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TP敏感的钾通道 (KATP)是将细胞膜电活动与细胞物质代谢联系在一起的重要通道 ,该通道是由磺酰脲受体 (SUR)和内向整流钾通道 (Kir6 .x)两种亚单位组成。SUR和Kir6 .2基因的突变可引起KATP通道对ATP、ADP Mg2 +敏感性的改变 ,引起KATP通道的活动性低下 ,从而导致遗传性高胰岛素血症 ;SUR1和Kir6 .2基因的突变及多态性还可能与 2型糖尿病 (T2DM)相关 ,其原因可能是SUR1基因变异导致高胰岛素血症 ;对不同人群的研究发现 ,SUR1基因的多态性与T2DM之间存在相关性 ,但各人群之间SUR1基因与T2DM相关的位点存在不一致性。
TP-sensitive potassium channel (KATP) is an important channel that links the electrical activity of cell membrane to the metabolism of cell substance. The channel is composed of two subunits: sulfonylurea receptor (SUR) and inward rectifier potassium channel (Kir6. X) composition. Mutations in SUR and Kir6.2 genes cause changes in the sensitivity of KATP channels to ATP and ADP Mg2 +, resulting in low activity of KATP channels, leading to hereditary hyperinsulinemia; mutations in SUR1 and Kir6.2 genes and more Morphology may also be associated with type 2 diabetes mellitus (T2DM), which may be due to SUR1 gene mutations leading to hyperinsulinemia; studies of different populations have found a correlation between SUR1 gene polymorphisms and T2DM, but each population There is an inconsistency between the SUR1 gene and T2DM-related sites.