Dominika Mihalikova, Paul Stamm, Miroslava Kvandova, Chinmayi Pednekar, Lea Strohm, Henning Ubbens, Matthias Oelze, Marin Kuntic, Claudius Witzler, Maria Teresa Bayo Jimenez, Sanela Rajlic, Katie Frenis, Qi Tang, Yue Ruan, Susanne Karbach, Hartmut Kleinert, Omar Hahad, Alex von Kriegsheim, Ning Xia, Tilman Grune, Huige Li, Swenja Kröller-Schön, Adrian Gericke, Wolfram Ruf, Philipp S Wild, Philipp Lurz, Thomas Münzel, Andreas Daiber, Thomas Jansen
{"title":"暴露于飞机噪音会加剧三种糖尿病小鼠模型的心血管和氧化损伤。","authors":"Dominika Mihalikova, Paul Stamm, Miroslava Kvandova, Chinmayi Pednekar, Lea Strohm, Henning Ubbens, Matthias Oelze, Marin Kuntic, Claudius Witzler, Maria Teresa Bayo Jimenez, Sanela Rajlic, Katie Frenis, Qi Tang, Yue Ruan, Susanne Karbach, Hartmut Kleinert, Omar Hahad, Alex von Kriegsheim, Ning Xia, Tilman Grune, Huige Li, Swenja Kröller-Schön, Adrian Gericke, Wolfram Ruf, Philipp S Wild, Philipp Lurz, Thomas Münzel, Andreas Daiber, Thomas Jansen","doi":"10.1093/eurjpc/zwae320","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods and results: </strong>C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. 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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":12051,"journal":{"name":"European journal of preventive cardiology","volume":null,"pages":null},"PeriodicalIF":8.4000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Exposure to aircraft noise exacerbates cardiovascular and oxidative damage in three mouse models of diabetes.\",\"authors\":\"Dominika Mihalikova, Paul Stamm, Miroslava Kvandova, Chinmayi Pednekar, Lea Strohm, Henning Ubbens, Matthias Oelze, Marin Kuntic, Claudius Witzler, Maria Teresa Bayo Jimenez, Sanela Rajlic, Katie Frenis, Qi Tang, Yue Ruan, Susanne Karbach, Hartmut Kleinert, Omar Hahad, Alex von Kriegsheim, Ning Xia, Tilman Grune, Huige Li, Swenja Kröller-Schön, Adrian Gericke, Wolfram Ruf, Philipp S Wild, Philipp Lurz, Thomas Münzel, Andreas Daiber, Thomas Jansen\",\"doi\":\"10.1093/eurjpc/zwae320\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods and results: </strong>C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. 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.</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":12051,\"journal\":{\"name\":\"European journal of preventive cardiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":8.4000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European journal of preventive cardiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/eurjpc/zwae320\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of preventive cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/eurjpc/zwae320","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Exposure to aircraft noise exacerbates cardiovascular and oxidative damage in three mouse models of diabetes.
Background: 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/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. 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.
期刊介绍:
European Journal of Preventive Cardiology (EJPC) is an official journal of the European Society of Cardiology (ESC) and the European Association of Preventive Cardiology (EAPC). The journal covers a wide range of scientific, clinical, and public health disciplines related to cardiovascular disease prevention, risk factor management, cardiovascular rehabilitation, population science and public health, and exercise physiology. The categories covered by the journal include classical risk factors and treatment, lifestyle risk factors, non-modifiable cardiovascular risk factors, cardiovascular conditions, concomitant pathological conditions, sport cardiology, diagnostic tests, care settings, epidemiology, pharmacology and pharmacotherapy, machine learning, and artificial intelligence.