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慢性高血糖可以损害胰岛β细胞的功能,其作用途径涉及多个方面,目前提出的作用机制主要包括氧化应激、内质网应激、炎症、晚期糖基化终末产物、低氧、β细胞去分化等。氧化应激和内质网应激在葡萄糖毒性对β细胞影响中的研究较为透彻,新发现的β细胞去分化在糖尿病的进展中也起到重要作用。葡萄糖毒性与糖尿病的进展息息相关,研究葡萄糖毒性的作用机制对保护胰岛β细胞功能具有重要意义。
Chronic hyperglycemia can damage the function of islet β cells. Its mechanism of action involves many aspects. The mechanisms of action currently proposed include oxidative stress, endoplasmic reticulum stress, inflammation, advanced glycation end products, hypoxia, β Dedifferentiation of cells. Oxidative stress and endoplasmic reticulum stress in glucose toxicity on the impact of β-cell research is more thorough, the newly discovered β-cell dedifferentiation also plays an important role in the progression of diabetes. Glucose toxicity is closely related to the progress of diabetes. It is of great significance to study the mechanism of action of glucose toxicity on the protection of pancreatic β-cell function.