So in this video, we're going to examine the absorptive state in greater detail. During this state, anabolism is going to exceed catabolism. We're building more than we are breaking down. And that makes sense because during the absorptive state, as an organism, we are digesting material and we're reabsorbing or absorbing that material uh up to about 4 hours postmeal. So, we're getting a glut of resources and with those resources, with those ample resources, we have plenty of nutrients for synthesis reactions. Any excess is then going to be stored during this period of time. So, carbohydrates, glucose most specifically, is going to be the major cellular energy fuel. The excess glucose that we have is going to be converted in the liver to glycogen or in some cases even fat. If we synthesize fat and protein, it's going to be released into the blood for storage via the atapost tissues. And we're going to be using these proteins called very low density lipoproteins. And we'll talk about them uh in greater detail in another video. With regards to triglycerides, the protein lipoprotein lipase, this is an enzyme that is going to catalyze the lipids of the kyomicrons. Remember that's when we're absorbing fats uh into via these little globules and the lactals and the lymphatic system. Uh and it's going to catalyze the lipids in the muscle as well as the fat tissues, right? their preferred energy source. The glycerol and the fatty acids are going to be converted to triglycerides for storage. The triglycerides are going to be used by the atapose cells, the liver, the skeletal and the cardiac muscles as the primary energy source. Amino acids, anything that is in excess will be daminated and used for ATP synthesis. With regards to the liver, it's going to store these amino acids as fat ultimately and this is where you're producing your ura waste. Uh if you're using damination reactions, most of the amino acids however that we do consume or that are in this particular phase are going to be used for protein synthesis. So here's sort of a flowchart showing you each of these three major pools. The amino acid pool, the glucose or carbohydrate pool, and the lipid pool. So the majority of the emphasis is going to be on synthesis. So we're taking amino acids and making them into proteins. We're taking glucose and converting it into glycogen. taking the glycerol and the fatty acids and converting those into triglycerides and storing them. Many of the cells are going to be using glucose as an energy source. Others, however, can use those lipids. So, here's an overview of the absorptive state. You have the GI tract. We're directly absorbing glucose. Excuse me for that. So, we're absorbing glucose and converting it into glycogen. We're absorbing amino acids, converting that into protein in the muscles. In the liver, we're also doing the same thing, processing those amino acids into proteins, most likely plasma proteins. But if you have an excess of amino acids, you'll convert them into keto acids and then shunt them into either energy production or convert them ultimately into fatty acids and store them as triglycerides. So all of this of course is under hormonal control and the primary hormone here is going to be insulin. So insulin is usually secreted under hyperglycemic conditions which are associated with diet. Right? When you're consuming foods, there's going to be a glut of carbohydrates coming in. So insulin secretion is primarily going to be stimulated by the blood levels of glucose as well as the blood levels of amino acids. Additional hormones can trigger uh gl uh additional hormones can trigger insulin release. One of which is a hormone called intestinal glucose dependent insulinotropic polyeptide or gip for short. Now of course this is a mouthful but it is quite a very descriptive name. So it's a string of amino acids hence the polyeptide. So it's a peptidebased hormone intestinal indicating where it is secreted glucose dependent. So this is the stimulus of the secretion of this particular hormone. And then this long word here insulinotropic. Well insulin is pretty obvious. Tropic is basically a hormone that triggers the release of another hormone. So anytime you hear the word tropic hormone, it's just a hormone in a cascade of hormones. So in this case, GIP which is released in response to glucose presence will stimulate the beta cells in the pancreas to ultimately release insulin. And they achieve this via the association with a receptor on cells which just for shortand we're going to just call the GIP receptor. And I mention this because most of you have probably heard of a drug called ompic. Ompic actually targets this particular receptor. So it's going to activate this receptor which results in insulin secretion. So this helps certain diabetics that are aren't as sensitive to insulin anymore. So, type 2 diabetics to sort of cause