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Biomedicines
Special Issues
Epigenetics and Metabolic Disorders
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Epigenetics and Metabolic Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (30 September 2025) | Viewed by 17755

Editor

Dr. Patrik Krumpolec

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Guest Editor
Medirex Group Academy, 949 05 Nitra, Slovakia
Interests: metabolic diseases; inflammatory bowel diseases; genomics; epigenetics

Special Issue Information

Dear Colleagues,

Metabolic diseases represent a wide spectrum of disorders arising from disruptions in the body's metabolic processes. The constantly increasing incidence and prevalence of metabolic disorders make this group of diseases not only an epidemiological issue but also an economic and societal problem.

One of the causes of metabolic diseases is epigenetic changes in the regulation of genes that control metabolic processes. Understanding epigenetic changes in the context of the development of metabolic diseases has the potential to influence processes related to the onset and progression of these diseases and may lead to new strategies in prevention and treatment.

This Special Issue welcomes original research and review articles dedicated to epigenetic processes underlying the onset and development of metabolic diseases. We encourage authors to contribute to this Special Issue with works related to (but not limited to) the following:

  • Prenatal epigenetic changes related to metabolic diseases;
  • Heredity and epigenetic changes underlying metabolic diseases;
  • The role of epigenetics in relationship of environmental factors and metabolic diseases;
  • Therapeutic interventions targeting abnormal epigenetic markers associated with metabolic diseases.

Dr. Patrik Krumpolec
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 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. Biomedicines 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 2600 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

  • metabolic diseases
  • epigenetics
  • DNA methylation
  • histone modification
  • non-coding RNA (ncRNA)-mediated gene regulation
  • heredity
  • environmental factors

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Published Papers (3 papers)

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Research

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17 pages, 3095 KB  
Article
Haplotypes, Genotypes, and DNA Methylation Levels of Neuromedin U Gene Are Associated with Cardio-Metabolic Parameters: Results from the Moli-sani Study
by Fabrizia Noro, Annalisa Marotta, Simona Costanzo, Benedetta Izzi, Alessandro Gialluisi, Amalia De Curtis, Antonietta Pepe, Sarah Grossi, Augusto Di Castelnuovo, Chiara Cerletti, Maria Benedetta Donati, Giovanni de Gaetano, Francesco Gianfagna and Licia Iacoviello
Biomedicines 2025, 13(8), 1906; https://doi.org/10.3390/biomedicines13081906 - 5 Aug 2025
Viewed by 1007
Abstract
Background/Objectives: Neuromedin U (NMU) is a highly conserved gene encoding a neuropeptide involved in the regulation of feeding behavior and energy homeostasis. We aimed to analyze the association between NMU genetic and epigenetic variations and cardio-metabolic parameters in an Italian population to identify [...] Read more.
Background/Objectives: Neuromedin U (NMU) is a highly conserved gene encoding a neuropeptide involved in the regulation of feeding behavior and energy homeostasis. We aimed to analyze the association between NMU genetic and epigenetic variations and cardio-metabolic parameters in an Italian population to identify the role of these variants in cardio-metabolic risk. Methods: A total of 4028 subjects were randomly selected from the Moli-sani study cohort. NMU haplotypes were estimated using seven SNPs located in the gene body and in the promoter region; DNA methylation levels in the promoter region, previously associated with lipid-related variables in the same population, were also used. Results: Among the haplotypes inferred, the haplotype carrying the highest number of minor variants (frequency 16.6%), when compared with the most frequent haplotype, was positively associated with insulin levels, HOMA-IR, and diastolic blood pressure, and negatively with HDL-cholesterol. The multivariable analysis that considered methylation levels along with their interactions with SNPs showed that increased methylation levels in two close CpG sites were associated with higher levels of lipid-related variables. Conclusions: This study supports a role for NMU as a regulator of human metabolism. This finding suggests that NMU could be a potential target for preventive interventions against coronary and cerebrovascular diseases, and that NMU genetic and epigenetic variability may serve as a biomarker for cardio-metabolic risk. Full article
(This article belongs to the Special Issue Epigenetics and Metabolic Disorders)
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Review

