymes serve as the glucose sensor for insulin release.
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Now let's talk about glute 4. So glute 4 as I said is in the adipose tissue and the muscle and it responds to glucose concentrations in the peripheral blood.
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So now I'm going to do a quick side-by-side comparison of glute 2 and glute 4. So glute 2 is in the hippocytes cells and in the pancreatic cells tissue while glute 4 is in the adipose tissue which is the blood.
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So KM is in glute 2, KM is high and higher than 15 millimetres or small M big M while glute 4 it is low and it is 5 M and it is near the normal glucose levels in the blood.
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So saturated, glute 2 is not saturated at normal glucose levels while glute 4 is saturated at normal glucose levels like normal glucose levels in the blood.
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Glute 2 is not responsive to insulin but it does detect glucose and causes insulin release from beta B cells in the pancreas and glute 4 is responsive to insulin.
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So I'm going to talk about right now how insulin promotes glucose entry into the cells. So glute 2, glute 4 at my bad, glute 4 is saturated when glucose raises above the 5 M and after that the only way to let more glucose into the cell is by insulin.
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So when it is glute 4 is saturated the only way that you can actually leave more glucose back into the cell is through insulin and causing a pre-group and glute 4 causes the pre-group to glute 4 to fuse to the memory.
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And glute 4, the way that it describes it is kind of like a 4 molecules almost like gates bind to each other and they do bind to the membranes.
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And glute 2, there are a lot when it binds to the membranes it almost pretty much becomes a gate when it binds to the membranes.
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So yeah and the endosythosis of glute 4 is when these gates become the 4 molecules binded together almost like think of an X.
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And exosythosis is when that X separates into the 4 gates and then embeds himself in the membrane.
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These are so important because insulin regulation of the glucose transports and in the muscle cells of adipus tissue forget this last sentence I realized I completely misphrased this.
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Alright so now I'm going to move on to the Khan Academy notes on glycolysis.
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So all cells can carry out glycolysis which is important but you should know that it happens in the cytoplasm as I talked about before.
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So let's see I'm trying to not say things that I already said so I'm just going to say something that is really important for the MCAT to know is about glycolysis because glycolysis is a high yield project is that the rate limit in steps of the reactions are really important to know.
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So let's look at the glute, the glycolysis rate limit in steps.
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When I am looking at the transport chain, the transport and the glycolysis mechanisms there are a lot of enzymes and a lot of steps.
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So glucose is transported into the cytoplasm and the six glucose and then ATP is added, the first ATP is added, turned into ADP and then we get to the glucose 6-phosphate.
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I summarized the transfer, I summarized and say it changes the glucose 6-phosphate into fructose and then the fructose 6-phosphate is changed using the PFK, is changed to PFK2, is changed into glucose 26-B.
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This is the difference between the two fructose 6-P is converted into fructose 26-P and it is with the rate limiting step and it is with PFK2 and with insulin.
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Fructose 6-P is also translated so it can either become fructose 26-B, like phosphate or fructose 6-B can become fructose 16-B phosphate.
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So it can either become 2-6-B phosphate or 1-6-B phosphate. The difference is what we use to convert it.
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Both of these are rate limiting steps. The 1-6 actually is the more favorite because that is the one that gives us the pyruvate and therefore let's us have a lot more ATP.
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But so what I'm understanding right now from the chart that I'm looking at is fructose 6-P phosphate, insulin converts it using the PFK2 into fructose 26-B.
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And then that's fructose 26-B can then go and help with converting the initial fructose into fructose 16-B with PFK1, the phosphofructokinase1, that's the enzyme that helps with this conversion.
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We either have 1 or 2. 1 gives us 16-B phosphate and 2 gives us 26-B phosphate.
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And again, this step is where we use that second ATP that we invest into the glycolysis reaction.
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So moving forward, there are a lot of steps happen.
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ATP and citrate inhibits the AMP inhibits these steps, the rate limiting step while AMP activates it.
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It makes sense that ATP and citrate are inhibitors because they are pretty much the product of what we get from these reactions.
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While AMP is an activator, it activates it.
