Enterostatin
From Wikipedia, the free encyclopedia
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| Names | |
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| IUPAC name
(2S)-2-[[(2S)-1-[2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]acetyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoic acid | |
| Other names
Procolipase activation peptide; APGPR; L-Alanyl-L-prolylglycyl-L-prolyl-L-arginine | |
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3D model (JSmol) |
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PubChem CID |
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| UNII | |
CompTox Dashboard (EPA) |
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| Properties | |
| C21H36N8O6 | |
| Molar mass | 496.569 g·mol−1 |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Enterostatin is a pentapeptide[1] derived from a proenzyme in the gastrointestinal tract called procolipase. It reduces food intake, in particular fat intake,[2] when given peripherally or into the brain.[3]
Function
Enterostatin has been detected in gut endocrine cells.[7] It is created in the intestine by pancreatic procolipase, the other colipase serving as an obligatory cofactor for pancreatic lipase during fat digestion. Enterostatin can be created in the gastric mucosa and the mucosal epithelia in the small intestine. A high fat diet will cause the procolipase gene transcription and enterostatin to release into the gastrointestinal lumen. Enterostatin appears in the lymph and circulation after a meal. Enterostatin has been shown to selectively reduce fat intake during a normal meal. The testing has been successful with different species.[8]
Signaling pathway
The signaling pathway of the peripheral mechanism uses afferent vagal to hypothalamic centers. The central responses are mediated through a pathway including serotonergic and opioidergic components.[9] Enterostatin cuts fat intake, bodyweight, and body fat. This reaction may involve multiple metabolic effects of enterostatin, which include a decrease of insulin secretion,[10] a growth in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. It has been demonstrated that enterostatin stimulates neurons in the amygdala, the arcuate nucleus, the lateral and the ventromedial hypothalamus that have anatomic and functional projections to the paraventricular nucleus (PVN) of the hypothalamus.[11] Additionally, enterostatin regulates the expression of Agouti-related peptide (AgRP) in a complex manner.[12]
A possible pathophysiological role is indicated by studies that have associated low enterostatin output and/or responsiveness to breeds of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion from pancreatic procolipase after a test meal, compared with persons of normal weight.[3]