Xenin
目录号 : GC37943
Xenin是最初从人胃粘膜分离出来的由25个氨基酸组成的多肽。 Xenin是可以减少食欲的肠激素。
Cas No.:144092-28-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Animal experiment: | Mice: Mice (wild-type and ob/ob mice) are fasted overnight (1800–1000 h) and injected with xenin intracerebroventricularly (0.1, 1, or 5 μg) or intraperitoneally (0.5, 5, 15, or 50 μg/g body wt) at 1000 h. To compare the feeding-suppressing effect between xenin and neurotensin, equimolar amounts (16.5 nmol) of xenin (50 μg/g body wt) or neurotensin (28 μg/g body) are injected intraperitoneally after an overnight fast. Control mice receive either intracerebroventricular injection of aCSF or intraperitoneal injection of saline. Preweighed food is provided to mice immediately after the injection. Cumulative food intake is measured at time points indicated in each figure up to 24 h after injection[2]. |
References: [1]. Cooke JH, et al. Peripheral and central administration of xenin and neurotensin suppress food intake in rodents. Obesity (Silver Spring). 2009 Jun;17(6):1135-43. | |
Xenin is a 25-amino acid peptide initially isolated from human gastric mucosa. Xenin is a gut hormone that can reduce food intake.
Xenin is abundantly expressed in gastric, duodenal, and jejunal mucosa, and is found at lower levels in the pancreas. Xenin is released into the circulation postprandially and has been reported to stimulatepancreatic endocrine and exocrine secretion, inhibit gastrin secretion, and influence gastrointestinal motility. Xenin is highly homologous to neurotensin. Xenin and neurotensin are reported to have similar biological effects[1].
Both intracerebroventricular and intraperitoneal administration of xenin inhibit fasting-induced hyperphagia in wild-type mice in a dose-dependent manner. The intraperitoneal injection of xenin also reduces nocturnal intake in ad libitum–fed wild-type mice. The intraperitoneal injection of xenin increases Fos immunoreactivity in hypothalamic nuclei, including the paraventricular nucleus and the arcuate nucleus. Xenin reduces food intake in agouti and ob/ob mice[2]. Gastric emptying rate is reduced by about 93% in xenin-treated mice compared to saline-treated control mice. The i.p. xenin injection significantly increases Fos-immunoreactive cells in the nucleus of the solitary tract of the brainstem, but not area postrema and dorsal motor nucleus of the vagus[3].
References:
[1]. Cooke JH, et al. Peripheral and central administration of xenin and neurotensin suppress food intake in rodents. Obesity (Silver Spring). 2009 Jun;17(6):1135-43.
[2]. Leckstrom A, et al. Xenin, a gastrointestinal peptide, regulates feeding independent of the melanocortinsignaling pathway. Diabetes. 2009 Jan;58(1):87-94.
[3]. Kim ER, et al. Xenin delays gastric emptying rate and activates the brainstem in mice. Neurosci Lett. 2010 Aug 30;481(1):59-63.
| Cas No. | 144092-28-4 | SDF | |
| 分子式 | C139H224N38O32S | 分子量 | 2971.57 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.3365 mL | 1.6826 mL | 3.3652 mL |
| 5 mM | 0.0673 mL | 0.3365 mL | 0.673 mL |
| 10 mM | 0.0337 mL | 0.1683 mL | 0.3365 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
工作液浓度： mg/ml；
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2.
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Xenin--a review
Peptides 1998;19(3):609-15.PMID:9533652DOI:10.1016/s0196-9781(97)00378-1.
Xenin, a 25 amino acid peptide, has been identified in human gastric mucosa in the search for a counterpart to the amphibian octapeptide xenopsin. Xenin is structurally related also to the hypothalamic and ileal peptide neurotensin and is, therefore, a member of the xenopsin/neurotensin/Xenin peptide family. The biological activities of these peptides are similar: Xenin has been shown to inhibit pentagastrin-stimulated secretion of acid, to induce exocrine pancreatic secretion and to affect small and large intestinal motility. In the gut, Xenin interacts with the neurotensin receptor. Radioimmunoassay and chromatography of postprandial plasma in humans indicate the release of Xenin into the circulation. The identification of a 35-amino acid precursor peptide of Xenin - proxenin, and a review of the Gen-bank revealed that Xenin represents the N terminus of a cytosolic coat protein (alpha-COP) from which Xenin can be cleaved by aspartic proteinases such as pepsin and cathepsin E. The physiological role of the peptide Xenin is not known.
Xenin and Related Peptides: Potential Therapeutic Role in Diabetes and Related Metabolic Disorders
Clin Med Insights Endocrinol Diabetes 2021 Sep 22;14:11795514211043868.PMID:34588834DOI:10.1177/11795514211043868.