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13 pages, 679 KB  
Review
Current Insights into Obesity and m6A Modification
by Chen Meng and Di Yang
Biomedicines 2025, 13(9), 2164; https://doi.org/10.3390/biomedicines13092164 - 5 Sep 2025
Cited by 2 | Viewed by 1895
Abstract
Obesity has emerged as a global health challenge, closely associated with multiple metabolic diseases, such as cardiovascular diseases, type 2 diabetes, and non-alcoholic fatty liver disease. The traditional “calories-in minus calories-out” paradigm is no longer sufficient to explain the heterogeneity of obesity; consequently, [...] Read more.
Obesity has emerged as a global health challenge, closely associated with multiple metabolic diseases, such as cardiovascular diseases, type 2 diabetes, and non-alcoholic fatty liver disease. The traditional “calories-in minus calories-out” paradigm is no longer sufficient to explain the heterogeneity of obesity; consequently, a growing body of research has turned its focus to epigenetic regulation—particularly chemical modifications at the RNA level. N6-methyladenosine (m6A) modification is one of the most abundant epigenetic modifications on RNA, which dynamically regulates the methylation reaction in specific sequences on mRNA through methyltransferases (writers), demethylases (erasers), and binding proteins (readers). Accumulating evidence in recent years has revealed that m6A modification plays a pivotal role in the pathogenesis and progression of obesity, particularly through its regulation of key biological processes, such as adipocyte differentiation, lipid metabolism, and energy homeostasis. Given its critical involvement in metabolic dysregulation, targeting m6A-related mechanisms may offer novel therapeutic avenues for obesity management. This review systematically summarizes the current understanding of m6A modification in obesity, elucidates its underlying molecular mechanisms, and evaluates its potential as a therapeutic target. By integrating recent advances in the field, we aim to provide new perspectives for the development of innovative strategies in obesity treatment. Full article
(This article belongs to the Special Issue Epigenetics and Metabolic Disorders)
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33 pages, 2598 KB  
Review
Integrated Management of Cardiovascular–Renal–Hepatic–Metabolic Syndrome: Expanding Roles of SGLT2is, GLP-1RAs, and GIP/GLP-1RAs
by Nikolaos Theodorakis and Maria Nikolaou
Biomedicines 2025, 13(1), 135; https://doi.org/10.3390/biomedicines13010135 - 8 Jan 2025
Cited by 35 | Viewed by 13771
Abstract
Cardiovascular–Kidney–Metabolic syndrome, introduced by the American Heart Association in 2023, represents a complex and interconnected spectrum of diseases driven by shared pathophysiological mechanisms. However, this framework notably excludes the liver—an organ fundamental to metabolic regulation. Building on this concept, Cardiovascular–Renal–Hepatic–Metabolic (CRHM) syndrome incorporates [...] Read more.
Cardiovascular–Kidney–Metabolic syndrome, introduced by the American Heart Association in 2023, represents a complex and interconnected spectrum of diseases driven by shared pathophysiological mechanisms. However, this framework notably excludes the liver—an organ fundamental to metabolic regulation. Building on this concept, Cardiovascular–Renal–Hepatic–Metabolic (CRHM) syndrome incorporates the liver’s pivotal role in this interconnected disease spectrum, particularly through its involvement via metabolic dysfunction-associated steatotic liver disease (MASLD). Despite the increasing prevalence of CRHM syndrome, unified management strategies remain insufficiently explored. This review addresses the following critical question: How can novel anti-diabetic agents, including sodium–glucose cotransporter-2 inhibitors (SGLT2is), glucagon-like peptide-1 receptor agonists (GLP-1RAs), and dual gastric inhibitory polypeptide (GIP)/GLP-1RA, offer an integrated approach to managing CRHM syndrome beyond the boundaries of traditional specialties? By synthesizing evidence from landmark clinical trials, we highlight the paradigm-shifting potential of these therapies. SGLT2is, such as dapagliflozin and empagliflozin, have emerged as cornerstone guideline-directed treatments for heart failure (HF) and chronic kidney disease (CKD), providing benefits that extend beyond glycemic control and are independent of diabetes status. GLP-1RAs, e.g., semaglutide, have transformed obesity management by enabling weight reductions exceeding 15% and improving outcomes in atherosclerotic cardiovascular disease (ASCVD), diabetic CKD, HF, and MASLD. Additionally, tirzepatide, a dual GIP/GLP-1RA, enables unprecedented weight loss (>20%), reduces diabetes risk by over 90%, and improves outcomes in HF with preserved ejection fraction (HFpEF), MASLD, and obstructive sleep apnea. By moving beyond the traditional organ-specific approach, we propose a unified framework that integrates these agents into holistic management strategies for CRHM syndrome. This paradigm shift moves away from fragmented, organ-centric management toward a more unified approach, fostering collaboration across specialties and marking progress in precision cardiometabolic medicine. Full article
(This article belongs to the Special Issue Epigenetics and Metabolic Disorders)
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