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Costanzo Physiology (Chapter 9E) Endocrine Physiology: Pancreas || Study This!
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hello and welcome to the next portion of the endocrine physiology chapter going over the endocrine pancreas of costanzo's physiology textbook if you enjoy the video please don't forget to give it a like and if you haven't subscribed already please consider doing so about 60 of you who watch these videos are not subscribed and it really helps the channel out so jumping into the endocrine pancreas remember this is different to our exocrine pancreas which secretes enzymes into our gi system to then break down our food products the endocrine pancreas secretes hormones into the bloodstream to mainly regulate our glucose concentrations so we have these areas called the islets of langerhans which contain the endocrine pancreas cells predominantly we have alpha cells beta cells some delta cells and then some other cells intermixed but the alpha cells secrete glucagon they the cells secrete insulin and then delta cells release somatostatin the other cells that aren't really depicted in here at least pancreatic polypeptide but there is less known about this actual hormone so we won't be covering that in this chapter so since we have this organization of the cells and these eyelets of langerhans they actually have some cells to cell communication either by gap junctions which is just the electrical communication between the cells or due to the blood supply that comes in once one cell has received its blood supply that venous blood from that cell actually disperses to the other cells so they are able to communicate with one another and then there's also adrenergic cholinergic and peptidogenic neurons as well that innervate these cells so we're going to go through each of those major hormones insulin is a big one because clearly it causes a pretty significant clinical disease and diabetes so starting with the synthesis and the structure of insulin it gets synthesized into first pre pro insulin from the mrna within the cell it is then cleaved early into pro insulin before getting shuttled away until the endoplasmic reticulum where it is modified to be folded into a folded form of insulin and then finally packaged up into some secretory granules in the golgi apparatus ready to be released as actual insulin now insulin gets regulated predominantly from glucose but it can be thought of as a hormone of abundance so any abundance of nutrients insulin is going to be secreted to try and store that energy in the body for use in the future so although increased glucose concentrations are by far the most important stimulatory factor increased amino acids or fatty acids will also stimulate insulin release in addition to glucagon which we'll talk about in a second cortisol which has a insulin resistant factor that will actually increase the secretion of insulin just because cortisol is going to increase our glucose and then also increase our insulin as well glucose-dependent and selenotropic peptide gip this is a hormone that's released from the gi system when we eat food and this causes an increased release of insulin due to oral glucose versus if we give glucose intravenously it's all because gip comes in and further stimulates insulin release potassium causes the release of insulin potassium is in our diet and this is important because insulin helps potassium get shuttled away into cells so when we eat insulin gets released to move those potassium from the diet into our cells vagal stimulation and some drugs will do it so sulfonylurea drugs increase the secretion of insulin and these are some treatments for type 2 diabetes we'll get into diabetes in a second here and then clearly obesity there will be abundant nutrients with obesity so that will stimulate increased insulin secretion the inhibitory factors of insulin secretion include low glucose which is understandable fasting and exercise because we no longer have an abundance for nutrients we actually want to start using those stores of energy so insulin is going to be bad in this situation so we inhibit the secretion there somatostatin remember our stopping hormone is going to stop our insulin secretion and then some drugs as well so getting into how insulin gets secreted first of all the stimuli mainly is glucose so we're going to focus on glucose here it enters the cell via the glute 2 transporter which is facilitated transfusion going to occur when we have hyperglycemia you know we have a high glucose concentration outside the cell it then gets facilitated diffusion into the salvia glut2 it gets oxidized essentially through glycolysis to produce some atp to produce some energy molecules these energy molecules actually ironically close the potassium channels on the cell by closing the potassium channels we stop the loss of a positive ion out of the cell so this actually depolarizes the cell because remember if we wanted to repolarize a cell then we increase the movement of potassium out of the cell by stopping potassium moving out of the cell we depolarize it so that depolarization causes an increase in calcium influx into the cell high intracellular calcium then results in exocytosis of our insulin into our bloodstream so that is how insulin gets stimulated to be released because of high glucose concentrations in our blood now that is a similar method for if we have increased amino acids or fatty acids etc so once insulin is in our bloodstream it will go to our cells and work via the intrinsic tyrosine kinase receptors remember these receptors are the ones with actual kinase enzymes as attached to the receptor so by the insulin binding it we get a conformational change so then the tyrosine kinase enzyme will now phosphorylate proteins and enzymes within the cell ultimately that will produce the effects that we'll talk about a little bit later in the video now once that tyrosine kinase receptor has been bound to insulin it actually gets internalized and degradated by intracellular proteases so insulin actually down regulates its own receptor so now it's going to be less sensitive to the presence of insulin now this is becomes a problem when we have constantly high insulin levels such as with diabetes mellitus specifically type 2 