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Molecular Research in Obesity and Obesity Related Disorders: 3rd Edition

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

Deadline for manuscript submissions: 30 September 2025 | Viewed by 1939

Special Issue Editor


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Guest Editor
1. Department of Biochemistry and Pharmacogenomics, Faculty of Pharmacy, Medical University of Warsaw, 02-097 Warsaw, Poland
2. Center for Preclinical Research, Medical University of Warsaw, 02-097 Warsaw, Poland
Interests: biochemistry and molecular medicine; molecular and cellular mechanisms of disease pathogenesis; pathogenesis of metabolic disorders; the role of interaction between genetic and environmental factors in the pathogenesis of non-communicable diseases; atherosclerosis; obesity; obesity-related metabolic diseases and cancers
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Special Issue Information

Dear Colleagues,

Obesity, a complex disease involving an excessive amount of body fat, significantly increases the risk of many metabolic diseases and various cancers. Although the main causes of excessive accumulation of adipose tissue are known and numerous efforts have been undertaken to fight the obesogenic environment, the number of overweight and obese people continues to grow. The obesity epidemic intensifies the need for research on the etiology of this disease, especially its molecular mechanisms. There is considerable evidence that supports the role of epigenetic mechanisms, as well as cross-talks between adipocytes and other cells, and between adipose tissue and other tissues in the development of obesity and obesity-related diseases.

For this Special Issue, we seek papers that focus on the molecular mechanisms associated with the development of obesity and obesity-related diseases, including adipocyte biology and adipose tissue disfunction, cell-to-cell metabolic cross-talk and cross-talk between microbiome and adipose tissue, and the molecular mechanisms underlying these processes. Data on specific molecular patterns of adipocytes and other cells involved in the development of adipose tissue dysfunction and its metabolic consequences are welcome. New insights into molecular mechanisms related to changes in eating behaviours that lead to obesity are also of importance.

Prof. Dr. Grażyna Nowicka
Guest Editor

Manuscript Submission Information

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Keywords

  • biochemistry and molecular medicine
  • molecular and cellular mechanisms of disease pathogenesis
  • pathogenesis of metabolic disorders
  • the role of interaction between genetic and environmental factors in the pathogenesis of non-communicable diseases
  • atherosclerosis
  • obesity
  • obesity-related metabolic diseases and cancers

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Published Papers (4 papers)

