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Environmental Toxicant Exposures and Metabolic Disease
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Environmental Toxicant Exposures and Metabolic Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (30 January 2023) | Viewed by 9665

Special Issue Editor

Prof. Dr. Todd Leff

E-Mail Website
Guest Editor
Wayne State University School of Medicine, Center for Integrative Metabolic and Endocrine Research, Detroit, MI 48201, USA
Interests: molecular biology of diabetes and insulin resistance; regulation of gene expression; nuclear receptors; environmental toxicology

Special Issue Information

Dear Colleagues,

The rates of metabolic diseases, especially obesity and type 2 diabetes mellitus, have been on the rise worldwide for the last several decades. The primary factors contributing to the increased incidence of these syndromes are a sedentary lifestyle and excess caloric consumption. However, there are likely to be numerous less well understood environmental factors that modify disease risk and contribute to the high rates of diabetes and obesity in the general population. Among the factors that may fall into this category are exposures to a wide variety of environmental chemicals found in both the built and natural environment. While there are numerous examples of environmental toxicants that have well-characterized negative effects on specific physiological processes, there is less understanding of how environmental chemicals alter susceptibility to chronic diseases that are already present in high levels in the general population. The goal of this Special Issue is report current research activities aimed at understanding the contribution of environmental chemical exposure on the susceptibility and/or severity of diabetes and obesity. We invite submissions of review articles and primary research articles that address any aspect of this general problem. This includes research on the interaction of any known natural or man-made chemical or toxicant with human or animal model physiology. Articles addressing this problem at any biological level, from molecular mechanism studies to epidemiology, are welcome.

Prof. Dr. Todd Leff
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • environmental toxicants
  • chemical exposures
  • metabolic disease
  • diabetes
  • obesity
  • endocrine disruptors
  • metals
  • PFASs
  • organic pollutants

Published Papers (5 papers)

