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同为肠促胰岛素,以GLP-1为基础的药物在临床中广泛应用,而以葡萄糖依赖性促胰岛素多肽(GIP)为基础的药物却迟迟未能进入临床。近来研究表明,GIP与IR有关。长期高脂高热量饮食,对肠道K细胞的刺激增加,K细胞数目及其分泌的GIP也随之增加。在T2DM的早期阶段,GIP的肠促胰素效应降低,但其促进脂质沉积和胰升血糖素分泌的作用仍然存在;GIP分泌增多,促进脂质过度沉积,进而诱发脂肪组织的炎症反应,降低IS,加重IR;GIP促进胰升血糖素分泌,加重高血糖症。长期的糖脂毒性,加速胰岛β细胞凋亡。因此,GIP可能是加速IR和T2DM进展的重要因素,GIP/GIPR信号系统异常,与IR的发病机制相关。本文将对GIP及GIP/GIPR信号系统在T2DM病理生理中的作用及其参与IR的分子机制进行简要综述。
GLP-1-based drugs, which are both incretin and GLP-1, are widely used clinically, and drugs based on glucose-dependent insulinotropic polypeptide (GIP) have not been able to enter the clinic yet. Recent studies have shown that GIP and IR related. Long-term high-fat high-calorie diet, the stimulation of intestinal K cells increased, K cells and the secretion of GIP also increased. In the early stage of T2DM, GIP has decreased incretin effect, but its effect of promoting lipid deposition and glucagon secretion still exists. GIP secretion increases lipid over-deposition, which in turn induces inflammatory reaction of adipose tissue. Reduce IS, increase the IR; GIP promote glucagon secretion, increase hyperglycemia. Long-term glycolipid toxicity, accelerate pancreatic β-cell apoptosis. Therefore, GIP may be an important factor in accelerating the progress of IR and T2DM. The GIP / GIPR signaling system is abnormal and related to the pathogenesis of IR. In this article, we will briefly review the role of GIP and GIP / GIPR signaling systems in the pathophysiology of T2DM and the molecular mechanisms involved in IR.