 The hormone gastrin is released from the anterum of the stomach. In the anterum actually there are certain cells known as D-cells which release the gastrin hormone and as we are telling that it is the hormone that means it is released into blood from these D-cells and via blood it travels and reaches to the fundus part of the stomach where the parietal cells are present. So let's see the details of this. See actually the mucosa of the stomach dips little deep and the opening of this dip in the mucosa on the lumen of the stomach is known as gastric pit. Okay one thing before we proceed to further we have certain questions at the end of the video which are more clinically oriented and we'll see that by understanding the physiology whether you are able to solve those questions or not which I think that you will be definitely able to do. So let's continue. So now our gastric glands are present here. So some of these are mucous cells, there are stem cells and there are G-cells also here which secrete our gastrin. So what are these D-cells? These G-cells are flasks shaped cells and their epics is thrown into folds which we call as microvilli. So this apical portion of the cell is thrown into fold. So this forms a microvillain. So what happens this exposes these G-cells to the gastric contents. Now why it is important to know is that these G-cells on their surface have certain receptors. So there are receptors for amino acids, there are receptors for peptides. There are also receptors for H-plus ions. So these chemicals can act on the G-cells and affect its function. So let us see what are the stimuli for the secretion of the gastrin from G-cells. So as I already told that there are receptors for amino acids and peptides and these basically stimulate the secretion of the gastrin from the G-cells. Now once you understand the function of gastrin you will realize that actually it's very important that these chemicals stimulate the secretion because this G-cell will release a gastrin which in turn will cause the release of the ethyl and pepsin in the stomach and these are the ones which are important for the digestion of the peptides. So it's basically food is itself causing its own digestion by called stimulating the release of the hormone. Okay apart from that what happens that when we eat there is gastric distention and this gastric distention causes the stimulation of the vagus nerve causing release of gastrin-releasing peptide. So there is again presence of receptor for this gastrin-releasing peptide which can act on G-cells and stimulate the secretion of gastrin. So there are local stimuli then there are neural stimuli plus there are certain stimuli from blood as well. So this basal portion which is near to the blood vessel actually epinephrine which is released from sympathetic neurons and calcium they can act on the G-cells and cause release of the gastrin. So since the gastrin is important for the secretion of HCl that is the reason that when there is a lot of stress and activation of the sympathetic activity this epinephrine you see stimulates the secretion of the gastrin and HCl secretion so stress can lead to increased acid secretion in stomach. Okay so these are the stimuli for secretion of gastrin. Local neural and some mediators from blood as well we can say humoidal but these are all the stimuli for secretion what we want is there should be some inhibitor of secretion also. So basically as I told you that H plus ions can also act on these G-cells so these H plus ions basically inhibit the secretion of gastrin from the G-cells. So in short let's see how the regulation of gastrin secretion occurs. So there can be multiple modes of stimulation of the G-cell which we said amino acids, peptides then now due to gastric distinction they can be vagus or from blood they can be epinephrine. So various stimuli can be present which will ultimately lead to the secretion of the gastrin. Now this gastrin goes and acts on the parietal cells present on pundas. So there are certain receptors on these parietal cells known as C-C-K-A receptors even though they are gastrin receptors they are known as C-C-K-A receptors. Now this causes release of hydrogen ions from the parietal cells into the gastric lumen causing a change in the pH in the gastric lumen. Now it's important that when adequate pH is reached it should not be like that G-cell continues secreting gastrin. So what happens that there is a negative feedback of operating that these H plus ions actually inhibit G-cells from secreting the gastrin. So you see the end product is being fed back and it is inhibiting the secretion of gastrin from the G-cell. There is another method also by which these hydrogen ions act. Basically they cause increase of secretion from the D-cells which release somatostatin and somatostatin acts on these G-cells causing the inhibition of the secretion. So we have seen that what are the stimulators of secretion of gastrin and what are the inhibitors. Now let's see what are the functions of gastrin. For remembering functions of any gastric hormone there is some fundamental which you should remember. If you remember this then I'm sure you will be able to actually guess the function of the hormone. So gastrin basically helps in digestion at the site where it is released and then moves the contents forward. It also maintains the site of secretion. Now if I ask you that what can gastrin do to helping digestion at the site. So obviously it should release the contents of the gastric juice that is the HCl and pepsin. Then how will it move the contents forward. It will move the contents forward by increasing the GI motility and this one maintaining the site of secretion that means it is trophic to the site of action that is maintains its growth. So yes these are the functions of the gastrin. Stimulation of gastric acid and pepsin secretion. Increase of gastric motility and it is trophic