PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study

Lobato, Sagrario; Castillo-Granada, A. Lourdes; Bucio-Pacheco, Marcos; Salomón-Soto, Víctor Manuel; Álvarez-Valenzuela, Ramiro; Meza-Inostroza, Perla Margarita; Villegas-Vizcaíno, Raúl

doi:10.1016/j.heliyon.2024.e28936

Heliyon

2024

DOI: 10.1016/j.heliyon.2024.e28936

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PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study

Sagrario Lobato,

A. Lourdes Castillo-Granada,

Marcos Bucio-Pacheco

et al.

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2024

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Cited by 2 publications

References 136 publications

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Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

Lobato,

Salomón-Soto,

Espinosa-Méndez

et al. 2024

Biomolecules

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Obesity, influenced by environmental pollutants, can lead to complex metabolic disruptions. This systematic review and meta-analysis examined the molecular mechanisms underlying metabolically abnormal obesity caused by exposure to a high-fat diet (HFD) and fine particulate matter (PM2.5). Following the PRISMA guidelines, articles from 2019 to 2024 were gathered from Scopus, Web of Science, and PubMed, and a random-effects meta-analysis was performed, along with subgroup analyses and pathway enrichment analyses. This study was registered in the Open Science Framework. Thirty-three articles, mainly case–control studies and murine models, were reviewed, and they revealed that combined exposure to HFD and PM2.5 resulted in the greatest weight gain (82.835 g, p = 0.048), alongside increases in high-density lipoproteins, insulin, and the superoxide dismutase. HFD enriched pathways linked to adipocytokine signaling in brown adipose tissue, while PM2.5 impacted genes associated with fat formation. Both exposures downregulated protein metabolism pathways in white adipose tissue and activated stress-response pathways in cardiac tissue. Peroxisome proliferator-activated receptor and AMP-activated protein kinase signaling pathways in the liver were enriched, influencing non-alcoholic fatty liver disease. These findings highlight that combined exposure to HFD and PM2.5 amplifies body weight gain, oxidative stress, and metabolic dysfunction, suggesting a synergistic interaction with significant implications for metabolic health.

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Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

Lobato,

Salomón-Soto,

Espinosa-Méndez

et al. 2024

Biomolecules

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Assessment of Cytotoxicity and Genotoxicity Induced by Diesel Exhaust Particles (DEPs) on Cell Line A549 and the Potential Role of Amide-Functionalized Carbon Nanotubes as Fuel Additive

Pino,

Alvarado,

Rojas

et al. 2024

Energies

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Epidemiological studies have consistently linked air pollution to severe health risks. One strategy to reduce the impact of combustion products from engines is adding additives to the fuel. Potential benefits have been observed in terms of performance and emissions, as well as in decreasing fuel consumption. However, the associated emission of particulate matter into the environment may have unforeseen health effects. This study examines the effects of diesel exhaust particles (DEPs) from diesel fuel mixed with amide-functionalized carbon nanotubes (CNTF). The aim is to analyze the properties of DEPs and determine their toxic effects on lung cells. The DEPs were characterized using scanning and transmission electron microscopy, while the polycyclic aromatic hydrocarbons (PAHs) were analyzed through gas chromatography. Various assays were conducted to assess cell viability, apoptosis, oxidative stress, and DNA damage. The addition of CNTF to diesel fuel altered the morphology and size of the particles, as well as the quantity and composition of PAHs. At the cellular level, diesel DEPs induce higher levels of reactive oxygen species (ROS) production, DNA damage, apoptosis, and cytotoxicity compared to both CNTF and diesel–CNTF DEPs. These findings suggest that the nano-additives enhance energy efficiency by reducing pollutants without significantly increasing cell toxicity.

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PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study

Cited by 2 publications

References 136 publications

Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

Assessment of Cytotoxicity and Genotoxicity Induced by Diesel Exhaust Particles (DEPs) on Cell Line A549 and the Potential Role of Amide-Functionalized Carbon Nanotubes as Fuel Additive

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