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

Liu, Lijie; Huang, Yi; Fang, Cong; Zhang, Hongyu; Yang, Jing; Xuan, Chuanying; Wang, Fanfan; Lu, Haiying; Cao, Shuangfeng; Wang, Yongfang; Li, Shengwei; Sha, Jun; Zha, Mingming; Guo, Min; Wang, Jian

doi:10.1371/journal.pone.0195411

Cited by 22 publications

(20 citation statements)

References 37 publications

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“…Although with inconsistent outcome, the stress response exhibits broad impact on hepatic inflammation while patients are prone to blame stress for the deterioration of their liver maladies . Beyond this, the noise disturbance contributes to insulin resistance getting in the way of glucose homeostasis, which might exacerbate status of type 2 diabetes worsening the liver dysfunction . Another explanation behind the noise evoked disorder is the impairment of endothelial function which might damnify the blood supply in liver tissue .…”

Section: Discussionmentioning

confidence: 99%

“…2 Beyond this, the noise disturbance contributes to insulin resistance getting in the way of glucose homeostasis, which might exacerbate status of type 2 diabetes worsening the liver dysfunction. 35 Another explanation behind the noise evoked disorder is the impairment of endothelial function which might damnify the blood supply in liver tissue. 2 Furthermore, the involvement of vibration 36 or coherence resonances, 37 immunoreaction 38 should not be excluded.…”

Section: Discussionmentioning

confidence: 99%

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Acid sphingomyelinase mediates the noise‐induced liver disorder in mice

Meng

Xie

et al. 2019

Clin Exp Pharma Physio

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Summary Noise‐induced structural and functional disorder of the liver has been realized, but the underlying mechanism remains to be characterized, which has limited the introduction of precautious measures. Over‐activation of acid sphingomyelinase (ASM)/ceramide (Cer) pathway takes centre stage in hepatocyte injury entailed by various stimulus. We aimed to investigate whether it mediated the noise elicited liver disorder on infrastructure, lipid metabolism, apoptosis, and oxidative stress. Mice were exposed to broad band noise (20–20k Hz, 90–110 dB) for 1, 3, 5 or 7 days by 3 hr/d. Doxepin hydrochloride (DOX), an ASM inhibitor was given by 5 mg/kg/d gavage. We showed that 5 or 7 days intense, broad band noise exposure caused significant infrastructure derangement and lipid droplets storage in hepatocytes. The content of cholesterol, free fatty acids or triglyceride was increased significantly in liver tissue upon noise stimulation. Moreover, the noise promoted apoptosis and superoxide generation in hepatocytes significantly, enhancing activity of aspartate aminotransferase (AST) or alanine amino transferase (ALT) in serum. Acid sphingomyelinase activity and Cer generation in liver tissue were elevated by noise exposure, which was normalized with DOX administrated. Accordingly, DOX alleviated steatosis, apoptosis, oxidative stress and enzymatic change in hepatocytes or serum of noise exposed mice substantially. In summary, our results suggest the ASM/Cer pathway contributes to the broad band noise elicited liver damage in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acid sphingomyelinase mediates the noise‐induced liver disorder in mice

Meng

Xie

et al. 2019

Clin Exp Pharma Physio

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“…The causal effect of stress exposure on glucose homeostasis has been investigated in various animal models [9,10]. As shown by Uchida et al [9], two weeks of restraint stress impaired insulin sensitivity in normal diet-fed mice and was accompanied by the augmented accumulation of macrophages and subsequent inflammatory response in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

“…This finding suggests the notion that moderate stress exposure, without directly affecting glucose homeostasis, can exert synergetic effects on the development of IR in combination with HFD feeding. Recently, Liu et al [10] investigated the effects of chronic noise exposure on IR in HFD-fed mice and found that insulin sensitivity tended to be decreased in 8-week-old HFD-fed stressed mice; however, this was not significantly different to insulin sensitivity in HFD-fed control mice. This may be attributed to the difference in the intensity and duration of stress exposure due to the different experimental protocols.…”

