Production of insulin and glucagon
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- Concerning the depolarization of the cell, how is it advantageous to the cell to pump more cations into the cell if it's already heavy on the positive charge? Would it not want to push positively charged molecules OUT of the cell instead of bringing more IN?(12 votes)
- The answer to this lies in the fact that two different forces are at work here: these two forces together are called the electrochemical potential. Electric potential is what you've taken into consideration, great. Chemical potential refers to the gradient for a given ion. It's true that the depolarization has made the cell more positively charged, but body goes through a lot of trouble to regulate it's ion concentrations, and it's especially vigilant with Ca2+ ions. Ca2+ concentration is kept 10,000 times higher outside the cell. That means, it'll take a lot of electric opposition by positive charges to stop Ca2+ ions from rushing in. And by exchanging a few K+ ions (Yes really a few, it doesn't take too many ions to depolarize a cell, but that's for another discussion) there won't be enough of a force to stop Ca2+.(15 votes)
- The previous video mentions that insulin is necessary for the cells to take in glucose in order to make ATP. However, in this video, it says that the glucose must first enter through the GLUT2 receptor and make ATP in order to depolarize the cell and activate the Ca2+ channel, which in turn allows insulin to be released. So how can it be said that insulin is necessary for glucose to enter the cell when glucose must first enter the cell and produce ATP in order for insulin to be released??(5 votes)
- Great question! There are multiple types of GLUT receptors. GLUT2 is not insulin-dependent, so glucose can enter the pancreas without the presence of insulin.(9 votes)
- I'm a little confused about the correction of "more potassium" to "less potassium outside the cell".
I might be completely misreading this, but isn't the membrane potential around -70mV, so there should be more potassium outside of the cell as it travels down the concentration gradient?
Does the correction refer to the intracellular environment?(3 votes)
- at5:00you mention that glucose enters the cell through the GLUT2 transporter. In the previous video glucose is said to be uptaken by the cell through the use of insulin but this video shows that GLUT2 is responsible for the cells uptake of glucose and that insulin is exocytosed. Can someone please clarify what im missing?
Also around6:15why is Calcium uptaken into the cell after K+ increases in the cell? Wouldn't the increase in positive charge in the cell yield a lower chance of Calcium entering the cell?(1 vote)
- Insulin is really cool in that, its effect on the cell is to tell it to produce GLUT2 transporters so that it can take in glucose. So both are necessary in order to uptake glucose.
For the second question, remember that at cell membranes, there are two gradients at play that determine movement of solutes. There's an electrical gradient, and a chemical gradient. The concentration of Ca 2+ outside of the cell is muuuuch higher than that inside the cell, so the chemical gradient favors the movement of Ca 2+ into the cell. . When K+ enters the cell, it unlocks the Calcium gate and allows the Ca 2+ to move down its concentration gradient.(4 votes)
- I'm confused about the potassium channel. Sal says potassium passively leaves the cell so at rest there's more potassium outside the cell but the correction says he meant "less", but how can there be less potassium outside the cell if potassium is passively leaving the cell? Also, he says when there's ATP it prevents potassium from leaving the cell so the cell membrane becomes depolarized. How can it be depolarized if the cell is more positively charged than the outside to begin with, and it gets even more positively charged when there's ATP?(1 vote)
- Under the resting condition, the potassium ions leave the cell through "leaky" (open) protein channels and will continue doing so as long as their concentration in the cell is higher than their concentration outside of the cell. This means that when potassium ions leave the cell, their concentration outside is less than inside of the cell. Therefore, the correction to the video is accurate.
When the ATP molecule closes the channels by binding to them, the potassium ions concentration begins to build up inside the cell due to the Na+/K+ antiporter that brings more potassium ions inside the cell. As under the resting conditions there is a negative resting membrane potential (around negative 50 to 70 mV), this leads to the cell membrane depolarization making it less negative.(1 vote)
- the video shows where the glucose is going into the cell glut2... after some steps ... the calcium help the insulin to leave the cell right? i thought the glucose cant get into the cell with out insulin. can you help me with this question please(1 vote)
- How can the beta cells be polarized by facilitated diffusion? What drives the movement of potassium from inside the cell to outside the cell if it is going against it's concentration gradient?(1 vote)
- How would the pancreas and liver respond to hypoglycaemia?(1 vote)
- Hypoglycemia means your blood glucose level is way too lower than the normal level. In that case, the pancreas will secrete glucagon and signal the liver to carry out glycogenolysis (breakdown of glycogen to glucose) in order to raise the blood sugar level. Noted gluconeogenesis is also promoted by increase level of glucagon, yet the liver will not go to that way unless your body is at a fasting state.(1 vote)
- Is there any more detail on how alpha cells release glucagon? Or do we only have discovered amino acids trigger glucagon release?(1 vote)
- why do they say in their edit that potassium is higher inside the cell compared to outside. Isn't potassium always leaving at rest making it higher outside compared to inside?(1 vote)
