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Yeah, cool. So, hi everyone today. We'll be covering the second half of the endo topics for phase one A. So our first lecturer is LEV and she will be taking you through glucose homeostasis. Hi. Yeah. So um as Alicia mentioned, I'm gonna be talking to you about glucose homeostasis and also a little bit about um diabetes a little bit later down. Uh the line. Um so just to get started, um I'll talk to you a little bit about glucose and the different responses in the body to like high and low glucose. Um A bit about the cells in the pancreas about insulin and how it's released. And then finally we'll go over some recap questions. Um and then yeah, I'll talk about diabetes as well. Um towards the end. So the Tylers for this session um in your syllabus are to know the principles of glucose homeostasis and to be able to apply them to different like scenarios. Um and then also to know about the incretin effect GLP one and also how insulin like binds to an insulin receptor um in like in the different like muscles and um a uh sorry adipocytes in the body. Um So before we start, wait, is this interactive? Like um I've made it to be interactive, but I don't really know how this format works. So, answers on the chat. Yeah, we can do the answers in the chat. And if no one responds, could you just do out of the answer? I'll continue. Yeah, that's fine. So I'll just read the question out. A girl feels hungry and she has a burger. Um and a hormone is produced by the pancreas in response to the increase in the girl's blood sugar. Um concentration after eating a burger, which option below best represents the physiological responses brought on by the increased levels of this hormone um in the bloodstream. So I'll give you guys like like a couple of seconds and if not, I'll just carry on. Should I just move on? Yeah. Sure. Yeah. OK. Um So the answer is b uh the hormone in question is insulin and insulin results in increased glycolysis, decreased lipolysis and increased protein synthesis. So we'll talk a little bit about that later on. Um So why is glucose actually important? Well, if your blood glucose concentration falls below like the normal range around like four millimoles per liter, um you become hypoglycemic and if this falls even further um towards like like below two millimoles per liter, this can lead to cerebral function being impaired and can result in unconsciousness, coma and eventual um death. So it's like very serious. Um and people presenting in A&E with hyperglycemia are like treated very, very urgently um because uh it can like escalate very quickly. So, how is it actually regulated? So, when our blood glucose levels are um low, uh four hormones are released. Uh Glucagon, Cortisol growth hormone and then the catecholamines. So, Glucagon is released from the pancreas. Um and I'll talk to you a little bit about that later on. Um but the other three are also involved in increasing blood glucose levels and blood glucose levels are decreased by insulin which is again released from the pancreas. So this is just a diagram to basically sum up um the different hormones involved in glucose regulation. So the pancreas is actually made up of majority of exocrine acinar cells. So, these secrete um uh enzymes to the small intestine. Um and this is involved in like digestion. Um But 2% of the pancreas is composed of islets of L hands. And these are the cells involved in glucose homeostasis. So you can see here. Um yeah, the majority of these cells are all like asthma cells and then you have these occasional islets of Langerhans. Um So there are three different types of cells in the islets of Langerhans alpha cells uh which are the cells that produce Glucagon beta cells which produce insulin. And then delta cells which produce somatostatin. These different cells communicate via paracrine communication. Um And there are two methods to this um paracrine communication between gap junctions, which is essentially where they exchange small molecules between them and then v tight junctions. Um It is in there like extracellular space in between them and like they're able to measure the different concentrations of hormones that they put out into those spaces and adjust their own like hormone output according to that. Um and in terms of what actually happens when uh your blood glucose drops. Um So, pancreatic glucagon is released and this initially causes increased lipolysis. Um So, the breakdown of fats, um increased gluconeogenesis and increased hepatic glycogenolysis. And again, also increases um amino acid uptake into the liver. And this is used uh for gluconeogenesis and uh this is all mediated via an increase in alpha adrenergic sympathetic um pathway activity. Um So, yeah, that mediates the whole process um and drives the blood glucose to increase uh to level it out. So this is just a diagram to show all of that. Sorry. Um So, as you can see here, insulin is actually inhibited in this instance. Um because we don't want to like decrease our blood sugar even further. Um Glucagon is released by the alpha cells. Somatostatin is still released by the delta cells, but it's because I'll explain it a bit later, but it sort of acts as like a counter regulatory hormone. Um So it's secreted slightly just to like really fine tune the levels of glucagon that's being released. Um So yeah, it's been mediated by the sympathetic nervous system. Um ad alpha adrenergic pathways. Um And then also there are um some immunoassays and gi hormones that are also involved in stimulating the alpha cells. Um but that's not very like relevant for you guys and your syllabus. Um So, on the other side, uh when you have high blood glucose, pancreatic insulin is released and this causes an increase in lipogenesis and a decrease in lipolysis also causes an increase in glycolysis, an increase in glycogenesis and an increase in glute mediated glucose transport into cells. Um And then finally, in terms of proteins, it causes increased protein synthesis and increased amino acid um transport. And this is mediated by the parasympathetic and beta adrenergic sympathetic pathway activity. Um instead of the alpha adrenergic um which is used for Glucagon. So again, yeah, as you can see here in this diagram, sorry. Um uh the beta cells are releasing insulin. Um alpha cells still release some glucon because they don't. Um essentially the body's trying to make sure that you don't overshoot into hypoglycemia um if too much insulin is produced. So some glucagon is still produced uh just to make sure that you're not becoming hypoglycemic. Um But uh and yeah, and somatostatin is still slightly released as well. Um And then the S NS uses the beta pathway this time to stimulate the beta cells. And again, the para sympathetic nerve system um also plays a part in this whole like process. So, like I mentioned, somatostatin acts as a sort of regulatory hormone it's released um in response to both insulin and glucon levels and uh essentially fine tunes the levels of hormones that are released so that the blood glucose levels are also fine tuned. Um And the slide is also just showing that insulin is also used for growth and development. Um This is mostly when your in utero insulin acts acts as like a um growth factor um for a fetus. Um But that's just a, a side note. So the incretin effect is on your syllabus. Um It's a bit of a weird one to get your head around, but once you like get your head around it, it like makes sense. Um So if you imagine giving someone 50 g of glucose either orally or via IV, um there will be the same rate of change of plasma glucose in your body. But if you compare the plasma insulin levels, um between these two methods of delivery, there will be a greater rate of change. So like a steeper spike. Um As you can see here, a steeper spike uh from the oral load in comparison to the IV load and this is due to hormone.