Dynamic recovery after acute single fine particulate matter exposure in male mice: Effect on lipid deregulation and cardiovascular alterations

Zhang, Xi; Jie, Zhang; Wu, Yan; Nan, Bingru; Huang, Qingyu; Du, Xiaodong; Tian, Meiping; Liu, Liangpo; Xin, Yuntian; Li, Yanbo; Duan, Junchao; Chen, Rui; Sun, Zhiwei; Shen, Heqing

doi:10.1016/j.jhazmat.2021.125504

Cited by 18 publications

(5 citation statements)

References 53 publications

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“…As a primary component in air pollution, PM2.5 directly enters the blood and contributes to multiorgan toxicities ( Goldberg and Villeneuve, 2008 ; Xu et al, 2016 ; Xu et al, 2018 ). Recently, accumulating research has shown that exposure to PM2.5 can act as an independent factor to disrupt the balance of lipid metabolism ( McGuinn et al, 2019 ; Zhang et al, 2021 ). Air pollution can increase the BMI of children and can increase the probability of developing obesity, as reported by most epidemiological studies ( Tong et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Multi-omics reveals hypertrophy of adipose tissue and lipid metabolism disorder via mitochondria in young mice under real-ambient exposure to air pollution

Gao

Yang

et al. 2023

Front. Pharmacol.

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Air pollution has become one of the most serious health risks as a result of industrialization, especially in developing countries. More attention has been drawn to the relationship between obesity/overweight and fine particulate matter (PM2.5). Especially for susceptible populations, the impact of air pollution on children and adolescents has attracted more public attentions. However, the detailed underlying mechanism influencing obesity or overweight under PM2.5 exposure is still unknown. Therefore, young mice were exposed to PM2.5 using the real-ambient exposure system that we previously established in Shijiazhuang city. Compared with the traditionally concentrated air particle (CAP) system, our real-ambient exposure system provides similar PM2.5 concentrations and characteristics as outdoor ambient air and minimizes the influence of external interfering factors. After 8 weeks of exposure to PM2.5, the weight of gonadal white adipose tissue (gWAT) and subcutaneous white adipose tissue (sWAT) was considerably increased, accompanied by a significantly enlarged size of adipocytes in sWAT. Importantly, multiomics analysis indicated altered metabolites involved in the lipid metabolism pathway, and transcriptomic analysis revealed notably changed signaling pathways related to fatty acid metabolism. Moreover, the mtDNA copy number, mitochondrial activity and fatty acid oxidation (FAO) were increased in the liver under PM2.5 exposure. Taken together, our research investigated the hypotrophy of adipose tissue in young mice, supported an imbalance in lipid metabolism based on multiomics analysis, and revealed disordered mitochondrial function under PM2.5 exposure. Our study provided new insight into the hazardous effects of air pollution, and extended our understanding on the underlying mechanism.

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Section: Discussionmentioning

confidence: 99%

Multi-omics reveals hypertrophy of adipose tissue and lipid metabolism disorder via mitochondria in young mice under real-ambient exposure to air pollution

Gao

Yang

et al. 2023

Front. Pharmacol.

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“…42 For example, targeted lipidomic analysis has shown that PM 2.5 exposure in mice on day 7 led to a significant decrease in phospholipids. 43 In the present study, untargeted lipidomics were used to analyze the changes in lipid profiles by PM 2.5 , and to the best of our knowledge, this is the first study to compare global lipidomic changes in preadipocytes in response to PM 2.5 .…”

Section: ■ Discussionmentioning

confidence: 99%

PPARγ As a Potential Target for Adipogenesis Induced by Fine Particulate Matter in 3T3-L1 Preadipocytes

Yun

Chen

Miao

et al. 2023

Environ. Sci. Technol.

