Enterostatin 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. An increased high fat diets 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.
Signaling pathwayedit
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. Inveterately, enterostatin cuts fat intake, bodyweight, and body fat. This reaction may involve multiple metabolic effects of enterostatin, which include a decrease of insulin secretion,[4] a growth in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. 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]
Effectsedit
Its effects include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. At the end level, it initiates a sensation of fullness of stomach which could be the reason for its role in regulation of fat intake and reduction of body weight. For enterostatin to be utilized it needs the presence of CCK A receptors. Studies based on rats who lack these receptors have found them to be un-responsive to enterostatin.[5]
When rats have been injected with high doses of enterostatin into the brain the rats ate progressively less food as the dose was increased.[6]: 969 In rats, examination of experiments involving the effects of peripheral or intracerebroventricular administration of enterostatin show this selectively slows down fat consumption.[7]: 8
Medical trialsedit
Although enterostatin-like immunoreactivities exist in blood, brain, and gut, and exogenous enterostatins decrease fat appetite and insulin secretion in rats, the roles of these peptides in human obesity remain to be examined.,[8]
Referencesedit
^York DA, Teng L, Park-York M (June 2010). "Effects of dietary fat and enterostatin on dopamine and 5-hydroxytrytamine release from rat striatal slices". Brain Res. 1349: 48–55. doi:10.1016/j.brainres.2010.06.036. PMID 20599830. S2CID 7112000.
^Fernstrom, etc; John D. Fernstrom; Ricardo Uauy; Pedro Arroyo (2000). Nutrition and Brain: 5th Nestle Nutrition Workshop, Mexico City. Karger Publishers. p. 76. ISBN978-3-8055-7166-1.
^Park M, Farrell J, Lemmon K, York DA (October 2009). "Enterostatin alters protein trafficking to inhibit insulin secretion in Beta-TC6 cells". Peptides. 30 (10): 1866–73. doi:10.1016/j.peptides.2009.06.021. PMC2755607. PMID 19563849.
^Jean-Pierre Montmayeur; Johannes le Coutre (September 14, 2009). Fat Detection: Taste, Texture, and Post Ingestive Effects. CRC Press; 1 edition. p. 359. ISBN978-1-4200-6775-0.
^Handbook of biologically active peptides. Londan: Academic Press. 2006. ISBN978-0-12-369442-3.
^George A. Bray; Donna H. Ryan (2006). Overweight and the Metabolic Syndrome: From Bench to Bedside. Springer; 1 edition. ISBN978-0-387-32163-9.
^C. Prasad; M. Imamura; C. Debata; F. Svec; N. Sumar; J. Hermon-Taylor (1999). Hyperenterostatinemia in Premenopausal Obese Women. The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 3 937-941.
February 21, 2024
enterostatin, pentapeptide, derived, from, proenzyme, gastrointestinal, tract, called, procolipase, reduces, food, intake, particular, intake, when, given, peripherally, into, brain, namesiupac, name, aminopropanoyl, pyrrolidine, carbonyl, amino, acetyl, pyrro. 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 Enterostatin NamesIUPAC name 2S 2 2S 1 2 2S 1 2S 2 aminopropanoyl pyrrolidine 2 carbonyl amino acetyl pyrrolidine 2 carbonyl amino 5 diaminomethylideneamino pentanoic acidOther names Procolipase activation peptide APGPR L Alanyl L prolylglycyl L prolyl L arginineIdentifiersCAS Number 117830 79 2 Y3D model JSmol Interactive imageChemSpider 2340236 NPubChem CID 3082883UNII C9R6HY7YRT YCompTox Dashboard EPA DTXSID20151927InChI InChI 1S C21H36N8O6 c1 12 22 19 33 29 10 4 6 14 29 17 31 26 11 16 30 28 9 3 7 15 28 18 32 27 13 20 34 35 5 2 8 25 21 23 24 h12 15H 2 11 22H2 1H3 H 26 31 H 27 32 H 34 35 H4 23 24 25 t12 13 14 15 m0 s1 NKey ITZMJCSORYKOSI