对磺酰脲(su)作用机制的研究可大致上分为三个阶段。早期(即五、六十年代,SU开始用于糖尿病治疗时)的研究提示磺酰脲的降糖作用是直接作用于β细胞,刺激内源胰岛素分泌。因为动物在切除胰腺后,药物的降糖作用消失。但只要保留10%的胰腺组织,降糖作用仍然存在。 70年代后,由于胰岛素放免测定及受体(R)分析的广泛应用,发现继续使用SU血浆胰岛素基础水平回复到甚或低于治疗前水平 The mechanism of action of sulfonylureas (su) can be roughly divided into three stages. Early (ie, the fifties and sixties, SU started for the treatment of diabetes) studies have shown that the hypoglycemic effect of sulfonylurea is a direct role in the beta cells, stimulating endogenous insulin secretion. Because the animals after the removal of the pancreas, the hypoglycemic effect of the drug disappeared. But as long as 10% of the retained pancreatic tissue, hypoglycemic effect still exists. After the 1970s, due to the extensive use of insulin radioimmunoassay and receptor (R) analysis, it was found that the continued use of SU plasma insulin levels returned to or even below pre-treatment levels