Flatt P R, Shibier O, Szecowka J, Berggren P O
Department of Biological and Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland, U.K.
Diabete Metab. 1994 Mar-Apr;20(2):157-62.
Sulphonylureas and the hyperglycaemic sulphonamide diazoxide are commonly employed in the therapy of non-insulin-dependent (Type 2) diabetes mellitus and insulinoma, respectively. Stimulatory effects of sulphonylureas on insulin secretion and the inhibitory action of diazoxide are thought to be primarily mediated through modulation of the activity of ATP-sensitive K+ channels (K(+)-ATP channels) in the beta-cell plasma membrane. Certain sulphonylureas are known to be internalised by the pancreatic B-cell. Recent studies suggest that these drugs and diazoxide can influence insulin secretion from electropermeabilized beta-cells in which K(+)-ATP channels and other plasma membrane ion channels are inoperative. This observation suggests that sulphonylureas and diazoxide interact with intracellular sites in the pancreatic B-cell which are directly involved in the regulation of the final stages of exocytosis.
磺脲类药物和高血糖磺酰胺类药物二氮嗪，分别常用于非胰岛素依赖型（2型）糖尿病和胰岛素瘤的治疗。磺脲类药物对胰岛素分泌的刺激作用以及二氮嗪的抑制作用，被认为主要是通过调节β细胞膜中ATP敏感性钾通道（K(+)-ATP通道）的活性来介导的。已知某些磺脲类药物可被胰腺β细胞内化。最近的研究表明，这些药物和二氮嗪可影响电穿孔β细胞的胰岛素分泌，在这些细胞中K(+)-ATP通道和其他质膜离子通道不起作用。这一观察结果表明，磺脲类药物和二氮嗪与胰腺β细胞内直接参与调节胞吐作用最后阶段的位点相互作用。
