 Body has mechanisms for both short-term regulation of food intake, that is when we are taking meat then how much will be the portion size for that particular meat, so that is short-term regulation of food intake and it also has mechanisms for long-term regulation of food intake which are important for control of weight and the amount of energy expenditure also. So this regulation both short-term and long-term happen at the level of the hypothalamus which has different nuclei and various chemicals can act on these nuclei, so let us see what are the nuclei which are important for regulation of food intake. Mainly nuclei are segregated into two centers, one is the feeding center which is the lateral nuclei and there is satitine center which is by ventromedial nucleus and paramentricular nucleus. Now when the feeding center that is the lateral nucleus is active and it is always active it is not inhibited okay. So when it is active it excites motor drive for eating which is present in the brain stem. So basically feeding center is for how much to eat and when to eat and how to eat that is the motor drive okay what is the behavior for eating that is present in the brain stem fine. So this feeding center is kept inhibited by satiety center, so satiety center actually inhibits this feeding center and then the feeding is going to stop. Now there are various chemicals and various mechanisms which act on these feeding center and satiety center to signal the body that it is time to eat or it is time to stop eating. So what are these signals? So for that we need to add one another nucleus that is the arquate nucleus of the hypothalamus. This arquate nucleus has two types of neurons that is the oryxinergic carneurons and the anorexinergic neurons. So oryxinergic neurons are those which will basically increase the hunger okay and anorexinergic neurons are those which will produce satiety or they will decrease the hunger. So in anorexic neurons we have POMC neurons that is pro opium melanocortin neurons which release alpha MSH which act on melanocortin receptors which are present on the neurons in the satiety center and it actually stimulates this neurons because of which satiety center is able to inhibit the feeding center. So it is due to the activation of these neurons that satiety center keeps inhibiting the feeding center. On the other hand the oryxinergic neurons are AGRP and NPY neurons which actually inhibit melanocortin receptor and because of this satiety center will be inhibited and it will not be able to inhibit the feeding center causing increase in the eating behavior. So that was all about the various nuclei which are present. Fine but now the point is that when these oryxinergic neurons and when these anorexinergic neurons will be activated. So as in the beginning I told you that there is both short term and long term regulation of food intake. So there should be signals which come in short term as well as there should be signals which come in long term isn't it? So short term that means when we are eating food that time when we are filled there should be signals which activate these anorexinergic neurons. Yes there are signals when we are eating food then there are certain GI hormones which are released and these GI hormones include PYY then there is GLP which actually increase the activity of these POMC neurons and that will cause the anorexia. So stoppage of feeding will occur because of these neurons and also CCK is also there. Then there is another hormone in short term which causes increase in the feeding behavior and that is ghrelin hormone. Ghrelin hormone released from axentic cells it causes activation of these oryxinergic neurons. So that is the short term control of food intake by GI hormones but when we eat and the food is absorbed that also determines the activation of these neurons and there are various theories for that. There is a glucostatic theory, glucostatic theory. Similarly there is amino static theory and lipostatic theory. So what it states is that when we eat and the absorption of these chemicals occurs in the body there will be increase in the blood glucose and there will be increase in blood amino acids as well and increase in fatty acids as well. Now these glucose amino acid and fatty acids actually increase the firing of neurons in the CETET center and that too of the ventromedial nucleus okay. So they increase the firing of neurons in the CETET center obviously it will cause the decreased activity of the neurons in the feeding center. So that is another aspect to that how regulation of food intake is occurring by GI hormones and by absorption of the carbohydrates amino acids and fatty acids after the food intake. Now another method is a long-term regulation of food intake and that is determined by the energy reserves of the body. So that long-term regulation is determined by the amount of adipose tissue in our body. Actually adipose tissue previously it was thought that it is a inert tissue in our body. It is just a storage place but now it has been found that it releases lot of chemicals and amongst these chemicals one very important chemical is leptin. So more the adipose tissue more is the release of the leptin in our body and this leptin acts on leptin receptors on the POMC neurons. So again here they will act and activate the POMC neurons causing increased activation of the CETET center and inhibition of the feeding center. So that is how energy reserves in our body determine how much we take food over long term and one more thing which we have not discussed and now and maybe it is little bit beyond this regulation of food intake but we should know that this reserves also determine that how much there will be energy expenditure because the activation of these POMC neurons in hypothalamus not only leads to inhibition of the feeding center but there are certain other aspects also which occur. Actually what this does is let me change the color this POMC it causes activation of the sympathetic nervous system and when sympathetic nervous system activation occurs there is increase in the metabolic rate and increase in metabolic rate causes increase in the energy production. So that the loss of the energy also continues if energy reserves in our body are too high plus it also causes decrease in insulin secretion and as we know that insulin is basically a hormone which is important for storing the fuel substrates isn't it? So if insulin secretion decreases then the storage of the fuel is also going to decrease and it may also be responsible for actually insulin resistance so that whatever insulin is there it is not able to act and the storage of the fuels is reduced. So that's how the regulation of food intake in our body occurs short-term regulation by a GI hormones are there and groupostatic amino static and lipostatic theories explain how the various fuels inhibit the food intake then long-term food intake is determined by the amount of the reserve fuel reserve in our body that is the adipose tissue which secretes various chemicals one of the very important ones being leptin. 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