Xenin bioactivity and its role in normal physiology has been investigated by several research groups since its discovery in 1992. The 25 amino acid peptide hormone is secreted from the same enteroendocrine K-cells as the incretin hormone glucose-dependent insulinotropic polypeptide (GIP), with early studies highlighting the biological significance of Xenin in the gastrointestinal tract, along with effects on satiety. Recently there has been more focus directed towards the role of Xenin in insulin secretion and potential for diabetes therapies, especially through its ability to potentiate the insulinotropic actions of GIP as well as utilisation in dual/triple acting gut hormone therapeutic approaches. Currently, there is a lack of clinically approved therapies aimed at restoring GIP bioactivity in type 2 diabetes mellitus, thus Xenin could hold real promise as a diabetes therapy. The biological actions of Xenin, including its ability to augment insulin secretion, induce satiety effects, as well as restoring GIP sensitivity, earmark this peptide as an attractive antidiabetic candidate. This minireview will focus on the multiple biological actions of Xenin, together with its proposed mechanism of action and potential benefits for the treatment of metabolic diseases such as diabetes.
Emerging therapeutic potential for Xenin and related peptides in obesity and diabetes
Diabetes Metab Res Rev 2018 Sep;34(6):e3006.PMID:29633491DOI:10.1002/dmrr.3006.
Xenin-25 is a 25-amino acid peptide hormone co-secreted from the same enteroendocrine K-cell as the incretin peptide glucose-dependent insulinotropic polypeptide. There is no known specific receptor for xenin-25, but studies suggest that at least some biological actions may be mediated through interaction with the neurotensin receptor. Original investigation into the physiological significance of xenin-25 focussed on effects related to gastrointestinal transit and satiety. However, xenin-25 has been demonstrated in pancreatic islets and recently shown to possess actions in relation to the regulation of insulin and glucagon secretion, as well as promoting beta-cell survival. Accordingly, the beneficial impact of xenin-25, and related analogues, has been assessed in animal models of diabetes-obesity. In addition, studies have demonstrated that metabolically active fragment peptides of xenin-25, particularly xenin-8, possess independent therapeutic promise for diabetes, as well as serving as bioactive components for the generation of multi-acting hybrid peptides with antidiabetic potential. This review focuses on continuing developments with Xenin compounds in relation to new therapeutic approaches for diabetes-obesity.
Minimum biological domain of xenin-25 required to induce anion secretion in the rat ileum
Peptides 2022 Jan;147:170680.PMID:34757144DOI:10.1016/j.peptides.2021.170680.
Xenin-25 has a variety of physiological functions in the gastrointestinal tract, including ion transport and motility. Xenin-25 and neurotensin show sequence homology, especially near their C-terminal regions. The sequence similarity between xenin-25 and neurotensin indicates that the effects of xenin-25 is mediated by the neurotensin receptor but some biological actions of xenin-25 are independent. We have previously reported that xenin-25 modulates intestinal ion transport and colonic smooth muscle activity. However, minimal biological domain of xenin-25 to induce ion transport was not clear. To improve the mechanistic understanding of xenin-25 and to gain additional insights into the functions of xenin-25, the present study was designed to determine the minimal biological domain of xenin-25 required for ion transport in the rat ileum using various truncated Xenin fragments and analogues in an Ussing chamber system. The present results demonstrate that the minimum biological domain of xenin-25 to induce Cl-/HCO3- secretion in the ileum contains the C-terminal pentapeptide. Furthermore, Arg at position 21 is important to retain the biological activity of xenin-25 and induces Cl-/HCO3- secretion in the rat ileum.
Effects of xenin-25 on insulin and glucagon secretions in healthy conscious sheep
Domest Anim Endocrinol 2021 Oct;77:106635.PMID:34111624DOI:10.1016/j.domaniend.2021.106635.
The aim of present study was to determine effect of an intravenous injection of xenin-25 on insulin and glucagon secretion in healthy conscious sheep. After feeding once at 17:00, the experiment was started from 9:00 on the next day. Xenin-25 was intravenously (i.v.) injected at a dose of 100 to 1000 pmol/kg with and without the simultaneous injection of glucose at a dose of 200 μmol/kg, and blood was withdrawn before and after the injections. A single xenin-25 injection at 100 and 300 pmol/kg significantly increased the plasma insulin concentration, whereas the 1000 pmol/kg dose did not elicit significantly enhanced insulin response. Plasma glucose and glucagon concentrations did not significantly change after a single xenin-25 injection. Xenin-25 injection significantly and dose-dependently augmented the glucose-induced insulin secretion. However, the changes in the plasma glucose and glucagon level after the glucose injection were not altered by Xenin injection. A prior intravenous injection of the neurotensin receptor subtype-1 (NTR-1) antagonist SR 48692 at 100 nmol/kg did not modify the glucose-induced change in plasma insulin caused by xenin-25 at 300 pmol/kg, and intravenous injection of the NTR-2 agonist levocabastine at 1000 pmol/kg did not augment the insulin response to the glucose injection. On the other hand, no xenin-25 immunopositive cells were detected in the ovine pancreas. The mRNAs of the three NTR subtypes were highly expressed in the ovine pancreas in comparison with the expression in the abomasum. These results suggest that xenin-25 released from the upper gastrointestinal tract plays a role of an insulinotropic factor in sheep, possibly through NTRs in the pancreatic islets, but not via NTR-2.