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Epigenetics of Metabolic Diseases

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

Deadline for manuscript submissions: 30 January 2026 | Viewed by 925

Special Issue Editor


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Guest Editor
1. Laboratory of Pharmacology, Department of Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece
2. Institute of Agri-Food and Life Sciences, University Research and Innovation Centre, Hellenic Mediterranean University, 71003 Heraklion, Greece
Interests: epigenetics; DNA methylation; biomarker; classifier; liquid biopsy; metabolic disease; diabetes; AutoML
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Special Issue Information

Dear Colleagues,

Metabolic diseases, including obesity, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), cardiovascular diseases, etc., as well as metabolic syndrome, represent growing challenges in global health. Recent advances in epigenetics have unveiled critical molecular mechanisms linking genetic and environmental factors to metabolic dysregulation and the onset and progression of various metabolic disorders. Epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNA regulation, play key roles in metabolic homeostasis and disease progression.

This Special Issue of IJMS, “Epigenetics of Metabolic Diseases” aims to highlight cutting-edge research on the molecular epigenetic mechanisms underlying metabolic diseases. We invite original research articles and reviews focusing on how epigenetic changes influence metabolic pathways, gene expression, and disease susceptibility. Studies utilizing high-throughput sequencing, single-cell epigenomics, and mechanistic insights into epigenetic regulators are particularly welcome. We encourage multi-omics approaches integrating epigenomics, transcriptomics, and metabolomics to deepen our understanding of metabolic disease pathogenesis. Through this Special Issue, we aim to advance the field of epigenetics in metabolism and foster new perspectives for precision medicine in metabolic disorders.

Dr. Makrina Karaglani
Guest Editor

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Keywords

  • epigenetics
  • metabolic diseases
  • DNA methylation
  • histone modifications
  • non-coding RNAs
  • obesity
  • diabetes
  • metabolic syndrome

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Published Papers (1 paper)

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Research

15 pages, 5472 KB  
Article
Fasting and Postprandial DNA Methylation Signatures in Adipose Tissue from Asymptomatic Individuals with Metabolic Alterations
by Fabiola Escalante-Araiza, Angélica Martínez-Hernández, Humberto García-Ortiz, Eira Huerta-Ávila, José Rafael Villafan-Bernal, Cecilia Contreras-Cubas, Federico Centeno-Cruz, GEMM Family Study, Edna J. Nava-González, José Damián Carrillo-Ruiz, Ernesto Rodriguez-Ayala, Raúl A. Bastarrachea, Francisco Barajas-Olmos and Lorena Orozco
Int. J. Mol. Sci. 2025, 26(23), 11306; https://doi.org/10.3390/ijms262311306 - 22 Nov 2025
Viewed by 347
Abstract
Cardiometabolic phenotypes such as obesity and impaired insulin action are key determinants of type 2 diabetes (T2D). Growing evidence highlights the postprandial state as a critical window in metabolic regulation, where epigenetic mechanisms, particularly DNA methylation in insulin-sensitive tissues, may play pivotal roles. [...] Read more.
Cardiometabolic phenotypes such as obesity and impaired insulin action are key determinants of type 2 diabetes (T2D). Growing evidence highlights the postprandial state as a critical window in metabolic regulation, where epigenetic mechanisms, particularly DNA methylation in insulin-sensitive tissues, may play pivotal roles. However, their dynamics across prandial states in subcutaneous adipose tissue (SAT) remain unclear. We analyzed genome-wide DNA methylation in paired fasting and postprandial SAT biopsies from 29 asymptomatic, drug-naïve individuals classified as controls (n = 8), prediabetes n = 9), or T2D (n = 12). Postprandial samples followed a standardized mixed-meal test. DNA methylation was quantified using the Illumina MethylationEPIC array and analyzed through the Chip Analysis Methylation Pipeline (ChAMP) pipeline. Differential methylation was more pronounced postprandially, especially in the T2D group. After adjusting for age and sex, 4599 differentially methylated CpG sites (DMCs) were identified, with increased hypermethylation in T2D. A total of 130 DMCs across 99 genes, including LCLAT1, HLA-C, ZNF714, and HOOK2, were shared by prediabetes and T2D groups. Over-representation analysis revealed 202 enriched pathways related to insulin resistance, AMPK signaling, and immune responses. Additionally, 110 Differentially Methylated Regions (DMRs), including ZNF577 and AGPAT1, were detected. These findings reveal early, prandial-dependent epigenetic alterations in SAT that precede overt dysglycemia, offering insights into personalized prevention in T2D. Full article
(This article belongs to the Special Issue Epigenetics of Metabolic Diseases)
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