Peptide YY is categorized into a family that comprises of neuropeptide Y, an orexigenic peptide and pancreatic polypeptide which produce from pancreatic endocrine cells. Peptide YY is a peptide with a tyrosine residue at the C and N which has 36 amino acid in it. It was secluded from the colonic extracts from in 1980 (Tatemoto and Mutt 1980). Peptide YY share the same tertiary shape with neuropeptide Y and pancreatic polypeptide, containing alpha helix and polyproline helix linked by a b turn which cause the U shaped peptide. (Glover, Haneef et al. 1983). PYY is homologous with PP and NPY peptide sequence and it is well kept between species. (Michael Conlon 2002)
For every hormone there must be a receptor to receive the hormone. In the case of peptide YY, the receptor works by the process of G protein Coupled Receptor. There are five different subtypes receptor for the peptide YY. (Larhammar 1996) and all of this inhibit the cyclic AMP build-up. The receptor are varied in spread and function and grouped into their attraction for peptide YY. Peptide YY binds to all receptor but PYY3-36 has high affinity for Y2 receptor and some affinity for Y1 and Y5 receptors. (Dumont, Fournier et al. 1995)
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After food intake, PYY is released in blood systemic circulation, with levels rising to a constant after one or two hours and remain at it up to 6 hours (Adrian, Ferri et al. 1985) . The levels are regulated by caloric intake and meal composition. Fatty meals cause a rise of higher levels compared with meals containing high protein or carbohydrate (Lin and Chey 2003). Other stimuli of releasing PYY are by the gastric acid, cholecsystokinin and infusion of bile acids into ileum or colon but not by gastric distension (Pedersen-Bjergaard, HÃ¸t et al. 1996) . Administration of intraduodenal meal increases plasma PYY before nutrients arrived at the distal part of gastrointestinal tract where PYY hormone is abundant secreted (Fu-Cheng, Anini et al. 1997).
PYY mechanism of action is by inhibiting food intake by interacting with the Y2 receptor (Y2R) in the hypothalamic arcuate nucleus. Y2R is an inhibitory presynaptic receptor in the arcuate nucleus. Studied mice whose it Y2R had been remove showed a malfunctioning inhibition of food intake and recover when are given peripheral direct injection of PYY hormone. The studied mice eat less food when are given after a fast. (Batterham, Cowley et al. 2002). This shows that the functioning of the PYY can cause mammals to eat less. When there is a deficiency in the hormone or the receptor itself, it can cause the animals to eat more. The anorectic effect of PYY also causes by the decrease of activity of Neuropeptide Y (NPY) which is a orixegenic hormones in the arcuate nucleus. PYY hormone signal decreases the hormonal signal of NPY while increasing alpha melanocytes stimulating hormones which is potent appetite inhibitor as well. This recommend that PYY maybe inhibitory to NPY (Broberger, Landry et al. 1997).
Peptide YY (PYY) is interrupted in gastrointestinal diseases and disorders. Changes in PYY appear to be an assimilative response to changes in pathophysiological conditions caused by the disease. This applies to GIT clinical disease e.g irritable bowel syndrome, inflammatory bowel disease, celiac disease, systemic sclerosis, and post-intestinal resection. Anomalies in PYY seem to add up to the development of symptoms present in irritable bowel syndrome, inflammatory bowel disease, gastroenteropathy in long-standing diabetes and Chronic idiopathic slow transit constipation (CST). The changes in PYY could, however, be favourable in some gastrointestinal disorders such as celiac disease, systemic sclerosis and post-intestinal resection state. Considering changes in PYY in GIT disease could be beneficial in clinical practice, where a receptor agonist or an antagonist can be used as a drug, depending on the ailment. Similar to other neuroendocrine peptides of the gut, PYY has broad physiological/pharmacological effects: it can bind to and trigger several receptors with independent actions. Thus, in order to use PYY as a drug, receptor-specific agonists or antagonists need to be developed.
