So now that we're somewhat familiar with the glycogen fast for lease enzyme in this video, we're going to continue to distinguish between the liver and muscle glycogen fast for lease. And so we're going to specifically focus on Alice Derek regulation of liver glycogen. Phosphor lays a and then later, in another video, we'll talk about Alice Derek regulation of muscle glycogen Foster Worley's. And so it turns out that we can better understand Alistair Regulation of liver glycogen phosphor lays A If we understand the role of glycogen breakdown in the liver, which is to form glucose for export to other tissues when blood glucose is low and so really, the liver is very, very unsophisticated, and so it's glycogen breakdown is toe form glucose for other tissues, and so, therefore, in the liver, the default glycogen phosphor lays form is going to be phosphor lace A. And so recall from our previous lesson videos that phosphor lays a is going to be the active form. And so in the liver, phosphor lace is going to stay active and keep providing glucose toe other tissues. Unless it's Alice. Derek Lee signaled to stop making glucose for other tissues And so if the blood glucose concentrations are already really, really high, such as after eating a glucose rich meal like a cookie, then in that instance, Glucose is going to act as an al hysteric inhibitor to phosphor Elise A via negative feedback, and we'll be able to talk more about this negative feedback down below in our image. And so really, what we're saying here is that liver glycogen phosphor lays a is going to remain in its active form and keep providing glucose toe other tissues on. It's really on Lee going to revert back to its inactive T state when it already detect sufficiently high glucose concentration in the blood. And so, if we take a look down below at our image notice, we're showing you here what happens in the liver after a glucose rich meal. So eating a cookie, for instance, and so notice what we have here at the top is the same exact reaction that we have seen before in our previous lesson videos, where we have a glycogen molecule here being broken down, shortening the chain here and releasing ah single glucose molecule as a glucose one phosphate and of course, uh, glycogen phosphor. Liz is going to catalyze this. Specifically liver glycogen phosphor lays in the liver. And so what you'll notice is that this glucose one phosphate that's released through subsequent reactions it can be converted into many different forms on one of those forms is just a glucose molecule like what we see here. And so this glucose molecule can also be obtained in our diet through eating things like cookies. And so if we eat a cookie at that point, that's gonna be considered a glucose rich meal. And our blood is going to contain a very high concentration of glucose, very sufficiently high concentration of glucose. And so it there. If we're already obtaining lots of glucose, then really there's no need for the liver. Phosphor leads to continue to provide glucose if we're obtaining it through our diet like this. And so when glucose concentration is high enough via negative feedback, it can actually act as an Alice Derek inhibitor to the phosphor lays a form, so notice that in the liver it's normally going to be in the phosphor, lays a our state, which is why we have this yellow background around it, showing that this is the form that it's normally in. However, when we eat a high glucose meal, there is negative feedback and that can transition. The enzyme from the, uh, fox world is a our state to the phosphor lays b t state. And so, of course, glucose eyes going to be al hysterically inhibiting, um, the enzyme here. So there's Alistair inhibition by glucose and which will also notice is to go from the phosphor lays a form to the phosphor Lisbie form. There also has to be a form of co violent modification. And so that's what we're showing here as well. And so this Covalin modification is very complex and includes multiple different types of hormones. And so we'll talk more about this Covalin modification later in our course in a different video. But for now, what we can see is Alice Terek, regulation by glucose, acting as an Alice Terek inhibitor and switching it from the on form to the off form down here. And so really, uh, this concludes the Alice Derek regulation of liver glycogen phosphor lays a and we'll be able to compare this to Alice Derek. Regulation of muscle glycogen fossil always be in our next lesson video. So I'll see you guys in our next video
A patient comes into your clinic suffering from anorexia nervosa. Her mother brought her in concerned as the patient has not eaten in over 3 days. She has the classic presentation including low body weight, decreased muscle mass, decreased glycogen, and decreased fat stores, and she is anemic (low red blood cell count). What would be the expected phosphorylation state and activity of the patient’s liver glycogen phosphorylase?
Phosphorylated & active.
Dephosphorylated & active.
Phosphorylated & inactive.
Dephosphorylated & inactive.
