European journal of preventive cardiology · 2025
Exposure to aircraft noise exacerbates cardiovascular and oxidative damage in three mouse models of diabetes.
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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
Аннотация
AIMS: 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.
METHODS AND RESULTS: 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.
CONCLUSION: 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.
METHODS AND RESULTS: 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.
CONCLUSION: 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.