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And we do not need glycolysis if we have enough energy.
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So therefore when we do have that ATP, we do not need glycolysis so it inhibits that step.
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Okay, so now let's take a look.
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So the glutes for the transporters, glutes 2 and glutes 4, as I said, they're not always bound to the membrane.
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They go and bind to the membrane later on.
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And when glucose travels through those binded transporters, the transporters, aka, like the way I see them, the ligands, that is what helps with gluteal, glycolysis being triggered and helps.
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But if we do have ATP or we have any of ATP or lactic acid or citrate that will cause this glycolysis not to occur.
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Okay.
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So let's see.
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Again, knowing the phosphofructo-chynase is really important because they are the fracture-phosphofructo-chynase 1, phosphofructo-chynase 2, because they are the rate-limiting enzyme.
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Alright.
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So in fermentation, NADH is converted into NAD+.
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Which again, we use NAD+.
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We use NAD+.
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And NADH in the electron-transport chain to give us ATP.
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Okay.
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So something to say also is that in yeast cells fermentation is the conversion of pyruvate and pyruvate is 3 carbons to ethanol, which is 2 carbons and carbon dioxide, which is 1 carbons.
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The 2 carbons, the ethanol, is the acyselcoa.
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While the end products are different, the results of both mammalian and yeast fermentation is the same, which is replenish-in-us with NAD+.
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Okay. There are.
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So this is time for a mnemonic.
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So the irreversible steps of glycolysis, we have 4 enzymes to know.
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And the best way to memorize these 4 enzymes that are irreversible steps are, this is the mnemonic.
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How glycolysis pushes forward the process-chynase?
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How glycolysis pushes forward the process? It's through chynases.
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So, hexo chynase.
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G is glycolysis.
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So, G, how glycolysis?
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The second word is G, so it's glucose chynase.
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Pushes, third word is P, so it's PFK1, which is pushes forwards of PF.
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The process, process is this word letter P, pyruvate, and chynases, it's the letter K.
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Chynase, so pyruvate chynase.
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So the 4 enzymes are hexokynase, glucose chynase, PFK1, pyruvate chynase.
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And these are irreversible enzymes for the irreversible steps of glycolysis.
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Okay, irreversible enzymes are, is blood.
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There you go, red blood cells are irreversible enzymes.
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Okay, so now we're going to talk about the effects of the two bisphosphoglycerate on hymo-clobin A.
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This is a mouthful to say, so I'm just going to briefly talk about what I understood from this.
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So, other physiological stages in the body promote a right shift of the oxygen dissociation curve.
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And what causes that is a high 2, 3 B, P, G, or a low pH or a high hydrogen concentration or a high PCO2.
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So, like a good way to remember it is, exercise is the right thing to do.
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Right, right, aka pushes the curve to the right, so a right shift.
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Alright, now let's go look at the functions of those four important enzymes that we talked about.
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Hexokynase, the function of it is it converts glucose to glucose 6-phosphate and it traps glucose in the cell through force-for-relation.
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It is regulated and it is hexokynase is inhibited by products of glucose to phosphates and it is irreversible, of course.
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Second one, so how glycolysis pushes forward the process kinases.
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The second one is G in letter G, so glucose kinase.
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The function of glucose kinase is it traps glucose in the liver, it stops it from leaving the liver and the pancreatic cells through force-for-relation.
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Pretty much think of it this way.
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So, when glucose enters the liver or the pancreatic cells, glyco kinase runs to that glucose and puts a key on it, which is the phosphate group.
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Once it has that key, it is no longer, it is too big, it can no longer go back out of the liver and the pancus.
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And it is insulin-reduced to glucose kinase, which makes sense.
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Insulin controls how much glucose concentrations in the liver and pancreatic cells.
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And of course, again, all of these are irreversible steps.
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And then we have the P, so how glycolysis pushes forward, so the PF, it's PFK1, which is the phosphofructokinase1, the function enzyme for the rate-limitant step.
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It is the enzyme for the rate-limitant step that we talked about, converted the fructose 1.