Liver vs Muscle Glycogen Phosphorylase
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So now that we've covered Alice Derek regulation of liver glycogen, phosphor lays a In this video, we're going to talk about Alice Derek, Regulation of muscle glycogen, phosphor. Let's be. And we can better understand this by understanding the role of glycogen breakdown in our muscle tissues. And so the role of glycogen breakdown in our muscle tissues, unlike the role of glycogen breakdown in our liver tissues, is to form glucose and energy for itself on Lee during a muscle contraction. And so, therefore, in our muscle tissues, the default glycogen Foster Wallace is going to be glycogen phosphor. Let's be. And that's because recall that glycogen phosphor Lisbie is going to stay in the inactive state unless it's al hysterically signaled to create energy for a muscle contraction. Now in our muscle cells during a muscle contraction. Uh, there's going to be drastic energy changes. And so for that reason, our muscle glycogen phosphor release enzymes are going to be sensitive to regulation by energy molecules such as G six, p, a, T, p and a MP. Now recall from your previous biology courses that G six p is just an abbreviation for glucose six phosphate and This is just an intermediate molecule of glide Kalle assist, and it can therefore be converted into a teepee via cellular respiration. And so what we can say is that when there are high concentrations of G six p and high concentrations of 80 p, that's going to indicate high energy within the cell. And, of course, high energy is going to associate with muscle relaxation. Since when the muscle is relaxed, there's a build up of these high energy molecules now, on the other hand, high a MP concentrations is going to indicate low energy within the South. And that's because it's gonna be associated with muscle contractions and muscle contractions, deplete a teepee and form a MP. And so during contractions, there's this depletion of energy within the cell. And so the depleted A teepee results in MAWR, a MP, and the resulting a MP is going to al hysterically. Activate phosphor Lisbie via positive feedback, and we'll be able to see that positive feedback down below in our image. Now, before we get to our image, it's important to note that the muscle glycogen phosphor lays B is going to stay and active, uh, and really Onley revert to its active our state when it detects low energy due to muscle contractions, that air depleting the energy within the self. And so let's take a look down below at our image to clear some of this up. And so what? I want you guys to notices that were specifically focusing on, uh, during intense muscle contractions, such as if you're pumping weights in the gym or if you're in the middle of a marathon or something like that, and so notice at the top here. What we have is the same exact reaction that we saw in our previous lesson videos, where glycogen phosphor Elise is responsible for breaking down the glycogen and shortening the glycogen chain while releasing a glucose as glucose one phosphate. And then, of course, subsequent reactions can convert the glucose one phosphate into glucose six phosphate, or G six p, which we know is an Intermediate Inc like Collis is. And then, of course, the G six p via cellular respiration can be converted into a teepee. And so a teepee and glucose six phosphate g six p r high energy indicators and indicate when they build up they indicate muscle relaxation and so here during intense muscle contractions. Uh, this energy that we've built up here, the A T P can be used in a muscle contraction if you're in the middle of a marathon and so the a t P will be converted into the low energy molecule A m p. And so a m p is going to al hysterically activate, uh, the phosphor. Let's be here and help shifted to the phosphor relates a r. C. And so this is going to occur via positive feedback here. And so you can see that we've got the positive feedback indicator here. And so the low energy molecule a MP is a signal to the cell that it is, um, contracting. Uh, it's performing a muscle contraction. And so the muscle contraction, which generates a MP, allows a MP to al hysterically activate the fossil fuels BT state, which uh is going to occur via positive feedback and shifted from the faucet worlds. Bt state to the phosphor lays a our state and that is going to allow form or glycogen breakdown and a replacement of the energy that was being depleted. And so what we can see here is that normally, uh, the in our muscle tissues, the phosphor Ellis is going to be in the B form, uh, in phosphor Lisbie form in the T State. And it's on Lee during a muscle contraction where it will shift into the fuss for lead a our state. And that's exactly what we were indicating above. And so what's also important to note is that, uh, this is what happens during intense muscle contraction. But of course, during relax ation, there's an energy buildup in the cell. And so, during relax ation, the A, t, P and G six p are going to build up in concentration. And so the resulting G six p and ATP that we see here these guys are actually capable of al hysterically inhibiting foster release s so that it can essentially convert back into the form that it's normally end during muscle relaxation. And so we can see that G six p and 80 p here again are capable of al hysterically inhibiting or Alice Derek inhibition here of phosphor Lisbie via negative feedback. And so muscle glycogen phosphor lays experiences both positive feedback as well as negative feedback as well. From these high energy molecules and positive feedback from low energy molecules. And so you may be wondering, why is it that liver phosphor lays is insensitive to regulation by these molecules? Well, that has to do with the fact that the liver does not undergo drastic energy changes like our muscles do. And so for that reason, there insensitive to regulation by these energy molecules. And so this year concludes our lesson on Alice Derek regulation of muscle glycogen, phosphor Lazenby, and we'll be able to get some practice utilizing these concepts in our next video, so I'll see you guys there.
Muscle glycogen phosphorylase displays multiple modes of allosteric regulation. Which of the following is true?
AMP promotes conversion of R to T state.
ATP favors the conversion of the T to R state.
G6P promotes conversion of the T to R state.
If ATP is needed, phosphorylation converts the enzyme from the phosphorylase b to the phosphorylase a form.
Phosphorylation is mediated by phosphoprotein phosphatase 1.