VPGPR Enterostatin (BioDeep_00000027882)

   

human metabolite Endogenous


代谢物信息卡片


(2S)-2-({[(2S)-1-[2-({[(2S)-1-[(2S)-2-amino-3-methylbutanoyl]pyrrolidin-2-yl](hydroxy)methylidene}amino)acetyl]pyrrolidin-2-yl](hydroxy)methylidene}amino)-5-carbamimidamidopentanoate

化学式: C23H40N8O6 (524.3070660000001)
中文名称:
谱图信息: 最多检出来源 Bos taurus(endogenous) 50%

分子结构信息

SMILES: CC(C)C(C(=O)N1CCCC1C(=O)NCC(=O)N2CCCC2C(=O)NC(CCCN=C(N)N)C(=O)O)N
InChI: InChI=1S/C23H40N8O6/c1-13(2)18(24)21(35)31-11-5-7-15(31)19(33)28-12-17(32)30-10-4-8-16(30)20(34)29-14(22(36)37)6-3-9-27-23(25)26/h13-16,18H,3-12,24H2,1-2H3,(H,28,33)(H,29,34)(H,36,37)(H4,25,26,27)/t14-,15-,16-,18-/m0/s1

描述信息

Enterostatin VPGPR (Val-Pro-Gly-Pro-Arg) is a pentapeptide released from procolipase during fat digestion. In addition to the pancreas, enterostatin-immunoreactive cells are also present in the antrum and proximal small intestine. Enterostatin selectively reduces fat intake, decreases insulin secretion, and also increases energy expenditure by activating brown adipose tissue during high-fat feeding. Enterostatins are pentapeptides derived from the NH2-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Enterostatin is generated by the action of trypsin on procolipase in the intestinal lumen. Its structure is highly conserved in evolution, with an amino acid sequence of XPXPR. Three enterostatin sequences, Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR), have been studied extensively and shown to be almost equally effective in their ability to decrease dietary fat preference. Enterostatins are selective inhibitors of appetite, particularly of fat intake. Hyperenterostatinemia in obesity is probably secondary to enterostatin resistance; therefore, the regulatory system is producing more enterostatin to counteract the resistance. This is very similar to hyperinsulinemia and hyperleptinemia in obesity. The diminution in the meal-induced secretion of enterostatin in obesity suggests a delay in the appearance of satiety, leading to increased caloric intake. In rats enterostatin decreases body weight by decreasing fat-calorie intake and increasing the sympathetic firing rate of the nerves in interscapular brown adipose tissue. Enterostatin levels are elevated in the plasma of obese women, and enterostatin secretion is diminished after satiety. Oral administration of enterostatin, however, has no effect on food intake, energy expenditure, or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance, and the physiology of enterostatin in humans remains to be defined. (PMID: 10084574, 9526102, 8886249) [HMDB]
Enterostatin VPGPR (Val-Pro-Gly-Pro-Arg) is a pentapeptide released from procolipase during fat digestion. In addition to the pancreas, enterostatin-immunoreactive cells are also present in the antrum and proximal small intestine. Enterostatin selectively reduces fat intake, decreases insulin secretion, and also increases energy expenditure by activating brown adipose tissue during high-fat feeding. Enterostatins are pentapeptides derived from the NH2-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Enterostatin is generated by the action of trypsin on procolipase in the intestinal lumen. Its structure is highly conserved in evolution, with an amino acid sequence of XPXPR. Three enterostatin sequences, Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR), have been studied extensively and shown to be almost equally effective in their ability to decrease dietary fat preference. Enterostatins are selective inhibitors of appetite, particularly of fat intake. Hyperenterostatinemia in obesity is probably secondary to enterostatin resistance; therefore, the regulatory system is producing more enterostatin to counteract the resistance. This is very similar to hyperinsulinemia and hyperleptinemia in obesity. The diminution in the meal-induced secretion of enterostatin in obesity suggests a delay in the appearance of satiety, leading to increased caloric intake. In rats enterostatin decreases body weight by decreasing fat-calorie intake and increasing the sympathetic firing rate of the nerves in interscapular brown adipose tissue. Enterostatin levels are elevated in the plasma of obese women, and enterostatin secretion is diminished after satiety. Oral administration of enterostatin, however, has no effect on food intake, energy expenditure, or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance, and the physiology of enterostatin in humans remains to be defined. (PMID: 10084574, 9526102, 8886249).

同义名列表

5 个代谢物同义名

(2S)-2-({[(2S)-1-[2-({[(2S)-1-[(2S)-2-amino-3-methylbutanoyl]pyrrolidin-2-yl](hydroxy)methylidene}amino)acetyl]pyrrolidin-2-yl](hydroxy)methylidene}amino)-5-carbamimidamidopentanoate; (2S)-2-{[(2S)-1-(2-{[(2S)-1-[(2S)-2-amino-3-methylbutanoyl]pyrrolidin-2-yl]formamido}acetyl)pyrrolidin-2-yl]formamido}-5-[(diaminomethylidene)amino]pentanoic acid; 2-[1-[N-(1-L-Valyl-L-prolyl)glycyl]-L-prolyl]-L-arginine; L-Valyl-L-prolylglycyl-L-prolyl-L-arginine; VPGPR Enterostatin



数据库引用编号

6 个数据库交叉引用编号

分类词条

相关代谢途径

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代谢反应

0 个相关的代谢反应过程信息。

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1 个相关的物种来源信息

在这里通过桑基图来展示出与当前的这个代谢物在我们的BioDeep知识库中具有相关联信息的其他代谢物。在这里进行关联的信息来源主要有:

  • PubMed: 来源于PubMed文献库中的文献信息,我们通过自然语言数据挖掘得到的在同一篇文献中被同时提及的相关代谢物列表,这个列表按照代谢物同时出现的文献数量降序排序,取前10个代谢物作为相关研究中关联性很高的代谢物集合展示在桑基图中。
  • NCBI Taxonomy: 通过文献数据挖掘,得到的代谢物物种来源信息关联。这个关联信息同样按照出现的次数降序排序,取前10个代谢物作为高关联度的代谢物集合展示在桑吉图上。
  • Chemical Taxonomy: 在物质分类上处于同一个分类集合中的其他代谢物
  • Chemical Reaction: 在化学反应过程中,存在为当前代谢物相关联的生化反应过程中的反应底物或者反应产物的关联代谢物信息。

点击图上的相关代谢物的名称,可以跳转到相关代谢物的信息页面。



文献列表

  • C Prasad, M Imamura, C Debata, F Svec, N Sumar, J Hermon-Taylor. Hyperenterostatinemia in premenopausal obese women. The Journal of clinical endocrinology and metabolism. 1999 Mar; 84(3):937-41. doi: 10.1210/jcem.84.3.5562. [PMID: 10084574]
  • C Prasad, C Debata, J U McGregor. Hormones in Foods: Presence of Enterostatin-Like Immunoreactivities in Bovine Milk. Nutritional neuroscience. 1999; 2(3):147-54. doi: 10.1080/1028415x.1999.11747273. [PMID: 27415149]
  • J Mei, M Bouras, C Erlanson-Albertsson. Inhibition of insulin release by intraduodenally infused enterostatin-VPDPR in rats. Peptides. 1997; 18(5):651-5. doi: 10.1016/s0196-9781(97)00125-3. [PMID: 9213357]