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刺激胰岛素而非胰高血糖素从胰岛释放的胆囊收缩素末端四肽的合成类似物。

Synthetic analogs of cholecystokinin terminal tetrapeptide that stimulate insulin but not glucagon release from pancreatic islets.

作者信息

Khalid P, Sharma S D, Khan M M, Rastogi A K, Kidwai J R, Mathur K B

出版信息

Acta Diabetol Lat. 1986 Jul-Sep;23(3):239-42. doi: 10.1007/BF02624710.

Abstract

Two synthetic analogs of CCK-4, Glp-Met-Asp-Phe-NH2 (I) and Pro-Met-Asp-Phe-NH2 (II) reported earlier to stimulate insulin release from the isolated rat pancreatic islets in vitro at concentrations as low as 10(-10) M, have now been found to be totally ineffective as glucagon releasers at concentrations as high as 10(-6) M or higher. It is evident that the replacement of Trp in CCK-4 by Glp and Pro residues leads to peptides which exhibit insulin releasing activity without stimulating the release of glucagon.

摘要

两种CCK - 4的合成类似物,即早前报道的Glp - Met - Asp - Phe - NH2(I)和Pro - Met - Asp - Phe - NH2(II),在体外低至10(-10)M的浓度下就能刺激分离的大鼠胰岛释放胰岛素,现在发现它们在高达10(-6)M或更高的浓度下作为胰高血糖素释放剂却完全无效。显然,用Glp和Pro残基取代CCK - 4中的Trp会产生具有胰岛素释放活性而不刺激胰高血糖素释放的肽。

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