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Mounting evidence has shown that ambient PM 2.5 exposure is closely associated with the development of obesity, and adipose tissue represents an important endocrine target for PM 2.5 . In this study, the 3T3-L1 preadipocyte differentiation model was employed to comprehensively explore the adipogenic potential of PM 2.5 . After 8 days of PM 2.5 exposure, adipocyte fatty acid uptake and lipid accumulation were significantly increased, and adipogenic differentiation of 3T3-L1 cells was promoted in a concentrationdependent manner. Transcriptome and lipidome analyses revealed the systematic disruption of transcriptional and lipid profiling at 10 μg/mL PM 2.5 . Functional enrichment and visualized network analyses showed that the peroxisome proliferator-activated receptor (PPAR) pathway and the metabolism of glycerophospholipids, glycerolipids, and sphingolipids were most significantly affected during adipocyte differentiation. Reporter gene assays indicated that PPARγ was activated by PM 2.5 , demonstrating that PM 2.5 promoted adipogenesis by activating PPARγ. The increased transcriptional and protein expressions of PPARγ and downstream adipogenesis-associated markers (e.g., Fabp4 and CD36) were further cross-validated using qRT-PCR and western blot. PM 2.5induced adipogenesis, PPARγ pathway activation, and lipid remodeling were significantly attenuated by the supplementation of a PPARγ antagonist (T0070907). Overall, this study yielded mechanistic insights into PM 2.5 -induced adipogenesis in vitro by identifying the potential biomolecular targets for the prevention of PM 2.5 -induced obesity and related metabolic diseases.

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“…Because air pollution persists and its harm to people is longterm, most studies are aimed at long-term air pollution exposure [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27]. A few studies have shown that short-term air pollution levels can also bring about changes in blood lipids [28][29][30][31][32][33][34][35]. The role of short-term air pollution is helpful for explaining the mechanism and process of blood lipid changes caused by air pollution.…”

Section: Association Between Air Pollution and Blood Lipidsmentioning

confidence: 99%

“…Many studies have reported that air pollutants are significantly associated with the increase in TG, TC, and LDL-C or the decrease in HDL-C. However, most studies reported that air pollution was associated with adverse changes in 1-3 lipid indexes, and the changes in the others are beneficial or not significant [6,10,[12][13][14][15][16][17][18]20,[22][23][24][25][26][27][28][29][30][31][32][33][34][35]38,48]. A few studies reported that air pollution was associated with adverse changes in all four conventional lipid indexes [19,21,56], such as the study of Wang et al, which showed that a 10 µg/m 3 increase in PM 2.5 concentration was associated with a 0.92% increase in TC, a 2.23% increase in TG, a 3.04% increase in LDL-C, and a 2.03% decrease in HDL-C [19].…”

Section: Indicators Of Lipid Healthmentioning

confidence: 99%

Association between Air Pollution and Lipid Profiles

Zhang,

Shi,

et al. 2023

Toxics

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Dyslipidemia is a critical factor in the development of atherosclerosis and consequent cardiovascular disease. Numerous pieces of evidence demonstrate the association between air pollution and abnormal blood lipids. Although the results of epidemiological studies on the link between air pollution and blood lipids are unsettled due to different research methods and conditions, most of them corroborate the harmful effects of air pollution on blood lipids. Mechanism studies have revealed that air pollution may affect blood lipids via oxidative stress, inflammation, insulin resistance, mitochondrial dysfunction, and hypothalamic hormone and epigenetic changes. Moreover, there is a risk of metabolic diseases associated with air pollution, including fatty liver disease, diabetes mellitus, and obesity, which are often accompanied by dyslipidemia. Therefore, it is biologically plausible that air pollution affects blood lipids. The overall evidence supports that air pollution has a deleterious effect on blood lipid health. However, further research into susceptibility, indoor air pollution, and gaseous pollutants is required, and the issue of assessing the effects of mixtures of air pollutants remains an obstacle for the future.

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Dynamic recovery after acute single fine particulate matter exposure in male mice: Effect on lipid deregulation and cardiovascular alterations

Cited by 18 publications

References 53 publications

Multi-omics reveals hypertrophy of adipose tissue and lipid metabolism disorder via mitochondria in young mice under real-ambient exposure to air pollution

Multi-omics reveals hypertrophy of adipose tissue and lipid metabolism disorder via mitochondria in young mice under real-ambient exposure to air pollution

PPARγ As a Potential Target for Adipogenesis Induced by Fine Particulate Matter in 3T3-L1 Preadipocytes

Association between Air Pollution and Lipid Profiles

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