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。

IF 8.4 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS European journal of preventive cardiology Pub Date : 2024-10-01 DOI:10.1093/eurjpc/zwae320
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}
引用次数: 0

摘要

背景:流行病学将噪声与糖尿病和肥胖症等代谢性疾病的风险增加联系起来。对人类和实验动物进行的转化研究表明,噪音会导致活性氧(ROS)介导的心血管损伤。噪声与糖尿病之间的相互作用,特别是潜在的叠加不利影响,仍有待确定:用链脲佐菌素(静脉注射,50 毫克/千克/天,持续 5 天)诱导 C57BL/6 小鼠患 1 型糖尿病,用 S961(皮下渗透微型泵,0.57 毫克/千克/天,持续 7 天)或喂食高脂饮食(HFD,20 周)诱导 2 型糖尿病。对照组和糖尿病小鼠暴露于平均声压级为 72 dB(A) 的飞机噪音中 4 天。虽然体重未受影响,但噪音减少了所有糖尿病模型的胰岛素分泌。在高频分解模型中,口服葡萄糖耐量试验仅显示噪音会加重病情。噪音会升高血压,加重糖尿病引起的主动脉、肠系膜和脑动脉内皮功能障碍。在所有糖尿病模型中,脑动脉血管、主动脉、心脏和离体线粒体中的 ROS 形成都因噪音而持续增加。线粒体呼吸受到糖尿病和噪音的影响,但没有叠加效应。在高密度脂蛋白胆固醇模型中,噪声增加了 ROS 并导致脂肪组织炎症。RNA测序数据和基因通路集群的改变也证实了噪声对糖尿病患者造成的叠加损害:结论:在所有三种糖尿病模型中,飞机噪声都会加剧原有糖尿病小鼠的氧化应激、炎症和内皮功能障碍。因此,噪声可能会加剧糖尿病患者已经增加的心血管风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
European journal of preventive cardiology
European journal of preventive cardiology CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
12.50
自引率
12.00%
发文量
601
审稿时长
3-8 weeks
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.
期刊最新文献
REDUCE-IT, biomarkers, and confirmation bias: are we missing the forest for the trees? Strike early-strike strong lipid-lowering strategy with proprotein convertase subtilisin/kexin type 9 inhibitors in acute coronary syndrome patients: real-world evidence from the AT-TARGET-IT registry. Eligibility for lipid-lowering therapy when applying systemic coronary risk estimation 2 according to guidelines on apparently healthy middle-aged individuals. Use of combination therapy is associated with improved LDL cholesterol management: 1-year follow-up results from the European observational SANTORINI study. Effects of omega-3 fatty acids on coronary revascularization and cardiovascular events: a meta-analysis.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1