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I can't, I'm going to look at that page, so yeah, it converts fructose 6p into fructose 1.6b, BIS, I don't know what BIS is, and P, which is phosphate.
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So it converts the fructose 6p to fructose 1.6bIS, phosphate.
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And it uses ATP, which is something to really remember, it uses that second ATP that we need and put into glycolysis as our investments.
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It is regulated, it is regulated by ATP inhibits it, citrate inhibits it, glucose inhibits it, which are the product of the glycolysis cycle.
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And it is activated by AMP, fructose 2.3bis, and insulin.
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The fructose 2.3bis is a substrate.
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And let's see here.
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Alright.
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The third one, the third, or at my back, let's see.
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The fourth irreversible enzyme is, remember the minimonic, how glycolysis pushes forward the process chynesis.
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The third, the fourth enzyme is, pushes process chynesis, which is pyruvate chynesis.
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Okay.
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So the function of it, it's substrate level phosphorylation.
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That's what pyruvate chynesis does.
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It's a substrate level phosphorylation, like it would phosphorylate,
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it's PEP to ADP, and it gives us pyruvate and ATP.
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And the regulation, it is regulated by, and inhibited by fructose 1.6bis, it is irreversible as well.
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Now we're going to talk about two very important reversible enzymes.
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So, I'm looking at my notes, and it looks like I need to double check something before I give myself a wrong information.
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Bear with me.
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Alright.
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So, another reversible enzyme is, the first reversible enzyme that is important to know is,
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glycerol dehydrate, three phosphate dehydrationation.
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Its function is, it's phosphorylate and makes any pH.
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It is, as I said, reversible.
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The other second and really important enzyme to know is, three phosphoglycerates canyes.
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The function of it is, it's phosphorylation, it's phosphorylation of the substrate level.
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And, uh, uh, la, la, la, la, la, la.
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I think I talked about this one.
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It is reversible anyway, and it is the one that converts the, oh, no I did not talk about it, so I feel good.
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Okay.
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I'm on track. So three phospholuciliserate kinase is the second reversible enzyme that
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is important to know. It also phosphorylates at the substrate level and it converts one
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three bifosphate to ADP and gives us three phosphorylation and ATP. So now we're just
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the intestine lactose is converted into using lactase is converted into glucose and galactose.
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So lactase is found in the diodenum which is the first part of the intestine. That galactose
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then in the blood travels into the blood vessels and is then converted into in our eyes sometimes
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it converts into galactitol that is in the lens of our eyes and I don't think this is
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important to know so I'm just going to skip over the enzymes in that to know but when it goes
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to this blood this blood goes to the liver brain or other issues or other tissues ATP goes in
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which is then converted into ADP and it gives us in the long run where in the liver brain and
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other tissues galactose is converted into glycolysis into glucose and or goes through galactose.
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All right an important source of galactose in the diet is the diacycaryth lactose and it is
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present present in milk. All right important enzymes to know from the two from the pathway I just
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talked about which starts in the intestine blood and brain which converts lactose into glucose
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is galactocainase and galactose one phosphate uridyl transferase. So galactocainase both of these
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are happened in the are found in the liver brain and other tissues and these so the galactocainase
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converts galactose into galactose one phosphate and uses one ATP the galactose one phosphate is
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then converted using the second importance in time to know which is galactose one p uridyl transferase
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and that one gives us glucose one galactose one p we have glucose one p and then that glucose
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then gets converted one p gets converted into the regular glucose and that glucose goes into the
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glycolysis the glycolysis goes into glycolysis. Now let's talk about fructose metabolism fructose
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is found in honey and fruits and we know fructose as a it is another diacycaryth
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okay so sucrose also three places intestine blood and liver and kidney so sucrose using sucrose
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is converted either directly gives us two things sucrose gives us gal glucose and fructose fructose
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fructose is a chemical like glucose this i'm going to say this from old biochemistry fructose is a
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five-member drink while glucose is a six-member drink okay so fructose from the intestine and gets
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absorbed into the blood and in the liver and kidney fructose is converted into fructose one
