Panten U, Schwanstecher M, Schwanstecher C
Institut für Pharmakologie und Toxikologie, Technische Universität Braunschweig, Germany.
Exp Clin Endocrinol Diabetes. 1996;104(1):1-9. doi: 10.1055/s-0029-1211414.
Binding of hypoglycemic sulfonylureas and their analogues to the sulfonylurea receptor in the beta-cell plasma membrane mediates closure of the ATP-sensitive K+-channel (KATP-channel) and thereby stimulation of insulin release. The sulfonylurea receptor is a member of the traffic ATPase family with two intracellular nucleotide binding folds. The receptor binding site for hypoglycemic drugs is located at the cytoplasmic face of the plasma membrane. Mutations in the sulfonylurea receptor gene have been detected which cause familial hyper-insulinism. Non-beta-cell sulfonylurea receptors do not contribute to the therapeutic benefit of sulfonylureas, but might be involved in presumed adverse effects of sulfonylureas in the cardiovascular and the central nervous system.
降糖磺脲类药物及其类似物与β细胞膜中的磺脲类受体结合，介导ATP敏感性钾通道（KATP通道）关闭，从而刺激胰岛素释放。磺脲类受体是具有两个细胞内核苷酸结合结构域的转运ATP酶家族成员。降糖药物的受体结合位点位于质膜的胞质面。已检测到磺脲类受体基因突变可导致家族性高胰岛素血症。非β细胞磺脲类受体对磺脲类药物的治疗益处无贡献，但可能参与磺脲类药物在心血管和中枢神经系统中的假定不良反应。
