Our hunger is control in the region of arcuate nucleus in the brain. Arcuate nucleus is located at the region between thalamus and pituitary gland. Specifically, the arcuate nucleus is located in the mediobasal hypothalamus at the base of the brain. The arcuate lies on either side of the third ventricle and just above the median eminence .Chronwall also said that ; The arcuate nucleus surrounds the ventral part of the third ventricle and contains densely packed small neurons with 1-3 dendrites. At least fifteen transmitters and neuropeptides have been found in perikarya of arcuate neurons(Chronwall 1985). It includes several significant populations of neurons, including neuroendocrine neurones, and appetite-regulating neurones.There are many enzymes that can increase or decrease our hunger. The arcuate nucleus can detect the level of lipid and sugar level in the blood circulation. Futhermore the arcuate nucleus can also measure the metabolites and hormones level in the body. Some of the examples of hormones that control the appetite are Ghrelin, PYY3-36, insulin , leptin, cholecystokinin(CKK), Glucagon-like-peptide(GLP-1) and also amylin. All of these enzymes have effects on human appetite centre. Amylin is secreted by pancreatic beta-cells.As a proof, this is what the authors of Antiulcer effects of amylin a review said : Amylin belongs to the calcitonin peptide family. Amylin is a peptide synthesized not only in the β cells of pancreatic islets, but in small quantities also in other organs like in the intestinal and gastric mucosa, lungs and central nervous system(Samonina, Kopylova et al. 2004).Futhermore, Amylin is secreted by pancreatic beta-cells(Lutz 2011). Amylin is secreted together with insulin. Amylin is not only secreted in pancreas, it also been secreted in small amounts in many other places such as intestinal, gastric mucosa and also central nervous system. This can be proof by : Amylin is a peptide synthesized not only in the β cells of pancreatic islets, but in small quantities also in other organs like in the intestinal and gastric mucosa, lungs and central nervous system(Samonina, Kopylova et al. 2004).Amylin is secreted together with insulin. When people have type 1 diabetes, the concentration of insulin and also amylin in their body is low. Like insulin, there is a deficiency of amylin in people with type 1 diabetes(Scherbaum 1998). The functions of amylin is not well known yet completely. The main function of amylin is help to slow the speed at which food is digested and glucose is released into the bloodstream. It acts as a control for insulin, working to moderate the metabolism of glucose in muscle tissue that is stimulated by insulin.
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Physiological Action of Amylin
Amylin is kind of a unique enzyme because it is related in controlling our hunger. Basically, there are many physiological function of amylin. One of the important function of amylin is that amylin acts as a satiation signal. So, how can amylin acts a satiation signal? Amylin can control our meal size by its endocrine factor.at the region of the arcuate nucleus. As a proof, Lutz Thomas in his book entitled The role of amylin in the control of energy homeostasis said that : In the complex system that controls eating, amylin functions as a potent satiation signal and is believed to be a physiological control of meal size.Certain criteria need to be fulfilled so that an endocrine factor is considered to be of physiological relevance. this requirement seems to be met by amylin for its satiation action (Lutz 2010). There were some experiment was conducted to show the effects of as a satiation signal. In one of the experiment, a 5-g meal was given overnight fasted rats. This action leads to an immediate rise in endogenous plasma amylin levels from about 3-5 pmol/l to 15-20 pmol/l .(Lutz 2010). From this experiment, we can see that the exogenous amylin has an acute onset of action and decreases eating in rats within a few minutes. As a proof, Lutz in his book Pancreatic amylin as a centrally acting satiating hormone, state that ; Concerning amylin as a satiating hormone, it is well established that amylin is released during meals, and that exogenous amylin leads to a dose-related reduction in meal size. Amylin has a rapid onset and brief duration of action.(Lutz 2005). The second function of amylin is that amylin can increases energy expenditure. How is the mechanism for amylin to increases energy expenditure? In the years recently, some studies was investigated to show the effect of enhanced amylin receptor signalling effect on energy expenditure. In one of the experiment, it has been showed that body weight and body fat loss in fasted rats treated with repeated peripheral injections of the amylin receptor agonist sCT were more pronounced than in saline-treated controls, indicating that sCT most likely increased energy expenditure.(Lutz 2010). Futhermore, Amylin control the nutrient fluxes by reduces energy intake, modulates nutrient utilization by inhibiting postprandial glucagon secretion, and increases energy disposal by preventing compensatory decreases of energy expenditure in weight-reduced individuals. The best investigated function of amylin which is cosecreted with insulin is to reduce eating by promoting meal-ending satiation. (Lutz 2012). As a short conclusion for the physiological action of amylin is that it can act as a satiation signal and also can increases energy expenditure.