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phosphate it gets phosphorylated using the fructose kinase that phosphorylated fructose is then
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is then converted by aldolase B into glyceroldehyde or DHAP two things not important for me to know
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at the end of the day in the liver and kidney fructose is phosphorylated then goes to more
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reactions to give us to go into three very important change three very important steps which is it
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goes into glycolysis glycosinesis or glycognusinesis so before we move on we're just going to talk
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about the two things to know which is the enzyme responsible for trapped in glucose in the cell
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is galactokines and the enzyme that links the two pathways between galactose
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the galactose metabolism and the glycolysis that enzyme that the linkin enzyme is galactose one
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phosphate uridilus so the enzyme that is responsible for trapped in fructose so the first one I
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talked about was galactose the fruit the enzyme responsible for trapped in fructose is fructokines
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and the one that is responsible the enzyme responsible for linkin the two pathways again the two
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metabolic pathways is aldolase B so the trapped enzyme is pretty much the same for the two the first
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one is for galactose is galactokines for fructose is fructokines the second one is a little different
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so the linkin enzyme for the for galactose is galactose one phosphate uridilase while the linkin
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enzyme is aldolase B okay so now I'm going to talk about pyruvate dehydrogenase
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okay so pyruvate dehydrogenase is in the liver and in the liver it is activated by insulin
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and in the nervous system it is not responsive to the is not responsive to hormones
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so that means I believe that even like in the nervous system insulin would not be able to
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activate pyruvate dehydrogenase and it makes sense because high levels high insulin levels
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to the liver that the individual is well fed thus the liver should not only burn glucose for
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energy but shifts the fassy acid the like equilibrium towards production and storage rather than
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oxidation I read that part's word by word if you can tell but I'm just going to try to explain it
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my own words that pretty much it's if we high levels of insulin shows us that we're already full
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and we do not really we do not really need to burn more glucose for energy all right let's move a
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close is converted in through glycolysis into pyruvate pyruvate dehydrogenase is a very
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important enzyme it converts pyruvate into acetyl CoA and that acetyl CoA is converted into
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is converted into the CO2 or H2O through the citric acid cycle or it is converted into fatty
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acids through fatty acid synthesis okay so pyruvate dehydrogenase again is inhibited by its
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the substrate which the products which is acetyl CoA
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it's inhibited by the products which is acetyl CoA and let's take a look so pyruvate let's see I'm
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going to say that the like what three things can happen to pyruvate first pyruvate could
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turn into oxalo acetate the acetyl acetyl and that happens using pyruvate carbose cyclase enzyme
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or pyruvate can turn into a silkyl CoA with the PDH I think that is the pyruvate dehydrogenase
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the one that I've been talking about the step I've been talking about. pyruvate could also turn
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into lactate and that is through lactate dehydrogenase. From memory I'm going to say it would turn
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into lactate if it was more of an anaerobic um an anaerobic process because of a lack of oxygen.
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Now what are the reactants of the pyruvate dehydrogenase complex?
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Small break 12 silver my cats okay
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okay so
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so
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what are the reactants of the pyruvate dehydrogenase complex and what are the products?
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So the reactants for pyruvate dehydrogenase in order for us to get the the results we first
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need pyruvate we also need NAD plus this is really really important that I feel like I didn't
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talk about enough is in 4 pyruvate to give us a cetyl CoA we need not only pyruvate the
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hydrogenase which is the enzyme we also need NAD plus to be inputted into that reaction and we
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also need CoA. Then that CoA gets converted and we get the acetyl CoA as our product we get NADH
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which is the we just um protonated the NAD plus and we get CO2 okay and I talked about that
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before and a very nice introduction that I gave which is the 3 carbinated pyruvate one of them
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gets oxidized and that one carbon becomes CO2 and so acetyl CoA
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um affects B the H versus pyruvate dehydrogenates by by inhibiting it and it is to prevent
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more pyruvate to be formed once if we have already have a COA why do we need the pyruvate dehydrogenase
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to keep producing pyruvate now that was half or almost half of the ninth chapter of biochemistry
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which is a complicated high yield chapter I'm going to take a break and we'll talk about
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us in the next episode and I'm going to start its 9.5 of the Khan Academy books.