PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study
Obesity is currently one of the most alarming pathological conditions due to the progressive increase in its prevalence. In the last decade, it has been associated with fine particulate matter suspended in the air (PM2.5). The purpose of this study was to explore the mechanistic interaction of PM2.5...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2024-04-01
|
| Series: | Heliyon |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844024049673 |
| _version_ | 1797219295407636480 |
|---|---|
| author | Sagrario Lobato A. Lourdes Castillo-Granada Marcos Bucio-Pacheco Víctor Manuel Salomón-Soto Ramiro Álvarez-Valenzuela Perla Margarita Meza-Inostroza Raúl Villegas-Vizcaíno |
| author_facet | Sagrario Lobato A. Lourdes Castillo-Granada Marcos Bucio-Pacheco Víctor Manuel Salomón-Soto Ramiro Álvarez-Valenzuela Perla Margarita Meza-Inostroza Raúl Villegas-Vizcaíno |
| author_sort | Sagrario Lobato |
| collection | DOAJ |
| description | Obesity is currently one of the most alarming pathological conditions due to the progressive increase in its prevalence. In the last decade, it has been associated with fine particulate matter suspended in the air (PM2.5). The purpose of this study was to explore the mechanistic interaction of PM2.5 with a high-fat diet (HFD) through the differential regulation of transcriptional signatures, aiming to identify the association of these particles with metabolically abnormal obesity. The research design was observational, using bioinformatic methods and an explanatory approach based on Rothman's causal model. We propose three new transcriptional signatures in murine adipose tissue. The sum of transcriptional differences between the group exposed to an HFD and PM2.5, compared to the control group, were 0.851, 0.265, and −0.047 (p > 0.05). The HFD group increased body mass by 20% with two positive biomarkers of metabolic impact. The group exposed to PM2.5 maintained a similar weight to the control group but exhibited three positive biomarkers. Enriched biological pathways (p < 0.05) included PPAR signaling, small molecule transport, adipogenesis genes, cytokine-cytokine receptor interaction, and HIF-1 signaling. Transcriptional regulation predictions revealed CpG islands and common transcription factors. We propose three new transcriptional signatures: FAT-PM2.5-CEJUS, FAT-PM2.5-UP, and FAT-PM2.5-DN, whose transcriptional regulation profile in adipocytes was statistically similar by dietary intake and HFD and exposure to PM2.5 in mice; suggesting a mechanistic interaction between both factors. However, HFD-exposed murines developed moderate metabolically abnormal obesity, and PM2.5-exposed murines developed severe abnormal metabolism without obesity. Therefore, in Rothman's terms, it is concluded that HFD is a sufficient cause of the development of obesity, and PM2.5 is a component cause of severe abnormal metabolism of obesity. These signatures would be integrated into a systemic biological process that would induce transcriptional regulation in trans, activating obesogenic biological pathways, restricting lipid mobilization pathways, decreasing adaptive thermogenesis and angiogenesis, and altering vascular tone thus inducing a severe metabolically abnormal obesity. |
| first_indexed | 2024-04-24T12:31:22Z |
| format | Article |
| id | doaj.art-139e895eb0aa49248de448e9467f829f |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-04-24T12:31:22Z |
| publishDate | 2024-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-139e895eb0aa49248de448e9467f829f2024-04-08T04:08:33ZengElsevierHeliyon2405-84402024-04-01107e28936PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical studySagrario Lobato0A. Lourdes Castillo-Granada1Marcos Bucio-Pacheco2Víctor Manuel Salomón-Soto3Ramiro Álvarez-Valenzuela4Perla Margarita Meza-Inostroza5Raúl Villegas-Vizcaíno6Departamento de Investigación en Salud, Servicios de Salud del Estado de Puebla, 15 South Street 302, Puebla, Mexico; Promoción y Educación para la Salud, Universidad Abierta y a Distancia de México. Universidad Avenue 1200, 1st Floor, quadrant 1-2, Xoco, Benito Juarez, 03330, Mexico City, Mexico; Educación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, Mexico; Corresponding author. Head of Departamento de Investigación en Salud, Servicios de Salud del Estado de Puebla, 15 South Street 302, Puebla, Mexico.Educación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, Mexico; Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, Guelatao Avenue 66, Ejército de Oriente Indeco II ISSSTE, Iztapalapa, 09230, Mexico