- [Voiceover] As you can see on this gentleman right here, he's got a liver, and then this organ down here is referred to as the pancreas. Now the pancreas sits in the retroperitoneum which relative to the liver, which sits in the peritoneum, or in the abdomen, the pancreas is found to the back and to the left, to the back and to the left. And what's distinctive about the pancreas is it's blood supply. And so we can go through that in a little more detail after I blow up the pancreas right here and move it over just a little bit. Now the pancreas is like most organs, in that it receives oxygen rich arterial blood flow and gives off oxygen poor blood flow through the venous system. So this is the venous blood right here. And this is the arterial blood. But in addition to these two things, the pancreas also receives blood flow from the intestine, which I can draw right here. The small intestine will deliver unique nutrient rich blood through the pancreas and this is nutrient rich blood through the portal venous system. This is the portal venous blood flow. And once this nutrient rich blood flows through the pancreas it will trigger hormone release. Hormones such as insulin and glucagon and that'll actually be released into the portal venous blood and travel along with the rest of the nutrients to the liver. And the cool thing about the hormones going straight to the liver first means that the effects they have there are four times greater than what you will see in the rest of the body. So insulin and glucagon from the pancreas will have four times greater effect in the liver than in the rest of the body. But now the thing about the pancreas is that it doesn't just contain insulin and glucagon hanging out in random cells, they're organized. So if we blow up a small part of the pancreas right over here, we would see this. Which is a collection of cells here, like an island, surrounded by other cells. These other cells on the outside secrete enzymes that go into the GI tract, and we won't worry too much about them now, but the cells here in this island are referred to as the islet of langerhans. So it's the islet of langerhans. Which is just a fancy term for an island of cells. And the way the cells are organized in here is very structured. You'll have what are called beta cells in the middle of the island and on the outside you'll have what are called alpha cells. So alpha cells on the outside. And the key thing to remember here is that your beta cells release insulin while the alpha cells release glucagon. The alpha cells release glucagon. And we can actually go into further detail about how beta cells, for instance, secrete insulin into the blood. Let's start by focusing on this beta cell right here. I'll be sure to label this. This is a beta cell right here. This is our beta cell and these guys store insulin. So I'll write insulin here in this secretory vesicle. And I'll show you how it's released into the blood stream. This secretory vesicle, much like many secretory vesicles in the body, will release their contents outside of the cell if there's calcium present. So I'll put this calcium receptor here for now. The other thing that's unique about beta cells is that they have these potassium channels. So potassium channels that allow potassium to leave beta cells through facilitated diffusion. So they're just naturally leaving the beta cell over time. Which means that at rest there's a lot more potassium ions living outside of the beta cell than there are inside of the beta cell. And that's an important distinction because that's how we prevent the beta cell from being depolarized or getting a more positive charge within the cell. And this potassium channel also has a receptor on it, that I promise I'll go into more detail about in a minute. But it grabs onto ATP, the basic molecule of energy. And in addition to the potassium channel, there's also this calcium channel. So it's a calcium channel that's sitting here like in most cells and open through depolarization. And we'll go into how that happens in a second. All right, so now we're ready. How does insulin leave the beta cell? Well the first thing that has to happen is that glucose needs to enter the cell somehow, because when there's a lot of glucose around we wanna store it away. That's what insulin's supposed to do. And the way it enters is through this unique transporter. It's called the glut 2 transporter. And it allow glucose to enter into your beta cell. Once we get glucose inside of the cell, glucose will undergo what it usually does in most cells, processes such as glycolysis or be broken down into things that are sent through the krebs cycle. And doing this second thing here will produce a lot of ATP molecules. We mentioned ATP already. ATP is that basic form of energy. And it's important in this cell, because once we start to build up the amount of ATP that's present, some of it will go down here to this potassium channel and bind the ATP receptor that sits here. Now the interesting thing about this ATP receptor is that once it locks in, it'll actually block off this channel. It'll prevent potassium from leaving, so the next thing that'll happen is that the amount of potassium in the cell will start to skyrocket because there's no way for it to get out anymore. So you'll have a lot more potassium, or a lot more positive charge inside of the cell, than you have relative to what's outside. And what that's going to do is cause depolarization, depolarization of the membrane of the beta cell. That then will go and activate these voltage gated calcium channels, allowing calcium to enter the beta cell, which in turn can also cause calcium dependent calcium release into the cell. But overall it starts increasing the amount of calcium that's present on the inside. And as you might remember, the insulin secretory vesicle has a calcium receptor here. So sure enough, the next thing that occurs is that calcium will bind this receptor, causing this vesicle to fuse with the membrane of the beta cell. That'll cause insulin to be kicked out of the beta cell and be released into the blood stream. This step here, as you might recall, this final step that kicks the insulin out of the cell, is what's called exocytosis. Exocytosis, where a vesicle fuses with the cell membrane to release it's contents into the outside, or the extracellular space. Which in this case, is the portal venous blood, which will send it to the liver. So that's how insulin is released from beta cells. What about glucagon? How is it released from alpha cells? Well, unfortunately we don't know as well how this process works. All we know so far is that amino acids trigger glucagon release. How it does this specifically is a question and even perhaps a Nobel Prize up for grabs, which I think is fair to say, because the Nobel Prize in 1923 went to two scientists named Banting and Best for discovering insulin. And the crazy thing about that is that Charles Best, who shares in the Nobel Prize was a medical student the time the study was done in 1921. And then two years later, he was able to share the Nobel Prize with his professor, which is just mind boggling to think about.