氧化应激
细胞凋亡
胰岛素抵抗
间歇性缺氧
磷酸化
缺氧(环境)
细胞生物学
化学
下调和上调
氧化磷酸化
胰岛素
内分泌学
内科学
医学
生物
生物化学
氧气
基因
有机化学
阻塞性睡眠呼吸暂停
作者
Shan Zeng,Yeying Wang,Li Ai,Liwei Huang,Zhijuan Liu,Chun‐Xia He,Qiao Bai,Yongxia Li
标识
DOI:10.1111/1440-1681.13843
摘要
Abstract This study explores the potential mechanisms of obstructive sleep apnoea (OSA) complicates type 2 diabetes mellitus (T2DM) by which chronic intermittent hypoxia (CIH) induces insulin resistance and cell apoptosis in the pancreas through oxidative stress. Four‐ and eight‐week CIH rat models were established, and Tempol (100 mg/kg/d), was used as an oxidative stress inhibitor. This study included five groups: 4‐week CIH, 4‐week CIH‐Tempol, 8‐week CIH, 8‐week CIH‐Tempol and normal control (NC) groups. Fasting blood glucose and insulin levels were measured in the serum. The expression levels of 8‐hidroxy‐2‐deoxyguanosine (8‐OHdG), tribbles homologue 3 (TRB3), c‐Jun N‐terminal kinase (JNK), phosphorylated JNK (p‐JNK), insulin receptor substrate‐1 (IRS‐1), phosphorylated IRS‐1 (Ser307) (p‐IRS‐1 ser307 ), protein kinase B (AKT), phosphorylated AKT (Ser473) (p‐AKT ser473 ), B cell lymphoma protein‐2 (Bcl‐2), cleaved‐caspase‐3 (Cl‐caspase‐3), and the islet cell apoptosis were detected in the pancreas. CIH induced oxidative stress in the pancreas. Compared with that in the NC group and CIH‐Tempol groups individually, the homeostasis model assessment of insulin resistance (HOMA‐IR) and apoptosis of islet cells was increased in the CIH groups. CIH‐induced oxidative stress increased the expression of p‐IRS‐1 Ser307 and decreased the expression of p‐AKT Ser473 . The expression levels of TRB3 and p‐JNK were higher in the CIH groups than in both the CIH‐Tempol and NC groups. Meanwhile, the expressions of Cl‐caspase‐3 and Bcl‐2 were upregulated and downregulated, respectively, in the CIH groups. Hence, the present study demonstrated that CIH‐induced oxidative stress might not only induce insulin resistance but also islet cell apoptosis in the pancreas through TRB3 and p‐JNK.
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