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The NuGOwiki Metabolite Database is a joint initiative of NuGO and HMDB
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| APGPR Enterostatin | |
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| Chemical Name | (2S)-2-[[(2S)-1-[2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]acetyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoic acid |
| Chemical Formula | C21H36N8O6 |
| CAS Number | 117830-79-2 |
| Chemical Information | HMDB06117 |
| Biochemical Taxonomy |
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| Functional Taxonomy | Not Available |
| Nutritional Taxonomy | Not Available |
| Metabolic Pathways | Not Available |
| Biofluid Location |
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| Tissue Location | Not Available |
| Normal Biofluid Concentrations |
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| Normal Tissue Concentrations | Not Available |
| Diseases / Conditions Related to Nutrition | Not Available |
| Other (Monogenic Disorders) | Not Available |
| Abnormal Biofluid Concentrations | Not Available |
| Abnormal Tissue Concentrations | Not Available |
| Physiological Processes | Not Available |
| Authors: | |
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Contents |
Introduction
guidelines
Enterostatin APGPR (Ala-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)
Biological Function
Catabolism
Diseases / Conditions Related to Nutrition
Other (Monogenic) Disorders