Peptide YY (PYY), human
(Synonyms: 多肽YY(人),Peptide Tyrosine Tyrosine) 目录号 : GC30452PeptideYY(PYY)是一种肠道激素，可调节食欲和抑制胰腺分泌。PeptideYY(PYY)可以通过神经肽Y受体(NeuropeptideYreceptors)介导其作用。
Cas No.:118997-30-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Animal experiment: |
Cats[3]The inhibitory effects of Peptide YY on pancreatic exocrine secretion are studied by using an anesthetized adult (4 kg) cat. Infusion of secretin and CCK (1.5 units/ kg/hr each) in saline solution is made through the saphenous vein by using a perfusion pump at a flow rate of 10 ml/hr. Infusion or single injection of Peptide YY (10-250 pmol/kg) is also made through the saphenous vein. Pancreatic juice from the cannulated pancreatic duct is collected in test tubes for 10-min periods by using a fraction collector. The volume of the juice and A280 are measured. Bicarbonate is determined by the titration method[3].Rabbits[2]New Zealand White rabbits are fed an atherogenic diet and control animals fed a normal diet for 4 weeks. Immunohistochemistry is used to determine the localization of Peptide YY and eNOS in the aorta. The aorta, carotid, renal, iliac, inferior mesenteric, and renal interlobular arteries are removed, mounted in organ baths, and subjected to doses of Peptide YY (1-100 nM) and then acetylcholine (1 μM)[2]. |
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References: [1]. Peptide YY, et al. The gut hormone peptide YY regulates appetite. Ann N Y Acad Sci. 2003 Jun;994:162-8. |
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Peptide YY (PYY) is a gut hormone that regulates appetite and inhibits pancreatic secretion. Peptide YY (PYY) can mediate its effects through the Neuropeptide Y receptors.
The gut hormone peptide YY ( PYY) belongs to the pancreatic polypeptide (PP) family along with PP and neuropeptide Y (NPY). These peptides mediate their effects through the NPY receptors of which there are several subtypes (Y1, Y2, Y4, and Y5)[1]. Pancreatic polypeptide YY (Peptide YY), a small peptide consisting of 36 amino acids, is originally isolated from porcine intestine and is secreted from the neuroendocrine cells (L cells) in the mucosa of the gastrointestinal tract, but it has been localized to other locations associated with the digestive system[2].
Peptide YY is capable of strongly inhibiting secretin-stimulated pancreatic secretion. A very low dose of Peptide YY (10-20 pmol/kg) significantly decreases the pancreatic secretion of bicarbonate as well as fluid that is stimulated by a single dose of secretin (0.1 unit/kg). A dose of Peptide YY of 100-200 pmol/kg causes a 70-80% reduction of the pancreatic bicarbonate and fluid secretion[3]. Peptide YY is localised to blood vessels and atherosclerotic plaques of rabbits. It causes vasoconstriction of the vascular tree[2].
[1]. Peptide YY, et al. The gut hormone peptide YY regulates appetite. Ann N Y Acad Sci. 2003 Jun;994:162-8. [2]. Tatemoto K, et al. Isolation and characterization of peptide YY (PYY ), a candidate gut hormone that inhibits pancreatic exocrine secretion. Proc Natl Acad Sci U S A. 1982 Apr;79(8):2514-8. [3]. Smith RM, et al. Role of Peptide YY in blood vessel function and atherosclerosis in a rabbit model. Clin Exp Pharmacol Physiol. 2015 Jun;42(6):648-52.
| Cas No. | 118997-30-1 | SDF | |
| 别名 | 多肽YY(人),Peptide Tyrosine Tyrosine | ||
| 化学名 | L-tyrosyl-L-prolyl-L-isoleucyl-L-lysyl-L-prolyl-L-α-glutamyl-L-alanyl-L-prolylglycyl-L-α-glutamyl-L-α-aspartyl-L-alanyl-L-seryl-L-prolyl-L-α-glutamyl-L-α-glutamyl-L-leucyl-L-asparaginyl-L-arginyl-L-tyrosyl-L-tyrosyl-L-alanyl-L-seryl-L-leucyl-L-arginyl-L-histidyl-L-tyrosyl-L-leucyl-L-asparaginyl-L-leucyl-L-valyl-L-threonyl-L-arginyl-L-glutaminyl-L-arginyl-L-tyrosinamide, trifluoroacetate salt | ||
| Canonical SMILES | Tyr-Pro-Ile-Lys-Pro-Glu-Ala-Pro-Gly-Glu-Asp-Ala-Ser-Pro-Glu-Glu-Leu-Asn-Arg-Tyr-Tyr-Ala-Ser-Leu-Arg-His-Tyr-Leu-Asn-Leu-Val-Thr-Arg-Gln-Arg-Tyr-NH2 | ||
| 分子式 | C194H295N55O57 | 分子量 | 4309.75 |
| 溶解度 | 1mg/mL in water | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.232 mL | 1.1602 mL | 2.3203 mL |
| 5 mM | 0.0464 mL | 0.232 mL | 0.4641 mL |
| 10 mM | 0.0232 mL | 0.116 mL | 0.232 mL |
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The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis
Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.
