Mihalikova Dominika, Stamm Paul, Kvandova Miroslava, Pednekar Chinmayi, Strohm Lea, Ubbens Henning, Oelze Matthias, Kuntic Marin, Witzler Claudius, Bayo Jimenez Maria Teresa, Rajlic Sanela, Frenis Katie, Tang Qi, Ruan Yue, Karbach Susanne, Kleinert Hartmut, Hahad Omar, von Kriegsheim Alex, Xia Ning, Grune Tilman, Li Huige, Kröller-Schön Swenja, Gericke Adrian, Ruf Wolfram, Wild Philipp S, Lurz Philipp, Münzel Thomas, Daiber Andreas, Jansen Thomas
Department for Cardiology, Cardiology 1, University Medical Center of the Johannes Gutenberg-University, Langenbeckstr. 1, 55131 Mainz, Germany.
Institute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy ofSciences, Bratislava, Slovakia.
Eur J Prev Cardiol. 2025 Mar 18;32(4):301-314. doi: 10.1093/eurjpc/zwae320.
Epidemiology links noise to increased risk of metabolic diseases like diabetes and obesity. Translational studies in humans and experimental animals showed that noise causes reactive oxygen species (ROS)-mediated cardiovascular damage. The interaction between noise and diabetes, specifically potential additive adverse effects, remains to be determined.
C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/day for 5 days) to induce type 1 diabetes mellitus, with S961 (subcutaneous osmotic mini-pumps, 0.57 mg/kg/day for 7 days) or fed a high-fat diet (HFD, 20 weeks) to induce type 2 diabetes mellitus. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4 days. While body weight was unaffected, noise reduced insulin production in all diabetes models. The oral glucose tolerance test showed only an additive aggravation by noise in the HFD model. Noise increased blood pressure and aggravated diabetes-induced aortic, mesenteric, and cerebral arterioles' endothelial dysfunction. ROS formation in cerebral arterioles, the aorta, the heart, and isolated mitochondria was consistently increased by noise in all models of diabetes. Mitochondrial respiration was impaired by diabetes and noise, however without additive effects. Noise increased ROS and caused inflammation in adipose tissue in the HFD model. RNA-sequencing data and alteration of gene pathway clusters also supported additive damage by noise in the setting of diabetes.
In all three models of diabetes, aircraft noise exacerbates oxidative stress, inflammation, and endothelial dysfunction in mice with pre-existing diabetes. Thus, noise may potentiate the already increased cardiovascular risk in diabetic patients.
流行病学研究表明，噪音与糖尿病和肥胖等代谢性疾病风险增加有关。对人类和实验动物的转化研究表明，噪音会导致活性氧（ROS）介导的心血管损伤。噪音与糖尿病之间的相互作用，特别是潜在的叠加不良影响，仍有待确定。
用链脲佐菌素（腹腔注射，50mg/kg/天，共5天）处理C57BL/6小鼠以诱导1型糖尿病，用S961（皮下渗透微型泵，0.57mg/kg/天，共7天）或喂食高脂饮食（HFD，20周）以诱导2型糖尿病。将对照小鼠和糖尿病小鼠暴露于平均声压级为72dB(A)的飞机噪音中4天。虽然体重未受影响，但噪音降低了所有糖尿病模型中的胰岛素分泌。口服葡萄糖耐量试验表明，在HFD模型中，噪音只会产生叠加性加重作用。噪音会升高血压，并加重糖尿病引起的主动脉、肠系膜和脑小动脉的内皮功能障碍。在所有糖尿病模型中，噪音均使脑小动脉、主动脉、心脏和分离的线粒体中的ROS生成持续增加。糖尿病和噪音均会损害线粒体呼吸，但无叠加效应。在HFD模型中，噪音会增加ROS并导致脂肪组织炎症。RNA测序数据和基因通路簇的改变也支持在糖尿病背景下噪音造成的叠加性损伤。
在所有三种糖尿病模型中，飞机噪音都会加剧已患糖尿病小鼠的氧化应激、炎症和内皮功能障碍。因此，噪音可能会增强糖尿病患者本就已增加的心血管疾病风险。
