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慢性噪声暴露会加剧胰岛素抵抗,并促进高脂肪饮食小鼠模型中 2 型糖尿病的表现。

Chronic noise-exposure exacerbates insulin resistance and promotes the manifestations of the type 2 diabetes in a high-fat diet mouse model.

机构信息

Medical College, Southeast University, Nanjing, China.

Institute of Life Sciences, Southeast University, Nanjing, China.

出版信息

PLoS One. 2018 Mar 30;13(3):e0195411. doi: 10.1371/journal.pone.0195411. eCollection 2018.

DOI:10.1371/journal.pone.0195411
PMID:29601606
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5877872/
Abstract

Epidemiological studies have revealed that noise exposure was associated with an increased risk of type 2 diabetes mellitus (T2DM). However, the exact nature of that association remains to be elucidated. The present study is designed to examine the effects of chronic noise exposure on the development of T2DM in combination with a high-fat-diet (HFD) in mice. Here we show that chronic noise exposure at 85 dB SPL (4 h /day, below the safety limit for occupational noise exposure) exaggerated multiple metabolic abnormalities induced by HFD in C57BL/6J male mice, including worsened glucose intolerance, insulin resistance, fasting hyperglycemia and dyslipidemia. Furthermore, noise exposure exhibited a paradoxical impact on fat accumulation and circulating levels of free fatty acid, indicating a potential stimulating effect of noise on lipolysis. These results provide first in vivo supporting evidence for the causative role of noise exposure in diabetogenesis and pinpoint a noise-associated increase in blood free fatty acid levels as a possible mediator accelerating the effect of noise on the development of insulin resistance and T2DM.

摘要

流行病学研究表明,噪声暴露与 2 型糖尿病(T2DM)的风险增加有关。然而,这种关联的确切性质仍有待阐明。本研究旨在探讨慢性噪声暴露与高脂肪饮食(HFD)联合作用对小鼠 T2DM 发展的影响。在这里,我们显示慢性噪声暴露在 85 dB SPL(4 h /天,低于职业噪声暴露的安全限值)可加重 C57BL/6J 雄性小鼠中 HFD 诱导的多种代谢异常,包括葡萄糖耐量恶化、胰岛素抵抗、空腹高血糖和血脂异常。此外,噪声暴露对脂肪积累和循环游离脂肪酸水平表现出矛盾的影响,表明噪声对脂肪分解有潜在的刺激作用。这些结果为噪声暴露在糖尿病发生中的因果作用提供了第一个体内支持证据,并指出与噪声相关的血液游离脂肪酸水平升高可能是加速噪声对胰岛素抵抗和 T2DM 发展影响的一个潜在介导因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/83f43f083db2/pone.0195411.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/0ae4d8e508a0/pone.0195411.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/85412a51ad26/pone.0195411.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/eb148d1d7a86/pone.0195411.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/83f43f083db2/pone.0195411.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/0ae4d8e508a0/pone.0195411.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/85412a51ad26/pone.0195411.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/eb148d1d7a86/pone.0195411.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e237/5877872/83f43f083db2/pone.0195411.g004.jpg

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