City, MexicoEducación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, Mexico; Facultad de Biología, Universidad Autónoma de Sinaloa, Americas Avenue, Universitarios Blvd., University City, 80040, Culiacán Rosales, MexicoEducación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, MexicoEducación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, MexicoEducación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, MexicoEducación Superior, Centro de Estudios, “Justo Sierra”, Surutato, Badiraguato, MexicoObesity is currently one of the most alarming pathological conditions due to the progressive increase in its prevalence. In the last decade, it has been associated with fine particulate matter suspended in the air (PM2.5). The purpose of this study was to explore the mechanistic interaction of PM2.5 with a high-fat diet (HFD) through the differential regulation of transcriptional signatures, aiming to identify the association of these particles with metabolically abnormal obesity. The research design was observational, using bioinformatic methods and an explanatory approach based on Rothman's causal model. We propose three new transcriptional signatures in murine adipose tissue. The sum of transcriptional differences between the group exposed to an HFD and PM2.5, compared to the control group, were 0.851, 0.265, and −0.047 (p > 0.05). The HFD group increased body mass by 20% with two positive biomarkers of metabolic impact. The group exposed to PM2.5 maintained a similar weight to the control group but exhibited three positive biomarkers. Enriched biological pathways (p < 0.05) included PPAR signaling, small molecule transport, adipogenesis genes, cytokine-cytokine receptor interaction, and HIF-1 signaling. Transcriptional regulation predictions revealed CpG islands and common transcription factors. We propose three new transcriptional signatures: FAT-PM2.5-CEJUS, FAT-PM2.5-UP, and FAT-PM2.5-DN, whose transcriptional regulation profile in adipocytes was statistically similar by dietary intake and HFD and exposure to PM2.5 in mice; suggesting a mechanistic interaction between both factors. However, HFD-exposed murines developed moderate metabolically abnormal obesity, and PM2.5-exposed murines developed severe abnormal metabolism without obesity. Therefore, in Rothman's terms, it is concluded that HFD is a sufficient cause of the development of obesity, and PM2.5 is a component cause of severe abnormal metabolism of obesity. These signatures would be integrated into a systemic biological process that would induce transcriptional regulation in trans, activating obesogenic biological pathways, restricting lipid mobilization pathways, decreasing adaptive thermogenesis and angiogenesis, and altering vascular tone thus inducing a severe metabolically abnormal obesity.http://www.sciencedirect.com/science/article/pii/S2405844024049673Metabolically abnormal obesityAirborne particulate matterCausalityTranscriptional signatures |
| spellingShingle | Sagrario Lobato A. Lourdes Castillo-Granada Marcos Bucio-Pacheco Víctor Manuel Salomón-Soto Ramiro Álvarez-Valenzuela Perla Margarita Meza-Inostroza Raúl Villegas-Vizcaíno PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study Heliyon Metabolically abnormal obesity Airborne particulate matter Causality Transcriptional signatures |
| title | PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study |
| title_full | PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study |
| title_fullStr | PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study |
| title_full_unstemmed | PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study |
| title_short | PM2.5, component cause of severe metabolically abnormal obesity: An in silico, observational and analytical study |
| title_sort | pm2 5 component cause of severe metabolically abnormal obesity an in silico observational and analytical study |
| topic | Metabolically abnormal obesity Airborne particulate matter Causality Transcriptional signatures |
| url | http://www.sciencedirect.com/science/article/pii/S2405844024049673 |
| work_keys_str_mv | AT sagrariolobato pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT alourdescastillogranada pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT marcosbuciopacheco pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT victormanuelsalomonsoto pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT ramiroalvarezvalenzuela pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT perlamargaritamezainostroza pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy AT raulvillegasvizcaino pm25componentcauseofseveremetabolicallyabnormalobesityaninsilicoobservationalandanalyticalstudy |