Medical College, Southeast University, No.87, Dingjiaqiao Street, Gulou, Nanjing, China.
Institute of Life Sciences, Southeast University, Nanjing, China.
Environ Health Prev Med. 2018 Feb 12;23(1):6. doi: 10.1186/s12199-018-0694-3.
Epidemiological studies have suggested that noise exposure may increase the risk of type 2 diabetes mellitus (T2DM), and experimental studies have demonstrated that noise exposure can induce insulin resistance in rodents. The aim of the present study was to explore noise-induced processes underlying impaired insulin sensitivity in mice.
Male ICR mice were randomly divided into four groups: a control group without noise exposure and three noise groups exposed to white noise at a 95-dB sound pressure level for 4 h/day for 1, 10, or 20 days (N1D, N10D, and N20D, respectively). Systemic insulin sensitivity was evaluated at 1 day, 1 week, and 1 month post-noise exposure (1DPN, 1WPN, and 1MPN) via insulin tolerance tests (ITTs). Several insulin-related processes, including the phosphorylation of Akt, IRS1, and JNK in the animals' skeletal muscles, were examined using standard immunoblots. Biomarkers of inflammation (circulating levels of TNF-α and IL-6) and oxidative stress (SOD and CAT activities and MDA levels in skeletal muscles) were measured via chemical analyses.
The data obtained in this study showed the following: (1) The impairment of systemic insulin sensitivity was transient in the N1D group but prolonged in the N10D and N20D groups. (2) Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation. (3) Plasma levels of TNF-α and IL-6, CAT activity, and MDA concentrations in skeletal muscles were elevated after 20 days of noise exposure.
Impaired insulin sensitivity in noise-exposed mice might be mediated by an enhancement of the JNK/IRS1 pathway. Inflammation and oxidative stress might contribute to insulin resistance after chronic noise exposure.
流行病学研究表明，噪声暴露可能会增加 2 型糖尿病（T2DM）的风险，而实验研究表明，噪声暴露会导致啮齿动物产生胰岛素抵抗。本研究旨在探讨噪声引起的小鼠胰岛素敏感性受损的机制。
雄性 ICR 小鼠随机分为四组：无噪声暴露的对照组和分别暴露于 95 分贝声压级白噪声 4 小时/天 1、10 或 20 天的三组（分别为 N1D、N10D 和 N20D）。通过胰岛素耐量试验（ITT）在噪声暴露后 1 天（1DPN）、1 周（1WPN）和 1 个月（1MPN）评估全身胰岛素敏感性。使用标准免疫印迹法检测动物骨骼肌中 Akt、IRS1 和 JNK 的磷酸化等几种与胰岛素相关的过程。通过化学分析测量炎症生物标志物（循环 TNF-α 和 IL-6 水平）和氧化应激（骨骼肌中 SOD 和 CAT 活性及 MDA 水平）。
本研究结果表明：（1）N1D 组全身胰岛素敏感性的损害是短暂的，但 N10D 和 N20D 组则是持久的。（2）噪声暴露导致 JNK 磷酸化和 IRS1 丝氨酸磷酸化增强，以及对外源性胰岛素刺激时 Akt 磷酸化降低。（3）20 天噪声暴露后，血浆 TNF-α 和 IL-6 水平、CAT 活性和骨骼肌 MDA 浓度升高。
噪声暴露小鼠的胰岛素敏感性受损可能是通过增强 JNK/IRS1 通路介导的。炎症和氧化应激可能导致慢性噪声暴露后的胰岛素抵抗。
