Metabolic Diseases—New Markers and Treatment Pathways

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 2858

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Special Issue Information

Dear Colleagues,

Metabolic diseases encompass a broad range of disorders affecting the body’s metabolism, including diabetes, obesity, and inherited metabolic disorders. Recent advances in biomedical research have identified new biomarkers that may improve the diagnosis, monitoring, and treatment of these conditions. Biomarkers such as circulating metabolites, inflammatory markers, and genetic variations offer insights into disease mechanisms and progression.

Novel treatment pathways are emerging, leveraging these biomarkers for personalized medicine approaches. For instance, the role of gut microbiota in metabolic health has prompted investigations into microbiome-targeted therapies, including prebiotics and probiotics, which may alter metabolic profiles favorably. Additionally, advancements in gene editing technologies, such as CRISPR-Cas9, are being explored to correct specific genetic defects underlying certain metabolic disorders.

Pharmacological developments include new classes of anti-diabetic medications that target metabolic pathways, potentially improving glycemic control while reducing cardiovascular risks. Emerging therapies also focus on the hormonal regulation of appetite and energy expenditure, aiming to tackle obesity at its roots.

Understanding the interplay between genetic, environmental, and lifestyle factors is crucial for developing effective interventions. Continued research into these new markers and treatment strategies offers hope for improving outcomes and the quality of life for individuals affected by metabolic diseases.

Prof. Dr. Anna Różańska-Walędziak
Guest Editor

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Keywords

  • metabolic diseases
  • diabetes
  • obesity
  • biomarkers
  • anti-diabetic medications

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Published Papers (2 papers)

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Research

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19 pages, 1948 KB  
Article
Elucidating Genetic Drivers of Chronic Inflammation in Obesity
by Leyla O. Rashidova, Danila D. Shashnin, Pavel S. Zubeev, Elena P. Abalikhina, Natalia G. Podprugina, Valeriy A. Kozlov, Sergey V. Stasenko, Tatiana A. Mishchenko and Maria V. Vedunova
Biomedicines 2026, 14(2), 447; https://doi.org/10.3390/biomedicines14020447 - 17 Feb 2026
Viewed by 770
Abstract
Background/Objectives: Obesity is characterized by chronic low-grade inflammation, which plays a central role in the development of its metabolic complications. The genetic factors influencing this inflammatory phenotype remain incompletely understood. This study aimed to analyze the associations of functional polymorphisms in genes involved [...] Read more.
Background/Objectives: Obesity is characterized by chronic low-grade inflammation, which plays a central role in the development of its metabolic complications. The genetic factors influencing this inflammatory phenotype remain incompletely understood. This study aimed to analyze the associations of functional polymorphisms in genes involved in extracellular matrix remodeling (MMP2, MMP9, MMP12, COL1A1), metabolism (MTHFR, CYP3A5), and vascular regulation (NOS3, AGTR1) with plasma cytokine profiles and to identify inflammatory subphenotypes in patients with obesity. Methods: The study included 127 individuals, comprising 73 patients with excess body weight (body mass index, BMI ≥ 25 kg/m2) and 54 individuals with normal weight (BMI 18.5–24.9 kg/m2). Genotyping of selected polymorphisms was performed using real-time PCR. Plasma concentrations of 47 cytokines and chemokines were measured by multiplex immunoassay. Results: Nominally significant associations between genetic variants and cytokine levels were identified. Polymorphisms COL1A1 rs1107946 (CA genotype) and MMP9 rs17576 (AG genotype) were associated with a favorable inflammatory profile (decreased IL-6 and increased IL-10, respectively). In contrast, the AGTR1 rs5186 (AC genotipe) variant was associated with elevated TNF-α, IP-10/CXCL10, while the MTHFR rs1801131 (AC genotipe) variant was linked to increased MIP-1β/CCL4, both reflecting a pro-inflammatory shift. Complex, pleiotropic associations were observed for MMP2 rs243865 (elevated IL-7 and Fractalkine/CX3CL1) and NOS3 rs1799983 (elevated MCP-1/CCL2 and Eotaxin/CCL11). Cluster analysis revealed distinct patient subpopulations with differing inflammatory signatures. In one well-defined subgroup, an exploratory model (test R2 = 0.537) identified IL-8, IL-15, and albumin as candidate biomarkers predictive of BMI. Conclusions: The study identifies candidate genetic polymorphisms and inflammatory biomarkers associated with distinct patterns of systemic inflammation in obesity. These hypothesis-generating findings underscore the phenotypic heterogeneity of obesity and provide a basis for further research into the stratification of patients by the risk of developing metabolic complications. Full article
(This article belongs to the Special Issue Metabolic Diseases—New Markers and Treatment Pathways)
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Review

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34 pages, 1175 KB  
Review
From Metabolism to Mind: The Cardio–Metabolic–Brain Axis and the Role of Insulin Resistance—A Review
by Joanna Cielecka, Zuzanna Szkamruk, Maciej Walędziak and Anna Różańska-Walędziak
Biomedicines 2026, 14(2), 394; https://doi.org/10.3390/biomedicines14020394 - 9 Feb 2026
Cited by 1 | Viewed by 1738
Abstract
(1) Background: Insulin resistance (IR) is increasingly recognized not only as a key factor in metabolic and cardiovascular disorders but also as an important contributor to cognitive decline. The growing prevalence of obesity, type 2 diabetes mellitus, and cardiovascular disease (CVD), paralleled by [...] Read more.
(1) Background: Insulin resistance (IR) is increasingly recognized not only as a key factor in metabolic and cardiovascular disorders but also as an important contributor to cognitive decline. The growing prevalence of obesity, type 2 diabetes mellitus, and cardiovascular disease (CVD), paralleled by rising rates of dementia, highlights the need for an integrative model linking these conditions. The emerging cardio–metabolic–brain axis proposes a unified model explaining how biomarkers of metabolic stress, adipose-tissue-derived mediators, and abnormalities in laboratory parameters interact with vascular injury and neurodegeneration. (2) Methods: A comprehensive literature review was conducted using MEDLINE, SCOPUS, and Web of Science databases, complemented by additional searches in Embase and Cochrane Library. Studies from the past decade were screened using keywords such as “insulin resistance”, “cardio-metabolic-brain axis”, “cognitive decline”, and “cardiovascular disease”. Both epidemiological and mechanistic studies were analyzed to summarize current evidence and identify research gaps. (3) Results and Conclusions: Evidence indicates that insulin resistance contributes to endothelial dysfunction, chronic inflammation, and oxidative stress, driving the metabolic abnormalities characteristic of obesity and type 2 diabetes and promoting both atherosclerosis and neurodegeneration. Individuals with elevated IR—regardless of diabetes status—display higher risks of cardiovascular events and measurable cognitive decline. Brain insulin resistance further impairs glucose utilization, disrupts synaptic function, and facilitates amyloid accumulation, reflecting mechanisms observed in Alzheimer’s disease. These findings support IR as a key biomarker linking metabolic stress, vascular injury, and neural vulnerability within the cardio–metabolic–brain axis. Early identification of IR, together with targeted lifestyle and pharmacological interventions, may therefore offer dual benefits for cardiovascular and brain health. Continued longitudinal research is needed to validate this integrative model and refine therapeutic strategies aimed at improving insulin sensitivity. Full article
(This article belongs to the Special Issue Metabolic Diseases—New Markers and Treatment Pathways)
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