which happens with obesity because usually with obesity you have such an abundant nutrients within your bloodstream you typically are always hyperglycemic then that's going to constantly cause the secretion of insulin the receptors get down regulated so now you no longer respond to insulin and you effectively have no useful insulin in your body and that is when you get diabetes mellitus now the actions of insulin is next now once again this is a hormone of abundance so it's going to function to try and shut all away all of our nutrients inside our body for use at a later date so it's able to decrease our blood glucose concentration by increasing the glucose transport into cells using the glute for transporters and increases the production of those transporters it promotes the formation of glycogen in the liver and muscle remember glycogen is just a big polymer of glucose that stores that glucose away it also inhibits the breakdown of glycogen and also inhibits the formation of new glucose via gluconeogenesis which creates glucose basically from amino acids it reduces the blood fatty acid and ketoacid concentration and stimulates all that fat in the bloodstream to actually get deposited in your fatty tissue and inhibits your lipolysis it decreases your amino acid concentration by increasing the uptake by tissues and increasing your protein synthesis and also promotes the uptake of potassium into your cells remember we talked about that you have high potassium in your diet so insulin at the same time getting secreted but the glucose is going to help shuttle away all that extra potassium into your cells so if you have an abnormality in your insulin you essentially end up with diabetes mellitus diabetes mellitus just means sugary urine and the reason behind the sugary urine is because you have high blood glucose concentrations now that's either because of type 1 diabetes mellitus which means you are not producing enough insulin and that usually occurs due to an autoimmune destruction of your beta cells so you no longer produce insulin or type 2 diabetes which is insulin resistance and that may occur due to a constant hyperglycemia state this is the one that's typically associated with obesity due to just having so much glucose in the bloodstream there are some other causes for insulin resistance but let's get into too much detail for this particular chapter so with diabetes since we have ineffective insulin either due to a low concentration or low receptor numbers we are going to have increased glucose within our bloodstream that's unable to get into our cells so that increased glucose in our bloodstream is going to make us pee more because that's going to be over the threshold for our kidneys being able to reabsorb it so you end up with more glucose and your urine which has an osmotic effect to drag water with it so you become polyuric subsequently polydipsic as well you'll also end up being hyperkalemic because your potassium can't get into your cells you start to break down your proteins because you don't have that stimulus to get your amino acids into your cells and start to produce your proteins you also increase the amount of fatty acid and keto acids in your bloodstream because you have reduced that hormone that tells that fatty acids to get into your fat cells and store away so that can result in an issue actually called diabetic ketoacidosis which is more of an emergency because you have so many of these acids in your bloodstream you get this metabolic acidosis that you have to treat emergently now the treatment for type 1 diabetes is obviously going to be giving insulin if you're able to give insulin you essentially solve the problem of not being able to produce it when it comes to type 2 diabetes that's slightly different that is non-insulin dependent the problem is not essentially related to insulin quantity is related to the fact that your insulin receptors have been down regulated so the best way to treat this is trying to reduce your blood glucose concentrations from diet restriction weight reduction and then also some drugs that help to try to promote some insulin secretion but also increase our sensitivity of insulin at our target cells so type 2 diabetes slightly different where there's more of an environmental component into the treatment now glucagon is the complete opposite of insulin so it is the hormone of starvation and that is really to remember from our alpha cells and it's trying to maintain normal glucose concentrations so it's going to be secreted for the opposite reasons of insulin whenever we have low sugar within our bloodstream so low glucose concentrations it will also interestingly be stimulated if we ingest protein but this will be reduced if we have glucose simultaneously being secreted so if we have high glucose high amino acids we won't have an increased glucagon because that'll be an issue because that'll try to increase the glucose even further so essentially glucagon is trying to increase or maintain normal glucose concentrations when we are hypoglycemic so it's able to break down glycogen via glycogenolysis it's also able to reproduce new glucose via gluconeogenesis from our amino acids it's also able to increase the breakdown of our fat tissue via lipolysis to increase the amount of available energy and then also help to produce more glucose so everything is centered around increasing our glucose concentrations and then the last hormone that we'll talk about is somatostatin remember this is the stopping hormone we talked about this with growth hormone we talked about this with our gastrointestinal hormones here it's once again showing its face but this time being secreted from the delta cells of the pancreas to actually reduce the stimulation for secretion for glucagon and insulin it's having this protective effect so we don't get an overwhelming response of insulin or glucagon whenever they get secreted so it's kind of dampening their response to a stimuli so this is all that we're going to cover for today going over the pancreas join us for the next video we're going to go over the regulation of calcium and phosphorus to finish up this chapter once again if you haven't subscribed please consider doing so as it does help the channel out see you next time
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