背景 脊髓中枢敏化是引起疼痛的主要机制之一，以往对肠促胰岛素的研究局限于胰岛素相关作用，最新的研究发现肠促胰岛素可能参与了疼痛中枢敏化过程。 目的 回顾近年来国内外关于肠促胰岛素参与疼痛中枢敏化的研究。 内容 肠促胰岛素的生理特点和受体表达分布，胰高血糖素样肽-l（glucagon like peptide-1, GLP-1）及其受体和葡萄糖依赖性促胰岛素分泌多肽（glucose-dependent insulinotropic polypeptide, GIP）及其受体参与中枢可塑性和痛觉中枢敏化的机制，GLP-1和GIP信号系统“交叉对话”参与中枢敏化的潜在机制。 趋向 肠促胰岛素信号系统及其“交叉谈话”机制是疼痛中枢敏化的重要新机制。
Background Central sensitization is a main mechanism underlying pain. Incretin is confined to mediate insulin-mimetic effects, but recent study indicates that incretin may affect the central sensitization of pain. Objective This article reviews the studies about the effects of incretin on central sensitization of spinal cord in pain. Content This review summarized physiological characters and receptor localization of incretin. Glucagon like peptide-1 (GLP-1) and its receptor, glucose-dependent insulinotropic polypeptide (GIP) and its receptor influence the neuronal plasticity and the central sensitization of pain. The cross-talk between GLP-1 and GIP signaling pathway is a potential mechanism of the central sensitization underlying pain. Trend Central sensitization underlying pain can be induced by incretin signaling system and their cross-talk is an important and novel concept.
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