a little bit more insulin secretion so that you're removing the excess glucose that is in circulation. So, you're going from a hypoglycemic state to maybe a normal glycemic state. Additionally, the parasympathetic nervous system can also trigger insulin secretion. So remember the parasympathetic system was activated during digestion and absorption. So overall insulin's impact on metabolism is huge. It is a hypoglycemic hormone meaning it gets activated under hypoglycemic conditions. So it's it helps to lower hence why we're saying it's a hypoglycemic hormone. It helps to lower blood sugar levels. So the process of glucose absorption is going to be primarily through facilitated diffusion into cells, meaning it's passive. It's going to go down concentration gradients and it's highly dependent on insulin. So insulin triggers cells or permits these cells to use glucose. The exception are the brain and the liver where insulin really doesn't have this role this permissive role. The hpatocytes and the neurons in the brain are taking glucose whenever they need it. That's why even subtle effects or subtle lowering of glucose levels can potentially impact these highly metabolic cells. So glucose oxidation is going to be stimulated for energy production within the cells within regular cells while in the liver you're going to be producing from that influx of glucose glycogen. So you're storing it for when you're not eating. So when you're fasting uh and between meals as well as triglyceride formation. So in this flowchart we have the stimulus which is an increase in blood glucose levels that ultimately activates GIP which triggers the beta cells to produce and secrete insulin. Insulin is going to target regular cells. So that promotes the uptake and use of glucose that is going to lower the plasma levels of glucose. Um you can also have active transport of amino acids into tissues since there's a glut of energy now you can promote right the anabolic reactions of protein synthesis. So if there is glucose in circulation, if there's an adequate amount of glucose, this actually inhibits gluconneogenesis that is the formation of new glucose uh outside of diet. So the breakdown of uh triglycerides, the breakdown of amino acids, that's not going to be promoted since glucose levels are sufficient. So let's examine some homeostatic imbalances. And of course the big one is diabetes. And there are two main types of diabetes. Uh and we're not really going to differentiate them uh too much. But the first type known as type one. This is an autoimmune condition where the immune system attacks and destroys those beta eyelet cells. And so as a consequence there is an inadequate supply of insulin which is why we refer to type one as insulin dependent diabetes. Oops. Insulin dependent. The second type of insulin is when you have uh a lack of sensitivity to the insulin. So that lack of sensitivity to the insulin, that's going to be referred to as type 2 diabetes. And that's not autoimmune. There are, of course, risk factors, obesity being one of them, that can trigger this, but it's not that you're not producing enough insulin. It's just that you're not as sensitive to that insulin. So we call this insulin independent. Now in both cases you might have the patient inject insulin to help regulate blood sugar. But again the emphasis here is the is on sensitivity versus production. So alternatively insulin receptors could be abnormal. Maybe there's a mutation uh and that's why you develop this condition. So bottom line is with diabetes you have elevated levels of blood glucose which means these individuals are hyper glycemic. So because of that insensitivity or lack of production of insulin, they can't effectively lower the blood glucose levels and the cells which require insulin as a permissive factor, they're unable to access that glucose and so they need energy in the form of fats and proteins. Well, the problem if you have excessive breakdown of fats and proteins, which you're usually storing during this absorptive state, then you have what's called protein wasting and you have excessive weight loss, right? Because now you're favoring catabolism more over the anabolism uh in this absorptive state. And the breakdown products from fats and proteins is the generation of acids, right? The breakdown of fats leads to ketones while the breakdown of uh proteins also leads to sort of acids uh keto acids remember. So this is going to lead to metabolic acidosis or in other words it's going to create pH imbalance and since you are hyperglycemic in the plasma of the blood you filter that blood in the kidneys. So you're going to have a higher than normal amount of glucose in that filtrate and ultimately you're not able to recapture all of that glucose. So there will be some limited amount of glucose lost in the urine which ordinarily there is none lost in the urine.