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Research

19 pages, 2618 KiB  
Article
Concentration of Polycyclic Aromatic Hydrocarbons (PAHs) in Human Serum and Adipose Tissues and Stimulatory Effect of Naphthalene in Adipogenesis in 3T3-L1 Cells
by Ewa Mlyczyńska, Alice Bongrani, Christelle Rame, Małgorzata Węgiel, Anna Maślanka, Piotr Major, Piotr Zarzycki, Pierre-Henri Ducluzeau, Arnaud De Luca, Celine Bourbao-Tournois, Pascal Froment, Agnieszka Rak and Joëlle Dupont
Int. J. Mol. Sci. 2023, 24(2), 1455; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24021455 - 11 Jan 2023
Cited by 2 | Viewed by 1845
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are one of the most prevalent classes of environmental pollutants. Some evidence shows that PAHs could be involved in human obesity. However, little is known about the distribution patterns of PAHs in human adipose tissue (AT) and the role [...] Read more.
Polycyclic aromatic hydrocarbons (PAHs) are one of the most prevalent classes of environmental pollutants. Some evidence shows that PAHs could be involved in human obesity. However, little is known about the distribution patterns of PAHs in human adipose tissue (AT) and the role of PAHs on adipogenesis/lipogenesis. The aims of this pilot study were to determine concentrations of 16 PAHs defined as high-priority pollutants in the plasma and adipose tissue of French and Polish bariatric patients, as well as their correlation with body mass index (BMI), plasma and AT adipokines expression levels. We finally investigated the role of naphthalene on cell proliferation, viability, and differentiation in 3T3-L1 preadipocytes. The concentration of most PAHs was similar in the three types of AT and it was significantly higher in AT as compared to plasma, suggesting bioaccumulation. Polish patients had higher PAH levels in AT than French ones. Only the concentration of naphthalene in AT was positively correlated with the BMI and serum or adipose chemerin, adiponectin and resistin expression, in French but not in Polish patients, who had significantly higher BMIs. Moreover, naphthalene exposure increased the cell proliferation of 3T3-L1 preadipocytes and lipogenesis, and increased the expression of genes involved in adipogenesis after cell differentiation. Taken together, PAHs and more particularly naphthalene could be an obesogenic molecule and increase the risk of obesity. Full article
(This article belongs to the Special Issue Environmental Toxicant Exposures and Metabolic Disease)
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15 pages, 496 KiB  
Article
Exposure to Endocrine Disruptors (Di(2-Ethylhexyl)phthalate (DEHP) and Bisphenol A (BPA)) in Women from Different Residing Areas in Italy: Data from the LIFE PERSUADED Project
by Fabrizia Carli, Sabrina Tait, Luca Busani, Demetrio Ciociaro, Veronica Della Latta, Anna Paola Pala, Annalisa Deodati, Andrea Raffaelli, Filippo Pratesi, Raffaele Conte, Francesca Maranghi, Roberta Tassinari, Enrica Fabbrizi, Giacomo Toffol, Stefano Cianfarani, Cinzia La Rocca, Amalia Gastaldelli and LIFE PERSUADED Project Group
Int. J. Mol. Sci. 2022, 23(24), 16012; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232416012 - 16 Dec 2022
Cited by 6 | Viewed by 1478
Abstract
Phthalates and bisphenol A (BPA) are plasticizers used in many industrial products that can act as endocrine disruptors and lead to metabolic diseases. During the LIFE PERSUADED project, we measured the urinary concentrations of BPA and Di(2-ethylhexyl)phthalate (DEHP) metabolites in 900 Italian women [...] Read more.
Phthalates and bisphenol A (BPA) are plasticizers used in many industrial products that can act as endocrine disruptors and lead to metabolic diseases. During the LIFE PERSUADED project, we measured the urinary concentrations of BPA and Di(2-ethylhexyl)phthalate (DEHP) metabolites in 900 Italian women representative of the Italian female adult population (living in the north, centre, and south of Italy in both rural and urban areas). The whole cohort was exposed to DEHP and BPA with measurable levels above limit of detection in more than 99% and 95% of the samples, respectively. The exposure patterns differed for the two chemicals in the three macro-areas with the highest urinary levels for DEHP in south compared to central and northern Italy and for BPA in northern compared to central and southern Italy. BPA levels were higher in women living in urban areas, whereas no difference between areas was observed for DEHP. The estimated daily intake of BPA was 0.11 μg/kg per day, about 36-fold below the current temporary tolerable daily intake of 4 μg/kg per day established by the EFSA in 2015. The analysis of cumulative exposure showed a positive correlation between DEHP and BPA. Further, the reduction of exposure to DEHP and BPA, through specific legislative measures, is necessary to limit the harmfulness of these substances. Full article
(This article belongs to the Special Issue Environmental Toxicant Exposures and Metabolic Disease)
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22 pages, 3714 KiB  
Article
BDE-47, -99, -209 and Their Ternary Mixture Disrupt Glucose and Lipid Metabolism of Hepg2 Cells at Dietary Relevant Concentrations: Mechanistic Insight through Integrated Transcriptomics and Proteomics Analysis
by Marialuisa Casella, Gabriele Lori, Lucia Coppola, Cinzia La Rocca and Sabrina Tait
Int. J. Mol. Sci. 2022, 23(22), 14465; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214465 - 21 Nov 2022
Cited by 3 | Viewed by 1557
Abstract
Polybrominated diphenyl ethers (PBDEs) are persistent organic chemicals implied as flame retardants. Humans are mainly exposed to BDE-47, -99, and -209 congeners by diet. PBDEs are metabolic disruptors with the liver as the main target organ. To investigate their mode of action at [...] Read more.
