基础医学与临床 ›› 2009, Vol. 29 ›› Issue (12): 1337-1340.

• 短篇综述 • 上一篇    下一篇

内质网应激参与糖脂毒性引起的胰岛β细胞凋亡

杨燕丽 向若兰 孙琦   

  1. 中国医学科学院北京协和医学院北京协和医院 北京大学医学部生理与病理生理系
  • 收稿日期:2009-11-03 修回日期:2009-11-06 出版日期:2009-12-20 发布日期:2009-12-20

ERS response mediate glucolipotoxicity-induced β-cell apoptosis

Yan-li YANG, Ruo-lan XIANG, Qi SUN   

  1. Peking Union Medical College Hospital, CAMS & PUMC Department of Physiology and Pathophysiology, Peking University Health Science Center
  • Received:2009-11-03 Revised:2009-11-06 Online:2009-12-20 Published:2009-12-20

摘要: 胰岛β细胞具有高度发达的内质网,是对内质网应激最敏感的细胞之一。高浓度的游离脂肪酸引起内质网应激反应进而诱导了β细胞的凋亡,葡萄糖则促进了脂肪酸通过内质网应激引起的β细胞凋亡。总之,内质网应激介导了糖脂毒性引起的β细胞凋亡。

关键词: 内质网应激, 糖脂毒性, β细胞凋亡

Abstract: As one of the most sensitive cells of endoplasmic reticulum stress (ERS), pancreatic β-cells have an abundance of endoplasmic reticulum. Fatty acids cause apoptosis of β-cells and might contribute to β-cell loss in type 2 diabetes via the induction of ERS. Glucose is an amplifier of the ERS response to fatty acid, leading to increased β-cell apoptosis. ERS response is mediate to glucolipotoxicity-induced β-cell apoptosis.

Key words: endoplasmic reticulum stress, glucolipotoxicity, β-cell apoptosis

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