AJNGGQMLSA N NInChI 1 C21H36N8O6 c1 12 22 19 33 29 10 4 6 14 29 17 31 26 11 16 30 28 9 3 7 15 28 18 32 27 13 20 34 35 5 2 8 25 21 23 24 h12 15H 2 11 22H2 1H3 H 26 31 H 27 32 H 34 35 H4 23 24 25 t12 13 14 15 m0 s1Key ITZMJCSORYKOSI AJNGGQMLBFSMILES O C N C H C O O CCC N C N N C H 2N C O CNC O C H 1N C O C H N C CCC1 CCC2PropertiesChemical formula C 21H 36N 8O 6Molar mass 496 569 g mol 1Except where otherwise noted data are given for materials in their standard state at 25 C 77 F 100 kPa N verify what is Y N Infobox references Contents 1 Function 2 Signaling pathway 3 Effects 4 Medical trials 5 ReferencesFunction editEnterostatin 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 An increased high fat diets 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 Signaling pathway editThe 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 Inveterately enterostatin cuts fat intake bodyweight and body fat This reaction may involve multiple metabolic effects of enterostatin which include a decrease of insulin secretion 4 a growth in sympathetic drive to brown adipose tissue and the stimulation of adrenal corticosteroid secretion 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 Effects editIts effects include a reduction of insulin secretion an increase in sympathetic drive to brown adipose tissue and the stimulation of adrenal corticosteroid secretion At the end level it initiates a sensation of fullness of stomach which could be the reason for its role in regulation of fat intake and reduction of body weight For enterostatin to be utilized it needs the presence of CCK A receptors Studies based on rats who lack these receptors have found them to be un responsive to enterostatin 5 When rats have been injected with high doses of enterostatin into the brain the rats ate progressively less food as the dose was increased 6 969 In rats examination of experiments involving the effects of peripheral or intracerebroventricular administration of enterostatin show this selectively slows down fat consumption 7 8 Medical trials editAlthough enterostatin like immunoreactivities exist in blood brain and gut and exogenous enterostatins decrease fat appetite and insulin secretion in rats the roles of these peptides in human obesity remain to be examined 8 References edit York DA Teng L Park York M June 2010 Effects of dietary fat and enterostatin on dopamine and 5 hydroxytrytamine release from rat striatal slices Brain Res 1349 48 55 doi 10 1016 j brainres 2010 06 036 PMID 20599830 S2CID 7112000 Fernstrom etc John D Fernstrom Ricardo Uauy Pedro Arroyo 2000 Nutrition and Brain 5th Nestle Nutrition Workshop Mexico City Karger Publishers p 76 ISBN 978 3 8055 7166 1 a b Erlanson Albertsson C York D July 1997 Enterostatin a peptide regulating fat intake Obesity Research Nature Publishing Group 5 4 360 72 doi 10 1002 j 1550 8528 1997 tb00565 x ISSN 1930 7381 PMID 9285845 Park M Farrell J Lemmon K York DA October 2009 Enterostatin alters protein trafficking to inhibit insulin secretion in Beta TC6 cells Peptides 30 10 1866 73 doi 10 1016 j peptides 2009 06 021 PMC 2755607 PMID 19563849 Jean Pierre Montmayeur Johannes le Coutre September 14 2009 Fat Detection Taste Texture and Post Ingestive Effects CRC Press 1 edition p 359 ISBN 978 1 4200 6775 0 Handbook of biologically active peptides Londan Academic Press 2006 ISBN 978 0 12 369442 3 George A Bray Donna H Ryan 2006 Overweight and the Metabolic Syndrome From Bench to Bedside Springer 1 edition ISBN 978 0 387 32163 9 C Prasad M Imamura C Debata F Svec N Sumar J Hermon Taylor 1999 Hyperenterostatinemia in Premenopausal Obese Women The Journal of Clinical Endocrinology amp Metabolism Vol 84 No 3 937 941 Retrieved from https en wikipedia org w index php title Enterostatin amp oldid 1174352781, wikipedia, wiki, book, books, library,