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Pathopyhsiological effects of amylin
Despite of having physiological effects, amylin also has its own pathophysiological effects. The meaning of pathophysiology is The disordered physiological processes associated with disease or injury. So, in this section the disordered physiological processes of amylin associated with disease or injury will be discussed.Amylin is closely related with the gastric mucosal stability. The lining cells of our stomach secretes a lot of types of hormones and enzymes. All of the enzymes and hormones are grouped together and so called gastric juice. A group of the lining cells in the stomach, namely parietal cell, secretes Hydrochloric acid. Our stomach is prone to ulcer because of many ulcerogenic factors. Our body have several mechanism to maintain the gastric musical stability due to the ulcerogenic factors. One of them is amylin itself.
In the book of Antiulcer effects of amylin , it says that amylin has a dose-dependent inhibitory action on gastric acid secretion , it may increase the gastric stability against different ulcerogenic factors(Samonina, Kopylova et al. 2004). Many experiments was conducted to investigate the relation of amylin with the gastric mucosal activity. In one of the experiments of acetic acid-induced ulcer, it has been revealed that amylin can decrease the ulcer area as compared to animals that not be given amylin as injection. The experiment is as follows ; In experiments with acetic acid-induced ulcer, we injected amylin since 5th day after the acid application on serosa, i.e. after the ulcers had been completely formed and continued amylin administration for 5 days. A considerable decrease of ulcer area was observed in the experimental animals as compared with controls not receiving amylin. On the 10th day the ulcer index was 87% less in the intervention animals compared to the controls under the same conditions, i.e. peptide had a therapeutic effect . Guidobono et al. (Guidobono, Pagani et al. 1997)have also shown curative effects of amylin in the indomethacin-induced ulcer model. The results obtained confirm data of other authors who have observed the gastroprotective effect of amylin in ethanol-, indometacin-, reserpine- and serotonin-induced gastric mucosal damages.(clementi, Caruso et al. 1996) (Clementi, Caruso et al. 1997) (Guidobono, Pagani et al. 1997) (Guidobono, Pagani et al. 1998, V.I. Gridneva 2001) (Guidobono, Coluzzi et al. 1994). From this experiment, it shows that amylin can decrease the ulcer area in animals stomach thus control the gastric stability.
Futhermore, amylin also influcences the vagal stimulated gastric acid secretion. Vagal stimulation is actually the stimulation comes from the Cranial Nerve 10 namely Vagus Nerve. Vagus nerve involve in autonomic nervous system , specifically in the part of parasympathetic stimulation. Parasymphathetic stimulation occurs when in relax and not stressful condition. During this time, Vagus nerve will function and it will increases the Gastrointestinal tract motility and also the secretion of hormones and enzymes along the gastrointestinal tract. Stimulation of vagus leads to a decrease of pH. Vagal stimulation after amylin administration is, however, not accompanied by pH decrease. Therefore, amylin eliminates the vagal activation on the gastric acid secretion. But amylin decreased not only vagus activated gastric acid secretion, but also carbacholine-stimulated one. The concentration of active protons runs up to 62.2http://www.pathophysiologyjournal.com/webfiles/images/transparent.gifmkmol/ml after the administration of carbocholine and only 33http://www.pathophysiologyjournal.com/webfiles/images/transparent.gifmkmol/ml, if amylin is given just after carbocholine. (Guidobono 1998).
In conclusion, amylin can control the gastric motility and also control the gastric acid secretion. Actually, there are many mechanism that amylin have in order to overcome the ulcer effects.
. Exogenous amylin has an acute onset of action and decreases eating in rats within a few minutes (31). Amylin's effect relies on an amylin-induced reduction in meal size; this reduction occurs without signs of a conditioned taste aversion or without an increase in kaolin consumption (31, 34). Administration of the amylin receptor antagonist AC187 stimulates eating by increasing meal size, presumably by a blockade of endogenous amylin action (40,50). The satiating effect of peripheral amylin seems to be mediated by direct action on area postrema (AP) neurons; neither subdiaphragmatic vagotomy nor capsaicin-induced lesions of peripheral neural afferents that project to the brain reduced amylin's effect, but this effect was abolished in rats with specific AP lesions. Further, local injection of amylin into the AP inhibited eating by reducing meal size, and AP injections of the amylin receptor antagonist AC187 had the opposite effect. The in vivo behavioral data are consistent with electrophysiological and immunohistochemical studies that confirmed a direct influence of amylin on the AP (30, 32, 40, 51, 52).