to gastric mucosa that is causes gastric mucosal growth. Okay so based on this let's solve certain questions. So your first question is there are two statements given. First is the assertion second is the reason and you have to choose between the options. So assertion says that in pernicious anemia there are elevated gastrin levels in blood. So you should know what is pernicious anemia. Actually pernicious anemia is basically a trophic gastritis where there is a loss of the parietal cells. So if parietal cells are not there what will happen is that hydrogen ions will not be released. So first statement is in pernicious anemia there are elevated gastrin levels in blood and second statement says that negative feedback inhibition of gastrin secretion does not occur in pernicious anemia. So what is your answer? The answer here is first one. Both A and R are true and R is correct explanation for A. Why? Now you see that pernicious anemia I told that there is loss of the parietal cells. So if parietal cells are not there hydrogen ions will not be produced and if hydrogen ions will not be produced we said that these hydrogen ions are having a negative feedback inhibition on G cells. So if hydrogen ions are lost the negative feedback on the G cells is lost causing increase in the levels of the gastrin. So yes first statement is correct in pernicious anemia definitely there are elevated gastrin levels in blood which is known as hyper gastrinemia and what is the cause of that? The second one negative feedback inhibition of gastrin secretion does not occur. So that's what our question is saying both A and R are true and R is correct explanation for A. Okay let's go to second question. Second question says that administration of proton pump inhibitors. Proton pump is basically hydrogen potassium ATPase which is present on the parietal cells and is responsible for the release of the HCl. So if we give proton pump inhibitors for two months that means we are blocking the production of HCl it can cause rebound increase in gastric acid secretion when the drug is stopped. Now it looks very complicated and here we are asking that whether this statement is true or false. Now this is used clinically actually if you see that a patient who has given proton pump inhibitors for two months we generally see a rebound increase in gastric acid secretion when the drug is stopped. Why is this occurring? See when HCl is not produced this proton pump inhibitor is actually a very powerful drug and it blocks this hydrogen potassium ATPase kind of completely. So HCl is not produced at all then what happens? Obviously there is increased gastrin levels as I told you before that if HCl is not there negative feedback is lost and it will cause increased gastrin levels. Now you see the functions of gastrin. One of the function of gastrin is that it is trophic to gastric mucosa that means if there are high levels of gastrin it will cause hyperplasia in the stomach. So what happens that whatever cells are there they proliferate so obviously the mucosal growth is occurring. So this gastrin whatever gastrin is there it acts on increased number of parietal cells. Getting the point so it's a little round about answer. So because of proton pump inhibitors gastrin has caused growth of the gastric mucosa what we call is that it is trophic and later on normal levels of gastrin are acting on increased number of parietal cells causing increase in gastric acid secretion. So and this is used in practice actually this drug if it is used for one or two months actually it should not be suddenly stopped. It should be either the dose should be decreased slowly or when we are stopping the drug we should switch to some other drug like H2 receptor blockers which suppress the secretion of the gastric acid as well. So yes this statement is true. Stopping the drug will cause increase in gastric acid secretion and I have explained you why this is true. Okay before finishing let's come to question number three. Gastronoma is a gastrin secretion tumor. Sorry this spelling is wrong it should be tumor and the secretion stimulates the secretion of gastrin from gastronoma. Again let us see whether it's correct or not. Yes gastronoma is a gastrin secretion tumor and a tumor which causes hypergastronomia we call it as Zollinger-Eleson syndrome the plethora of symptoms which occur we call it as Zollinger-Eleson syndrome. Now the secretion which we did not see till now what happens the secretion is released from intestine that you'll see in the video on secretion. Actually this secretion also inhibits the secretion of gastrin from the G cells. See secretion is released from intestine and its main function is to maintain pH in the intestine. So if lot of acid is being secreted acid enters into the intestine as well. So this secretion basically neutralizes that acid in the intestine and also decreases the production of acid in the stomach. Anyways the question says that secretion stimulates the secretion of gastrin from gastronoma. So yes what we have discussed physiologically actually secretion inhibits the secretion of gastrin from G cells but when it comes to gastrinoma secretion actually stimulates the secretion of gastrin from gastronoma and these gastronomas mostly these are present in pancreas. So this is known as secretion stimulation test. So you see here both statements are true gastronoma yes it is a gastrin secretion tumor secretion does stimulate the secretion of gastrin from gastronoma though physiologically it actually inhibits the secretion from G cells. Okay so in this case answer is both A and R are true but R is not the correct explanation for A because these are two correct statements which don't have any relationship to each other as far as the reasoning is concerned. Okay that's all for the hormone gastrin for now thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel Physiology Open. Thank you.