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慢性噪声对大鼠葡萄糖代谢及肠道菌群-宿主炎症内稳态的影响。

Effects of chronic noise on glucose metabolism and gut microbiota-host inflammatory homeostasis in rats.

机构信息

Department of Occupational Hygiene, Tianjin Institute of Health and Environmental Medicine, Tianjin, China.

School of Medicine and Life Sciences, University of Jinan-Shandong Academy of Medical Sciences, Jinan, China.

出版信息

Sci Rep. 2016 Nov 4;6:36693. doi: 10.1038/srep36693.

DOI:10.1038/srep36693
PMID:27811997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5095650/
Abstract

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3-14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation.

摘要

慢性噪声暴露已被认为与糖尿病风险增加有关。然而,将慢性噪声应激与葡萄糖代谢联系起来的机制的实验证据有限。我们通过检查连续 30 天暴露于噪声的大鼠的葡萄糖代谢、免疫反应和肠道微生物群/宿主炎症平衡的变化来解决这个问题。慢性噪声暴露会导致血糖和皮质酮水平至少在噪声停止后 14 天内升高。应激大鼠的肝脏中还存在糖原和甘油三酯水平升高,以及通过胰岛素诱导的胰岛素受体/胰岛素受体底物 1/糖原合酶激酶 3β信号转导导致肝胰岛素产生受损,这种情况在噪声暴露停止后持续 3-14 天。慢性噪声改变了肠道中变形菌门和放线菌门的百分比,与对照组相比,盲肠中罗斯伯里亚菌的比例增加,而粪杆菌的比例减少。这些动物的肠道中免疫球蛋白 A、白细胞介素 1β 和肿瘤坏死因子 α 的水平也升高,这与葡萄糖调节和胰岛素敏感性的噪声诱导异常相对应。这些结果表明,终身环境噪声暴露可能通过改变肠道微生物群组成和肠道炎症对糖尿病的发生和发展产生累积影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/a8fb969290bd/srep36693-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/07050fcc5973/srep36693-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/215a1aa5453b/srep36693-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/678e6b2bdaa0/srep36693-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/17a7d5ae08c1/srep36693-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/a8fb969290bd/srep36693-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/07050fcc5973/srep36693-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/215a1aa5453b/srep36693-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/678e6b2bdaa0/srep36693-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/17a7d5ae08c1/srep36693-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58ce/5095650/a8fb969290bd/srep36693-f5.jpg

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