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    浙江省科技型企業---加速您的多肽研究
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    Enterostatins、腸抑素
    • Enterostatins、腸抑素

      Definition

      Enterostatin is a pentapeptide generated by the action of trypsin on procolipase in the intestinal lumen. Pharmacologic studies have suggested a role for these peptides in appetite regulation and insulin secretion 1.

      Related Peptides

      Enterostatins belong to a family of peptides (e.g., Val-Pro-Asp-Pro-Arg, VPDPR; Ala-Pro-Gly-Pro-Arg, APGPR; and Val-Pro-Gly-Pro-Arg, VPGPR) derived from the tryptic cleavage of amino-terminal pentapeptide from procolipase 1.

      Discovery

      In 1993, Mei et al., identified the peptapeptide obtained from the tryptic cleavage of the N-terminal of procolipase and named it enterostatin 2.

      Structural Characteristics

      Enterostatin 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 3. Modifications in the N-terminus of VPDPR abrogate biological function, other modifications result in retention of biological activity. The importance of the N-terminal residue of enterostatin was investigated by replacing the L-valine with (i) D-valine, (ii) L-tyrosine or (iii) addition of an L-tyrosine to generate the hexapeptide, YVPDPR. Replacement of the N-terminal L-valine residue with D-valine abrogated the insulin inhibitory activity of the peptide. This demonstrates that the N-terminal valine may be necessary for biological function and is consistent with a previous report showing a lack of effect of D-VPDPR on high-fat food consumption 4.

      Mode of Action

      A high-fat diet easily promotes hyperphagia giving an impression of an uncontrolled process. Fat digestion itself however provides control of fat intake through the digestion, carried out by pancreatic lipase and its protein cofactor colipase, and through enterostatin, released from procolipase during fat digestion 5. Neural mechanisms arising from the intestine involving vagal afferent nerves may be important for the early satiety mechanism induced by enterostatin during a meal 6. Enterostatin acts through an opioid pathway, rather as a µ-antagonist acting antagonistic to ß-casomorphin. In its mechanism of action enterostatin gives an exothermic reaction, while the opiate has an endothermic reaction. The decreased thermogenesis by opiates could explain an increased appetite and body weight, while an increased thermogenesis by enterostatin could explain a reduction in appetite and loss of body weight. The hypocholesterolemic effects of APGPR and VPDPR are mediated by a CCK1 receptor-dependent mechanism 7.

      Functions

      Enterostatin released from the exocrine pancreas and gastrointestinal tract, selectively inhibits fat intake through activation of an afferent vagal signaling pathway 8. Recent studies indicate that enterostatin modulates insulin release in response to a variety of agents that affect first phase as well as the second phase of insulin release 4.

      References

      1. Imamura M, Sumar N, Hermon-Taylor J, Robertson HJ, Prasad C (1998). Distribution and characterization of enterostatin-like immunoreactivity in human cerebrospinal fluid. Peptides, 19(8):1385-1391.

      2. Mei J, Bowyer RC, Jehanli AMT, Patel G, Erlanson-Albertsson C (1993). Identification of enterostatin, the pancreatic procolipase activation peptide in the intestine of rat. Pancreas, 8:488-493.

      3. Prasad C, Imamura M, Debata C, Svec F, Sumar N, Hermon-Taylor J (1999). Hyper- enterostatinemia in Premenopausal Obese Women. J Clin Endocrinol Metab., 84(3):937-941.

      4. Tadayyon M, Liou S, Briscoe CP, Badman G, Eggleston DS, Arch JRS, York DA (2002). Structure-function studies on enterostatin inhibition of insulin release. Int J Diabetes & Metabolism., 10:14-21.

      5. Berger K, Winzell MS, Mei J, Erlanson-Albertsson C (2004). Enterostatin and its target mechanisms during regulation of fat intake. Physiol Behav., 83(4):623-630.

      6. Mei J, Sörhede-Winzell M, Erlanson-Albertsson C (2002). Plasma Enterostatin: Identification and Release in Rats in Response to a Meal. Obes Res., 10(7):688694.

      7. Takenaka Y, Shimano T, Mori T, Hou IC, Ohinata K, Yoshikawa M. (2008). Enterostatin reduces serum cholesterol levels by way of a CCK1 receptor-dependent mechanism. Peptides.,29(12):2175-2178.

      8. Lin L, Thomas SR, Kilroy G, Schwartz GJ, York DA (2003). Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors Am J Physiol Regul Integr Comp Physiol., 285(2):321-328.

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