Section: Discussionmentioning

confidence: 99%

Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue

Motoyama

Yamada

Yamamoto

et al. 2020

Cells

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Social stress (SS) has been linked to the development of cardiovascular disease (CVD), which is closely associated with insulin resistance (IR); however, the causal effect of SS on IR remains unclear. The 8-week-old male C57BL/6 mice were exposed to SS by housing with a larger CD-1 mouse in a shared home cage without physical contact for 10 consecutive days followed by high-fat diet (HFD) feeding. Control mice were housed in the same cage without a CD-1 mouse. After 6 weeks of HFD, insulin sensitivity was significantly impaired in stressed mice. While the percentage of classically activated macrophages in epididymal white adipose tissue (eWAT) was equivalent between the two groups, the percentage of lymphocyte antigen 6 complex locus G6D (Ly-6G)/neutrophil elastase (NE)-double positive cells markedly increased in stressed mice, accompanied by augmented NE activity assessed by ex vivo eWAT fluorescent imaging. Treatment with an NE inhibitor completely abrogated the insulin sensitivity impairment of stressed mice. In vitro NE release upon stimulation with a formyl peptide receptor 1 agonist was significantly higher in bone marrow neutrophils of stressed mice. Our findings show that SS-exposed mice are susceptible to the development of HFD-induced IR accompanied by augmented NE activity. Modulation of neutrophil function may represent a potential therapeutic target for SS-associated IR.

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“…resistance, promoting the manifestation of diabetes in mice 18 . A cross-sectional study also reported that impaired fasting glucose was associated with noise-induced hearing loss among automobile manufacturing workers 19 .…”

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confidence: 99%

Occupational noise exposure and its association with incident hyperglycaemia: a retrospective cohort study

Chang

Liu

et al. 2020

Sci Rep

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noise pollution is reported to be associated with diabetes, but few studies have elucidated the associations between noise frequency characteristics. We aimed to evaluate the relationships between different noise frequency components and incident hyperglycaemia. An industry-based cohort of 905 volunteers was enrolled and followed up to 2012. Octave-band frequencies of workstation noise and individual noise levels were measured in 2012 to classify subjects' exposures retrospectively. We applied Cox regression models to estimate the relative risk (RR) of hyperglycaemia. An increased RR for hyperglycaemia of 1.80 (95% confidence interval [CI]: 1.04, 3.10) was found among subjects exposed to ≥ 85 A-weighted decibels (dBA) compared with those exposed to < 70 dBA. The highexposure groups at frequencies of 31.5, 63, 125, 250, 500, 1000, and 2000 Hz had a significantly higher risk of hyperglycaemia (all p values < 0.050) than the low-exposure groups. A 5-dB increase in noise frequencies at 31.5, 63, 125, 250, 500 Hz, and 1000 Hz was associated with an elevated risk of hyperglycaemia (all p values < 0.050), with the highest value of 1.27 (95% CI: 1.10, 1.47) at 31.5 Hz (p = 0.001). Occupational noise exposure may be associated with an increased incidence of hyperglycaemia, with the highest risk observed at 31.5 Hz. Growing numbers of field studies have reported an association between occupational noise exposure and cardiovascular disease (CVD) morbidity and mortality 1-10. In 2019, the World Health Organization (WHO) and the International Labour Organization (ILO) provided a joint methodology (WHO/ILO joint methodology) for estimating the work-related burden of CVD and injury due to workplace noise exposure 11. Noise exposure is regarded as an environmental stressor through direct (i.e., sleep disturbance) and indirect (i.e., annoyance) pathways that pose adverse health effects. Acute noise exposure may activate the hypothalamus-pituitary-adrenal axis and the sympathetic-adrenal-medulla axis to elevate the levels of stress hormones, including cortisol, catecholamine, adrenalin, and noradrenalin. Repeated and chronic stimuli may cause overproduction of stress hormones (e.g., cortisol) that increase the levels of fatty acids and glucose to partially restore homeostasis. In addition, catecholamines also boost the energy supply by breaking down triacylglycerol. Such increases in stress hormones may lead to pathophysiologic alterations in blood pressure, blood lipids, blood viscosity, and blood glucose, which promote the development of hypertension, arteriosclerosis, and CVD 12-14. Because the overproduction of cortisol may inhibit pancreatic insulin secretion and reduce insulin sensitivity in the liver, skeletal muscles, and adipose tissue 14 , it is plausible that long-term noise exposure may produce adverse changes in blood glucose. Noise pollution has been reported to be associated with diabetes in many animal and environmental epidemiological studies; however, few studies have elucidated the relationship between noise fre...

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

Cited by 22 publications

References 37 publications

Acid sphingomyelinase mediates the noise‐induced liver disorder in mice

Acid sphingomyelinase mediates the noise‐induced liver disorder in mice

Social Stress Increases Vulnerability to High-Fat Diet-Induced Insulin Resistance by Enhancing Neutrophil Elastase Activity in Adipose Tissue

Occupational noise exposure and its association with incident hyperglycaemia: a retrospective cohort study

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