The Effects of Trace Elements and Endocrine-Disrupting Compounds on Metabolic Health

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Environmental Metabolomics".

Deadline for manuscript submissions: 15 August 2026 | Viewed by 698

Editors


E-Mail Website
Guest Editor
Department of Toxicology, Dairy Technology and Food Storage, West Pomeranian University of Technology in Szczecin, 71-459 Szczecin, Poland
Interests: trace elements; micronutrients; dietary exposure; mineral bioavailability; trace element toxicity; nutritional determinants; food safety; health risk assessment; oxidative stress; element metabolism; human nutrition
Special Issues, Collections and Topics in MDPI journals

E-Mail
Guest Editor
Department of Toxicology, Dairy Technology and Food Storage, West Pomeranian University of Technology in Szczecin, Papieża Pawła VI 3, 71-459 Szczecin, Poland
Interests: environmental toxicology; food safety; instrumental analysis; chemical contaminants (heavy metals, pesticides, PCBs, PAHs, and others) in food, beverages, drinking water, breast milk, and blood
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, entitled "The Effects of Trace Elements and Endocrine-Disrupting Compounds on Metabolic Health", is devoted to the role of trace elements and endocrine-active compounds in the proper functioning of human metabolic health.

Trace Elements can play a dual role in ensuring metabolic health: they can be essential (in which case it is necessary to ensure adequate levels in the body) but also insignificant or even harmful (in the case of toxic elements). Despite the proven impact of these elements on the development of inflammation in the body, oxidative stress, and the normal aging process of cells, their impact continues to be marginalized. Some of these elements, such as cadmium, lead, mercury, and arsenic, are also classified as endocrine-disrupting chemicals (EDCs).

Endocrine-disrupting compounds (including BPA, phthalates, pesticides, parabens, and PCBs) disrupt metabolic health by acting as endocrine disruptors, causing inflammation, oxidative stress, and altering the gut microbiota.

Trace elements and endocrine-disrupting compounds can damage cells, disrupt insulin signaling, interfere with energy utilization, and overload the body's detoxification systems, leading to an increased risk of obesity, type 2 diabetes, fatty liver disease, and insulin resistance.

When analyzing the importance of elements and endocrine-active substances in ensuring metabolic health, particular attention should be paid to the following:

  • Dose–response relationships;
  • Multi-element interactions;
  • Individual variability (genetics, gender, diet, and environmental exposure).

Understanding all these aspects will contribute to the development of new targeted strategies for the prevention and treatment of metabolic disorders.

In light of recent findings, we invite you to submit articles on the impact of trace elements and endocrine-active substances on metabolic health.

Dr. Kamila Pokorska-Niewiada
Dr. Agata Witczak
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • the role of trace elements and/or EDCs in the development of metabolic syndrome
  • trace elements and endocrine-active substances in biological samples, their potential use as biomarkers of metabolic disorders
  • progress in research on multifactorial relationships determining metabolic health/development of metabolic diseases
  • progress in clinical research on the importance of elements and EDCs in metabolic pathways
  • the impact of genetic and environmental disorders on metabolite levels and fluxes

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

16 pages, 3170 KB  
Article
Integrated Multi-Omics Links Bisphenol AF (BPAF) Exposure to Hepatic Lipid Metabolism Disruption via Succinate Dehydrogenase Dysfunction and Mitochondrial Impairment
by Ning Wang, Jing Xu, Jing Leng, Jia-Le Xu, Da-Sheng Lu, Fan Zhang, Dong-Sheng Yu, Ke-Lei Qian, Gong-Hua Tao, Ping Xiao and Xin-Yu Hong
Metabolites 2026, 16(7), 440; https://doi.org/10.3390/metabo16070440 - 24 Jun 2026
Viewed by 327
Abstract
Background/Objective: Bisphenol AF (BPAF), a fluorinated analogue of bisphenol A, is an environmental contaminant associated with hepatotoxicity and metabolic disruption. However, the systematic molecular mechanisms linking early transcriptional events to metabolic dysfunction in the liver remain poorly defined. The aim of this study [...] Read more.
Background/Objective: Bisphenol AF (BPAF), a fluorinated analogue of bisphenol A, is an environmental contaminant associated with hepatotoxicity and metabolic disruption. However, the systematic molecular mechanisms linking early transcriptional events to metabolic dysfunction in the liver remain poorly defined. The aim of this study is to elucidate the association between BPAF exposure and hepatic lipid accumulation by integrating transcriptomics, cellular metabolomics, and targeted phenotypic assays. Methods: We performed RNA-sequencing on livers from mice exposed to BPAF (0.1–10 mg/kg/day, 28 days), and performed non-targeted metabolomics on AML12 murine hepatocytes co-cultured with RAW264.7 macrophages in a Transwell system (0–2500 nM BPAF, 48 h). Key metabolic pathways were identified through integrated bioinformatics and validated using enzymatic assays, qRT-PCR, Western blotting, and phenotypic staining (lipid droplets, ROS). Results: Multi-omics integration revealed significant disruption of PPAR signaling and the tricarboxylic acid (TCA) cycle. A striking dose-dependent accumulation of succinate was observed in exposed cells, concomitant with a significant inhibition of succinate dehydrogenase (SDH) activity (52% reduction at 2500 nM, p < 0.001). Transcriptomic data confirmed the downregulation of mitochondrial fatty acid β-oxidation genes. Phenotypic validation indicated that BPAF exposure is associated with oxidative stress, pro-inflammatory cytokine release (TNF-α, IL-6), and pronounced intracellular lipid droplet accumulation in hepatocytes. Conclusions: This study suggests that BPAF exposure is associated with SDH dysfunction, TCA cycle arrest, and lipid dysregulation. Whether BPAF directly inhibits SDH or acts through upstream mitochondrial targets warrants further structural and kinetic investigation. Full article
Show Figures

Graphical abstract

Back to TopTop