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Amylin binds strongly to the AP (63), and all identified components of the specific amylin receptor complex, i.e., the calcitonin core receptor (CT-R), together with several receptor-activity modifying proteins (RAMPs) that confer amylin affinity and selectivity, are expressed in the AP. The RAMPs regulate the transport of the core receptors to the cell surface and their glycosylation state which determines ligand specificity (21, 36, 42, 71). The amylin receptor arises from the interaction of RAMP 1 or RAMP 3 with the CT-R, and both RAMP1 and RAMP3 mRNA have been discovered in the mouse AP (71). Further, amylin-induced c-Fos mRNA and RAMP3 mRNA expression colocalize in the rat AP (7), and amylin-sensitive AP neurons carry the CT-R (8). One critical experiment still needs to be done, i.e., to test whether the CT-R and pertinent RAMPs colocalize on the same, amylin-activated AP neurons.
Amylin is secreted by pancreatic beta-cells and seems to function as a physiological signal of satiation and possibly also as an adiposity signal. Amylin's satiating effect is mediated via a direct action at area postrema (AP) neurons. The central pathways mediating amylin's effects rely on connections from the AP to the nucleus of the solitary tract and lateral parabrachial nucleus. Amylin was shown to interact, probably at the brainstem, with other satiating signals, namely cholecystokinin, glucagon-like peptide 1 and peptide YY, and other adiposity signals, namely leptin and insulin. The interaction with leptin, which is thought to involve the hypothalamus, may have important implications for the development of new and improved hormonal anti-obesity treatments. Steve Woods has contributed to the recent literature on amylin's eating inhibitory effect by some frequently cited publications. Steve's work concentrated more on the central administration of amylin and on amylin's potential role as an adiposity signal. His work will be reviewed here and discussed in the context of other important findings on amylin's role in the control of energy homeostasis.(Lutz 2011)
According to previous studies, the area postrema (AP) of the hindbrain may play an important role in mediating the anorectic effect of the pancreatic hormone amylin. Peripheral amylin has been suggested to directly act on AP neurons to bring about its anorectic effect. Cyclic GMP may act as second messenger in this regard. In the present study, we wanted to further delineate the role of the AP in amylin's effect and to find out whether endogenous amylin might reduce feeding via the AP. Rats with chronic cannulas aiming at the AP were infused with various doses of amylin, its agonist salmon calcitonin (sCT) or a cyclic guanosine monophosphate (cGMP) analogue. Amylin and sCT inhibited food intake for about 2 h after food presentation, mainly by reducing meal size when infused into the AP [e.g., 1 h food intake after amylin (0.4 μg/rat) infusion in 12-h deprived rats: NaCl 4.0±0.5 vs. amylin 2.4±0.5, P<.05]. The effect was comparable in ad libitum fed and 12-h food-deprived rats with a minimal effective dose of 0.04 μg/rat. Similar to amylin and sCT, the cGMP analogue 8-Br-cGMP (200 nmol/rat) also reduced food intake and meal size. Infusion of the amylin antagonist AC 187 (30 μg) into the AP significantly reduced the anorectic effect induced by an intraperitoneal injection of amylin (5 μg/kg). Furthermore, AC 187 alone increased feeding when infused into the AP. This study is in line with previous work pointing to an important role of the AP in mediating the anorectic effect of amylin. Furthermore, we provide evidence for a physiological role of endogenous amylin to reduce food intake. This may also involve an action via the AP.(Mollet, Gilg et al. 2004)
Amyloid formation by the neuropancreatic hormone, islet amyloid polypeptide (IAPP or amylin), one of the most amyloidogenic sequences known, leads to islet amyloidosis in type 2 diabetes and to islet transplant failure. Under normal conditions, IAPP plays a role in the maintenance of energy homeostasis by regulating several metabolic parameters, such as satiety, blood glucose levels, adiposity and body weight. The mechanisms of IAPP amyloid formation, the nature of IAPP toxic species and the cellular pathways that lead to pancreatic β-cell toxicity are not well characterized. Several mechanisms of toxicity, including receptor and non-receptor-mediated events, have been proposed. Analogs of IAPP have been approved for the treatment of diabetes and are under investigation for the treatment of obesity. © 2013 Federation of European Biochemical Societies.(Abedini and Schmidt 2013)
Although weight loss can usually be achieved by restricting food intake, the majority of dieters regain weight over the long-term. In the hypothalamus, hormonal signals from the gastrointestinal tract, adipose tissue and other peripheral sites are integrated to influence appetite and energy expenditure. Diet-induced weight loss is accompanied by several physiological changes which encourage weight regain, including alterations in energy expenditure, substrate metabolism and hormone pathways involved in appetite regulation, many of which persist beyond the initial weight loss period. Safe effective long-term strategies to overcome these physiological changes are needed to help facilitate maintenance of weight loss. The present review, which focuses on data from human studies, begins with an outline of body weight regulation to provide the context for the subsequent discussion of short- and long-term physiological changes which accompany diet-induced weight loss.(Sumithran and Proietto 2013)