K_(ATP)通道开放剂与β细胞休息学说  

K_(ATP)- channel opener and β-cell rest

作　　者：李娟[1] 邹大进[1] 

机构地区：[1]第二军医大学附属长海医院内分泌科,上海200433

出　　处：《国际内分泌代谢杂志》2006年第B04期1-3,共3页International Journal of Endocrinology and Metabolism

摘　　要：2型糖尿病发病的中心环节为胰岛素抵抗和β细胞功能受损。胰岛素抵抗、高胰岛素血症及持续的糖毒性可加剧胰岛β细胞功能衰竭。大量研究表明,KATP通道开放剂(二氮嗪)开放KATP 通道,可强制过度疲劳的β细胞休息,抑制胰岛素的分泌,增加胰岛内胰岛素含量,恢复了胰岛素的脉冲式分泌,从形态和功能上保护了β细胞。适度的胰岛休息可以减轻β细胞的代谢压力,提高β细胞功能,是值得今后重点研究的方向。Type 2 diabetes is characterized by insulin resistant and impaired β-cell function. It has been suggested that this defect of β-cell function is partly due to insulin resistance, hyperglycemia and glucotoxieity. It has been reported that induction of β-cell rest by activation of β-cell KATP-channels preserves insulin stores and pulsatile insulin secretion. It protected from both functionally and morphologically by suppression of excessive insulin secretion. Therefore, the concept of β-cell rest may provide a strategy to protect β-cells.

关 键 词：2型糖尿病 糖毒性 β细胞休息 KATP通道开放剂 

分 类 号：R587.1[医药卫生—内分泌]