Involvement of chronic stresses in rat islet and INS-1 cell glucotoxicity induced by intermittent high glucose
Involvement of chronic stresses in rat islet and INS-1 cell glucotoxicity induced by intermittent high glucose
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DOI：
10.1016/j.mce.2008.03.004
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发表时间：
2008-09-10
影响因子：
4.1
通讯作者：
Li, Guang-Wei
中科院分区：
文献类型：
--
作者：
Hou, Zhi-Qiang;Li, Hong-Liang;Li, Guang-Wei
为探讨间歇性高糖（IHG）和持续性高糖（SHG）对大鼠胰岛β细胞功能的毒性作用及其可能机制，将大鼠胰岛和INS-1 β细胞分别暴露于SHG（25 mmol/l）和IHG（11.1和25 mmol/l葡萄糖，每12 h交替）72 h。结果表明，IHG对大鼠胰岛和INS-1细胞胰岛素释放反应的损害比SHG更明显。同时，IHG暴露的胰岛和INS-1细胞的内质网和氧化应激水平更明显地增加。但SHG和IHG对细胞活力、胰岛素含量和基因表达的影响无显著性差异。综上所述，本研究提示IHG对大鼠胰岛β细胞功能的毒性作用可能是由于细胞应激过度激活所致。(c)2008爱思唯尔爱尔兰有限公司保留所有权利。
in order to investigate the toxic effect of intermittent high glucose (IHG) and sustained high glucose (SHG) on rat pancreatic beta cell functions and the potential involved mechanisms, isolated rat islets and INS-1 beta cells were exposed to SHG (25 mmol/l) or IHG (11.1 and 25 mmol/l glucose alternating every 12 h) for 72 h. The results showed that IHG induced a more significant impairment of insulin release response in rat islets and INS-1 cell than SHG. Simultaneously, the intracellular levels of endoplasmic reticulum and oxidative stress were more markedly increased in islets and INS-1 cells exposed to IHG. However, there was no significant difference between reducing cell viability, insulin content and gene expression induced by SHG and IHG. Taken together, this study suggested the more serious toxic effect on rat pancreatic beta cell function induced by IHG treatment may be due to excessive activation of cellular stress. (c) 2008 Elsevier Ireland Ltd. All rights reserved.