Irritable bowel syndrome is a chronic common disease affecting the worldâ€™s population. IBSâ€™ symptom includes diarrhea, constipation, or both of the syndrome and abdominal pain or discomfort. The pathogenesis is relatively unknown but there a multifactorial of the occurrence of this disease, which is heritability and genetics, environment and social learning, dietary or intestinal microbiota, low-grade inflammation, and disturbances in the neuroendocrine system (NES) of the gut. In the large intestine of an IBS patient, PYY cell abundancy was low, Other than that the number of serotonin cell also low alongside with the amount of cholecsystokinin (CCK). Serotonin acts on the receptors which are located on the myenteric plexus in the stomach and relax the stomach thus delaying gastric emptying. Serotonin also is a stimuli for the secretion of chloride and water from the small intestine. Due to this, motility in the colon of the IBS patients is reduced because chloride and salt is reduced. As compensation for this, PYY is reduced. Another hormone is the cholecsystokinin. CCK stimulates the release of PYY because CCK stimulates the release of bile salts and bile salts is a stimuli of PYY. Thus low CCK, leads to low bile salts which in turn leads to low PYY secretion. Therefore, PYY is reduced in IBS patient.
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Inflammatory bowel disease (IBD) comprises two different disorders with their standalone clinic pathologies of unknown cause. The diseases are ulcerative colitis (UC) and Crohnâ€™s disease (CD). Both UC and CD are different in organ specificity and histopathological characteristic. In the context of PYY hormones, UC and CD cause the colonic PYY cell to be decreased but serotonin and enteroglucagon immunoreactivities were elevated. Enteroglucagon and peptide YY cells are localized in the same organ of the body which is in the colorectal endocrine cell type which L cell. The L cell inreases the production of enteroglucagon and decreases the expression of PYY. In the ileal mucosa of a patient with CD, PYY cell density decreased so as serotonin but in UC biopsies of patient was found out that the serotonin in this patient is elevated. Evidence shows that inflammation and immune cells interact with the the gut, which regulates gastrointestinal motility and sensitivity (61). Thus, serotonin secretion by enterochromaffin (EC) cells can be greater or weakened by secretory products of immune cells such as CD4+ T lymphocytes (62). Furthermore, serotonin modulates the immune response (62)..Based on the above, the relation between serotonin and PYY is similar to the patient in IBS.
Chronic idiopathic slow transit constipation (CST) is a common clinical problem. The problem is characterised by chronic severe constipation. In examination, histopathological fail to identify any abnormality in the colon of the patient. The number of PYY in tissue taken from colonic tissue in CST patient is high but remain unaffected for basal and peak plasma of PYY. It seem difference for the findings above but by taking CST as individually, it was found that commotion in the neuroendocrine system is the most plausible cause for the disease and this disturbance affects the different neuroendocrine peptides in the patient. The increase of number of colonic PYY cells and PYY synthesis causes increase absorption, decrease water secretion, strengthening ileal brake and inhibiting intestinal motility which in turn causes constipation.
Another disease that related to PYY is the celiac disease. Celiac disease is the deterioration of the microvilli or the mucosa extending from the lining or lumen of the small intestine. This disease will cause the nutrient from food intake not absorbable. In the patient with celiac disease, the basal and plasma level of PYY are elevated. The elevated level of PYY decrease after a 8 months gluten free diet. The vicissitudes in the endocrine cells of the small intestine in patients with celiac disease are considered to be a selective process to meet the new demands exerted by the marked decrease in intestinal absorptive area; these changes contribute to the manifestation of the symptoms seen in patients with celiac disease, such as diarrhea and steatorrhea. The elevated levels of circulating PYY in patients with celiac disease appear to be involved in this hormonal process, and are probably a response as an attempt to slow down the intestinal transit time and increase intestinal absorption.
Surgical removal of stomach is usually the last resort when medical therapy has not working against gastrointestinal disease such as colonrectal carcinoma and inflammatory bowel disease. The removal a part of gastric cause several problem such as dumping syndrome and malabsorption. The serum levels of neuroendocrine hormones is investigated in the patient with gastroctomy in the distal part and the findings show that PYY level increase. This increase is to compensate the fast rate gastric transit and try to slow it down. This shows that when a surgery of resection occur, the synthesis of PYY increase to slow down the motility of gastric.
Advantages and Disadvantages
Advantages of peptide YY is that peptde YY can be used as fuel partitioning. By discriminating use of body energy stores and metabolic pathways is what define fuel partitioning