Crystal structures of human neuropeptide Y (NPY) and peptide YY (PYY)
Neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) form the evolutionarily conserved pancreatic polypeptide family. While the fold is widely utilized in nature, crystal structures remain elusive, particularly for the human forms, with only the structure of a distant avian form of PP reported. Here we utilize a crystallization chaperone (antibody Fab fragment), specifically recognizing the amidated peptide termini, to solve the structures of human NPY and human PYY. Intriguingly, and despite limited sequence identity (~50%), the structure of human PYY closely resembles that of avian PP, highlighting the broad structural conservation of the fold throughout evolution. Specifically, the PYY structure is characterized by a C-terminal amidated α-helix, preceded by a backfolded poly-proline N-terminus, with the termini in close proximity to each other. In contrast, in the structure of human NPY the N-terminal component is disordered, while the helical component of the peptide is observed in a four-helix bundle type arrangement, consistent with a propensity for multimerization suggested by NMR studies.
News in gut-brain communication: a role of peptide YY (PYY) in human obesity and following bariatric surgery?
Recent advances in obesity research focused on neuroendocrine control of food intake, appetite and body weight balance. Gut hormones, which are sequentially released from different regions of the gut, send signals to the areas of appetite control in the central nervous system causing a release of counter-regulatory hormones also originating from the gastrointestinal system. Ghrelin, a peptide secreted from the gastric fundus is released just before meal intake and stimulates hunger and food intake. Recently, peptide YY has been suggested to counteract ghrelin by inducing satiety and reducing appetite and caloric intake. While the effects of PYY on various gastrointestinal functions are well described, its action on weight loss is less known. Controversial results on the effect of exogenous administration of PYY(3-36) opened the discussion on the respective roles of PYY and/or PYY(3-36) in body weight homeostasis in man.
Established and emerging roles peptide YY (PYY) and exploitation in obesity-diabetes
Purpose of review: The antiobesity effects of activation of hypothalamic neuropeptide Y2 receptors (NPYR2) by the gut-derived hormone, peptide YY (PYY), are established. However, more recent insight into the biology of PYY has demonstrated remarkable benefits of sustained activation of pancreatic beta-cell NPYR1, that promises to open a new therapeutic avenue in diabetes.
Recent findings: The therapeutic applicability of NPYR2 agonists for obesity has been considered for many years. An alternative pathway for the clinical realisation of PYY-based drugs could be related to the development of NPYR1 agonists for treatment of diabetes. Thus, although stimulation of NPYR1 on pancreatic beta-cells has immediate insulinostatic effects, prolonged activation of these receptors leads to well defined beta-cell protective effects, with obvious positive implications for the treatment of diabetes. In this regard, NPYR1-specific, long-acting enzyme resistant PYY analogues, have been recently developed with encouraging preclinical effects observed on pancreatic islet architecture in diabetes. In agreement, the benefits of certain types of bariatric surgeries on beta-cell function and responsiveness have also been linked to elevated PYY secretion and NPY1 receptor activation.
Summary: Enzymatically stable forms of PYY, that selectively activate NPYR1, may have significant potential for preservation of beta-cell mass and the treatment of diabetes.
Peptide YY: more than just an appetite regulator
Replenishment of beta cell mass is a key aim of novel therapeutic interventions for diabetes, and the implementation of new strategies will be aided by understanding the mechanisms employed to regulate beta cell mass under normal physiological conditions. We have recently identified a new role for the gut hormone peptide YY (PYY) and the neuropeptide Y (NPY) receptor systems in the control of beta cell survival. PYY is perhaps best known for its role in regulating appetite and body weight, but its production by islet cells, the presence of NPY receptors on islets and the demonstration that Y1 activation causes proliferation of beta cells and protects them from apoptosis, suggest a role for this peptide in modulating beta cell mass. This review introduces PYY and its potential role in glucose homeostasis, then focuses on evidence supporting the concept that PYY and NPY receptors are exciting new targets for the preservation of beta cells.