Daniels A J, Chance W T, Grizzle M K, Heyer D, Matthews J E
Glaxo Wellcome Inc., Departments of Metabolic Diseases and Medicinal Chemistry, Research Triangle Park, NC 27713, USA.
Peptides. 2001 Mar;22(3):483-91. doi: 10.1016/s0196-9781(01)00358-8.
Neuropeptide Y has been proposed to play a major role in the hypothalamic regulation of feeding behavior through the activation of specific, central NPY receptor(s). In an effort to design small molecule antagonists of NPY receptors, we have synthesized a series of substituted dipeptides based on defined pharmacophores, previously identified by us and others as essential for the interaction with the peptide receptors. GI264879A behaves as a functional antagonist of Y1 receptors while displaying no binding selectivity for the different NPY receptor subtypes. We demonstrate here that administration of GI264879A to rats causes a significant decrease in food intake and body weight partly through a mechanism dependent on the integrity of the vagus nerve.
有人提出,神经肽Y通过激活特定的中枢NPY受体,在下丘脑对摄食行为的调节中起主要作用。为了设计NPY受体的小分子拮抗剂,我们基于特定的药效基团合成了一系列取代二肽,这些药效基团先前已被我们和其他人确定为与肽受体相互作用所必需的。GI264879A表现为Y1受体的功能性拮抗剂,而对不同的NPY受体亚型没有结合选择性。我们在此证明,给大鼠施用GI264879A会导致食物摄入量和体重显著下降,部分是通过一种依赖迷走神经完整性的机制实现的。