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在1型糖尿病中,β细胞与δ细胞电气合的丧失是导致低血糖引起的葡萄糖分泌障碍的基础

Thomas G Hill¹, Rui Gao¹, Anna Benrick²

¹Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK.

Nature metabolism

|September 23, 2024

概括

在1型糖尿病中,缺乏对低葡萄糖的葡萄糖激素反应是由于过度的索马托斯塔丁. 这种受损的反调节会增加1型糖尿病患者的低血糖风险.

科学领域:

内分泌学在内分泌学.
糖尿病研究糖尿病研究
细胞生理学细胞生理学

背景情况:

1型糖尿病 (T1D) 的特征是胰岛素和葡萄糖分泌受损.
患有T1D的患者往往缺乏对血葡萄糖下降的逆调节性葡萄糖反应,从而增加低血糖的风险.
之前在动物上的研究表明,SSTR抗体可以恢复葡萄糖分泌,但人类的相关性尚不清楚.

研究的目的:

研究人类T1D小岛中葡萄糖分泌受损背后的细胞机制.
为了确定低葡萄糖对葡萄糖反应的缺陷是否保留在人类T1D中.
阐明 somatostatin 在 T1D 中对抗调节的丧失中的作用.

主要方法:

从T1D捐赠者和非肥胖糖尿病小鼠中分离出来的人类小岛被使用.
测量了对低葡萄糖的反应中的葡萄糖分泌.
研究了体静止素和细胞间通信 (间隙结) 的作用.

主要成果:

人类T1D岛屿,就像T1D小鼠的岛屿一样,在低葡萄糖的情况下未能刺激葡萄糖分泌.
这种缺陷与体静止素的高分泌有关,导致对膜抑制葡萄糖释放.
"电动车"机制,即β细胞的高极化通常会抑制体静止素,由于β细胞的破坏而丧失.

结论:

在T1D中,自免疫性β细胞的破坏破坏了正常抑制体静止素分泌的过程.
这导致过量的体静止素,损害了葡萄糖的逆调节,增加了低血糖的风险.
剩余的β细胞功能可能对维持反调节反应和减少低血糖症的严重性至关重要.

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