Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Switzerland; Transfaculty Research Platform Molecular and Cognitive Neurosciences, University of Basel, Switzerland.
WAKING Team, Lyon Neuroscience Research Center (CRNL) - INSERM U1028, CNRS UMR5292, University Claude Bernard Lyon 1, Lyon, France.
Environ Int. 2018 Dec;121(Pt 1):1011-1023. doi: 10.1016/j.envint.2018.05.036. Epub 2018 Jul 4.
Epidemiological evidence indicates an association between transportation noise exposure and a higher risk of developing type 2 diabetes. Sleep disturbances are thought to be one of the mechanisms as it is well established that a few nights of short or poor sleep impair glucose tolerance and insulin sensitivity in healthy good sleepers.
The present study aimed to determine the extent to which exposure to nocturnal transportation noise affects glucose metabolism, and whether it is related to noise-induced sleep alterations.
Twenty-one young healthy volunteers (nine women) participated in a six-day laboratory study starting with a noise-free baseline night, then four nights sleeping with randomly-presented transportation noise scenarios (three road and one railway noise scenario) with identical average sound level of 45dB but differing in eventfulness and ending with a noise-free recovery night. Sleep was measured by polysomnography. Glucose tolerance and insulin sensitivity were measured after the baseline, the last noise night and the recovery nights with an oral glucose tolerance test using Matsuda and Stumvoll insulin sensitivity indexes. Eleven participants were assigned a less eventful noise scenario during the last noise night (LE-group), while the other ten had a more eventful noise scenario (ME-group). Baseline metabolic and sleep variables between the two intervention groups were compared using a non-parametric Mann-Whitney U test while mixed models were used for repeated measure analysis.
All participants had increased glucose (mean±SE, 14±2%, p<0.0001) and insulin (55±10%, p<0.0001) after the last noise night compared to the baseline night. 2h-glucose level tended to increase only in the ME-group between baseline (5.1±0.22mmol·L) and the last noise night (6.1±0.39mmol·L, condition: p=0.001, interaction: p=0.08). Insulin sensitivity assessed with Matsuda and Stumvoll indexes respectively decreased by 7±8% (p=0.001) and 9±2% (p<0.0001) after four nights with transportation noise. Only participants in the LE-group showed beneficial effects of the noise-free recovery night on glucose regulation (relative change to baseline: glucose: 1±2%, p=1.0 for LE-group and 18±4%, p<0.0001 for ME-group; Stumvoll index: 3.2±2.6%, p=1.0 for LE-group and 11±2.5%, p=0.002 for ME-group). Sleep was mildly impaired with increased sleep latency of 8±2min (<0.0001) and more cortical arousals per hour of sleep (1.8±0.6arousals/h, p=0.01) during the last noise night compared to baseline. No significant associations between sleep measures and glucose tolerance and insulin sensitivity were found.
In line with epidemiological findings, sleeping four nights with transportation noise impaired glucose tolerance and insulin sensitivity. Based on the presented sound exposure, the eventfulness of the noise scenarios seems to play an important role for noise-induced alterations in glucose regulation. However, we could not confirm our hypothesis that transportation noise impairs glucose regulation via deterioration in sleep quality and quantity. Therefore, other factors, such as stress-related pathways, may need to be considered as potential triggers for noise-evoked glucose intolerance in future research.
流行病学证据表明，交通噪声暴露与 2 型糖尿病风险增加之间存在关联。睡眠障碍被认为是其中的一种机制，因为已有充分的证据表明，几晚的短暂或不佳的睡眠会损害健康的良好睡眠者的葡萄糖耐量和胰岛素敏感性。
本研究旨在确定夜间交通噪声暴露对葡萄糖代谢的影响程度，以及其是否与噪声引起的睡眠改变有关。
21 名年轻健康志愿者（9 名女性）参加了一项为期六天的实验室研究，从无噪声的基础夜间开始，然后随机呈现交通噪声场景（三个道路噪声场景和一个铁路噪声场景），平均声级为 45dB，但事件发生率不同，持续四晚，最后以无噪声的恢复夜间结束。睡眠通过多导睡眠图进行测量。在基础、最后一个噪声夜间和恢复夜间后，使用口服葡萄糖耐量试验，使用 Matsuda 和 Stumvoll 胰岛素敏感性指数，测量葡萄糖耐量和胰岛素敏感性。11 名参与者在最后一个噪声夜间被分配到一个事件较少的噪声场景（LE 组），而另外 10 名参与者则被分配到一个事件较多的噪声场景（ME 组）。使用非参数曼-惠特尼 U 检验比较两组干预措施的基线代谢和睡眠变量，同时使用混合模型进行重复测量分析。
与基础夜间相比，所有参与者在最后一个噪声夜间后血糖（平均±SE，14±2%，p<0.0001）和胰岛素（55±10%，p<0.0001）均升高。在 ME 组中，2h 血糖水平仅在基线（5.1±0.22mmol·L）和最后一个噪声夜间（6.1±0.39mmol·L，条件：p=0.001，交互：p=0.08）之间出现增加趋势。使用 Matsuda 和 Stumvoll 指数评估的胰岛素敏感性分别下降了 7±8%（p=0.001）和 9±2%（p<0.0001），在经历四晚交通噪声后。只有 LE 组在噪声恢复夜间对葡萄糖调节显示出有益的效果（与基线相比的相对变化：血糖：1±2%，p=1.0 为 LE 组，18±4%，p<0.0001 为 ME 组；Stumvoll 指数：3.2±2.6%，p=1.0 为 LE 组，11±2.5%，p=0.002 为 ME 组）。与基础夜间相比，最后一个噪声夜间的睡眠潜伏期延长了 8±2min（<0.0001），每小时的皮质唤醒次数增加了 1.8±0.6 次（p=0.01）。睡眠测量与葡萄糖耐量和胰岛素敏感性之间没有显著关联。
与流行病学发现一致，连续四晚暴露于交通噪声会损害葡萄糖耐量和胰岛素敏感性。基于所呈现的声音暴露，噪声场景的事件发生率似乎对噪声引起的葡萄糖调节改变起着重要作用。然而，我们不能证实我们的假设，即交通噪声通过睡眠质量和数量的恶化来损害葡萄糖调节。因此，在未来的研究中，需要考虑其他因素，如应激相关途径，作为噪声诱发葡萄糖不耐受的潜在触发因素。