Polybrominated diphenyl ethers (PBDEs) are persistent organic chemicals implied as flame retardants. Humans are mainly exposed to BDE-47, -99, and -209 congeners by diet. PBDEs are metabolic disruptors with the liver as the main target organ. To investigate their mode of action at a human-relevant concentration, we exposed HepG2 cells to these congeners and their mixture at 1 nM, analyzing their transcriptomic and proteomic profiles. KEGG pathways and GSEA Hallmarks enrichment analyses evidenced that BDE-47 disrupted the glucose metabolism and hypoxia pathway; all the congeners and the MIX affected lipid metabolism and signaling Hallmarks regulating metabolism as mTORC1 and PI3K/AKT/MTOR. These results were confirmed by glucose secretion depletion and increased lipid accumulation, especially in BDE-47 and -209 treated cells. These congeners also affected the EGFR/MAPK signaling; further, BDE-47 enriched the estrogen pathway. Interestingly, BDE-209 and the MIX increased ERα gene expression, whereas all the congeners and the MIX induced ERβ and PPARα. We also found that PBDEs modulated several lncRNAs and that HNRNAP1 represented a central hub in all the four interaction networks. Overall, the PBDEs investigated affected glucose and lipid metabolism with different underlying modes of action, as highlighted by the integrated omics analysis, at a dietary relevant concentration. These results may support the mechanism-based risk assessment of these compounds in relation to liver metabolism disruption. Full article
(This article belongs to the Special Issue Environmental Toxicant Exposures and Metabolic Disease)
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15 pages, 6375 KiB  
Article
Transcriptome Analysis of Particulate Matter 2.5-Induced Abnormal Effects on Human Sebocytes
by Hye-Won Na, Hyun Soo Kim, Hyunjung Choi, Nari Cha, Young Rok Seo, Yong Deog Hong and Hyoung-June Kim
Int. J. Mol. Sci. 2022, 23(19), 11534; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911534 - 29 Sep 2022
Cited by 1 | Viewed by 1742
Abstract
Particulate matter 2.5 (PM2.5), an atmospheric pollutant with an aerodynamic diameter of <2.5 μm, can cause serious human health problems, including skin damage. Since sebocytes are involved in the regulation of skin homeostasis, it is necessary to study the effects of [...] Read more.
Particulate matter 2.5 (PM2.5), an atmospheric pollutant with an aerodynamic diameter of <2.5 μm, can cause serious human health problems, including skin damage. Since sebocytes are involved in the regulation of skin homeostasis, it is necessary to study the effects of PM2.5 on sebocytes. We examined the role of PM2.5 via the identification of differentially expressed genes, functional enrichment and canonical pathway analysis, upstream regulator analysis, and disease and biological function analysis through mRNA sequencing. Xenobiotic and lipid metabolism, inflammation, oxidative stress, and cell barrier damage-related pathways were enriched; additionally, PM2.5 altered steroid hormone biosynthesis and retinol metabolism-related pathways. Consequently, PM2.5 increased lipid synthesis, lipid peroxidation, inflammatory cytokine expression, and oxidative stress and altered the lipid composition and expression of factors that affect cell barriers. Furthermore, PM2.5 altered the activity of sterol regulatory element binding proteins, mitogen-activated protein kinases, transforming growth factor beta-SMAD, and forkhead box O3-mediated pathways. We also suggest that the alterations in retinol and estrogen metabolism by PM2.5 are related to the damage. These results were validated using the HairSkin® model. Thus, our results provide evidence of the harmful effects of PM2.5 on sebocytes as well as new targets for alleviating the skin damage it causes. Full article
(This article belongs to the Special Issue Environmental Toxicant Exposures and Metabolic Disease)
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18 pages, 7191 KiB  
Article
Recombinant FGF21 Attenuates Polychlorinated Biphenyl-Induced NAFLD/NASH by Modulating Hepatic Lipocalin-2 Expression
by Hye Young Kim and Young Hyun Yoo
Int. J. Mol. Sci. 2022, 23(16), 8899; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23168899 - 10 Aug 2022
Cited by 4 | Viewed by 2266
Abstract
Although recent studies have demonstrated that polychlorinated biphenyls (PCB) exposure leads to toxicant-associated steatohepatitis, the underlying mechanism of this condition remains unsolved. Male C57Bl/6 mice fed a standard diet (SD) or 60% high fat diet (HFD) were exposed to the nondioxin-like PCB mixture [...] Read more.
Although recent studies have demonstrated that polychlorinated biphenyls (PCB) exposure leads to toxicant-associated steatohepatitis, the underlying mechanism of this condition remains unsolved. Male C57Bl/6 mice fed a standard diet (SD) or 60% high fat diet (HFD) were exposed to the nondioxin-like PCB mixture Aroclor1260 or dioxin-like PCB congener PCB126 by intraperitoneal injection for a total of four times for six weeks. We observed hepatic injury, steatosis, inflammation, and fibrosis in not only the Aroclor1260-treated mice fed a HFD but the PCB126-treated mice fed either a SD or a HFD. We also observed that both types of PCB exposure induced hepatic iron overload (HIO). Noticeably, the expression of hepatic lipocalin-2 (LCN2) was significantly increased in the PCB-induced nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) models. The knockdown of LCN2 resulted in improvement of PCB-induced lipid and iron accumulation in vitro, suggesting that LCN2 plays a pivotal role in PCB-induced NAFLD/NASH. We observed that recombinant FGF21 improved hepatic steatosis and HIO in the PCB-induced NAFLD/NASH models. Importantly, recombinant FGF21 reduced the PCB-induced overexpression of hepatic LCN2 in vivo and in vitro. Our findings indicate that recombinant FGF21 attenuates PCB-induced NAFLD/NASH by modulating hepatic lipocalin-2 expression. Our data suggest that hepatic LCN2 might represent a suitable therapeutic target for improving PCB-induced NAFLD/NASH accompanying HIO. Full article
(This article belongs to the Special Issue Environmental Toxicant Exposures and Metabolic Disease)
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