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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。
The pathogenesis of type 2 diabetes is characterized by insulin resistance and impaired beta-cell function. Insulin resistance, hyperinsulinemia and persistent glucose toxicity can exacerbate pancreatic beta-cell failure. Numerous studies have shown that KATP channel openers (diazoxide) open KATP channels, can force the over-fatigue of beta cells to rest, inhibit insulin secretion, increase insulin content in islets and restore insulin pulse secretion, morphologically and functionally Protects the beta cells. Moderate islet resuscitation can reduce β-cell metabolic stress and improve β-cell function, it is worth focusing on the direction of future research.