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Research

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15 pages, 2372 KiB  
Article
Geniposide Mitigates Insulin Resistance and Hepatic Fibrosis via Insulin Signaling Pathway
by Seung-Hyun Oh, Min-Seong Lee and Byung-Cheol Lee
Int. J. Mol. Sci. 2025, 26(16), 8079; https://doi.org/10.3390/ijms26168079 - 21 Aug 2025
Viewed by 44
Abstract
Insulin resistance is a key driver of metabolic disorders, including type 2 diabetes and non-alcoholic fatty liver disease (NAFLD), progressing to non-alcoholic steatohepatitis (NASH). This study investigated the effects of geniposide (GP) on insulin sensitivity and hepatic fibrosis in a high-fat diet (HFD)-induced [...] Read more.
Insulin resistance is a key driver of metabolic disorders, including type 2 diabetes and non-alcoholic fatty liver disease (NAFLD), progressing to non-alcoholic steatohepatitis (NASH). This study investigated the effects of geniposide (GP) on insulin sensitivity and hepatic fibrosis in a high-fat diet (HFD)-induced NASH model. C57BL/6 mice were fed an HFD for five weeks and subsequently divided into normal chow (NC), HFD, HFD with GP 50 mg/kg (GP50), and HFD with GP 100 mg/kg (GP100) groups. The treatments were administered orally for 12 weeks. GP treatment significantly reduced body weight as well as epididymal fat and liver weights, while no differences were observed in food intake. Improvements in glucose and lipid metabolism were observed in oral glucose tolerance tests, homeostatic model assessment of insulin resistance (HOMA-IR), and blood lipid profiles. Histological analyses revealed that GP suppressed adipocyte hypertrophy and hepatic lipid accumulation and hepatic fibrosis. To further elucidate molecular mechanisms of GP, quantitative real-time polymerase chain reaction (qRT-PCR) analysis was conducted in the liver tissue. GP downregulated expression of inflammatory markers, including F4/80, tumor necrosis factor (TNF)-α, and interleukin (IL)-6. GP treatment modulated genes involved in insulin signaling including Janus kinase 2 (JAK2), insulin receptor (INSR), insulin receptor substrate 2 (IRS-2), and protein kinase B (AKT1) gene expression levels. This suggests GP suppresses inflammation and mitigates insulin resistance by activating the INSR–IRS2–Akt pathway. Additionally, GP enhanced adenosine monophosphate-activated protein kinase (AMPK) expression, suggesting its potential role in improving glucose and lipid metabolism. In conclusion, GP improves insulin resistance, inflammation, and hepatic fibrosis, highlighting its therapeutic potential for NASH and related metabolic disorders. Full article
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13 pages, 269 KiB  
Article
Association of Genetically Predicted Activity of AMP Deaminase 1 with Clinical and Biochemical Parameters in Diabetic Individuals with Coronary Artery Disease
by Maria Pietrzak-Nowacka, Ewa Gątarska, Krzysztof Safranow, Agnieszka Boroń, Kazimierz Ciechanowski, Jeremy S. C. Clark, Andrzej Ciechanowicz and Dorota Kostrzewa-Nowak
Int. J. Mol. Sci. 2025, 26(16), 8071; https://doi.org/10.3390/ijms26168071 - 21 Aug 2025
Viewed by 47
Abstract
Some reports indicated the association of rs17602729 and rs34526199 functional polymorphisms of the AMPD1 gene encoding adenosine monophosphate deaminase 1 (AMPD1) with the risk of coronary artery disease (CAD) and/or its intermediate phenotype. Therefore, the aim of our study was to analyze the [...] Read more.
Some reports indicated the association of rs17602729 and rs34526199 functional polymorphisms of the AMPD1 gene encoding adenosine monophosphate deaminase 1 (AMPD1) with the risk of coronary artery disease (CAD) and/or its intermediate phenotype. Therefore, the aim of our study was to analyze the association of both AMPD1 polymorphisms with the predisposition to disease and both clinical and biochemical phenotypes but solely in diabetic individuals with CAD. The study group consisted of 196 adult diabetic individuals with CAD, and the control group comprised 200 healthy newborns. Both AMPD1 polymorphisms were identified by a SNaPshot minisequencing reaction. Clinical and laboratory data were taken from patients’ records. There were no significant differences between both groups in the frequency distributions of AMPD1:rs17602729 and rs34526199 alleles or genotypes. BMI and the frequency of obesity in TT rs17602729 homozygotes (no AMPD1 activity) were significantly lower and the serum concentration of HDL cholesterol was significantly higher compared to other patients. The concentrations of total cholesterol and LDL cholesterol in homozygotes for wild-type AMPD1:rs17602729 (c.34C) and rs34526199 (c.860A) alleles (full AMPD1 activity) were significantly lower compared to its values in other patients. Our results suggest that genetically predicted activity of AMPD1 is associated with variation in body mass and lipid metabolism in diabetic Polish people with CAD. Full article

Review

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20 pages, 1779 KiB  
Review
Epicardial Adipose Tissue—A Novel Therapeutic Target in Obesity Cardiomyopathy
by Kacper Wiszniewski, Anna Grudniewska, Ilona Szabłowska-Gadomska, Ewa Pilichowska-Paszkiet, Beata Zaborska, Wojciech Zgliczyński, Piotr Dudek, Wojciech Bik, Marcin Sota and Beata Mrozikiewicz-Rakowska
Int. J. Mol. Sci. 2025, 26(16), 7963; https://doi.org/10.3390/ijms26167963 - 18 Aug 2025
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Abstract
Obesity is strongly associated with an increased risk of heart failure. Recent studies indicate that epicardial adipose tissue plays a critical role in the development of obesity-related cardiomyopathy. This distinct visceral fat depot, located between the myocardium and the visceral pericardium, is involved [...] Read more.
Obesity is strongly associated with an increased risk of heart failure. Recent studies indicate that epicardial adipose tissue plays a critical role in the development of obesity-related cardiomyopathy. This distinct visceral fat depot, located between the myocardium and the visceral pericardium, is involved in direct cross-talk with the adjacent myocardium, influencing both its structural integrity and electrophysiological function. This review aims to provide an up-to-date overview of the morphological, metabolic, immunological, and functional alterations of this adipose compartment in the context of obesity, and to explore its contribution to the pathogenesis of heart failure. Moreover, the article synthesizes current evidence on the potential cardioprotective effects of emerging anti-obesity pharmacotherapies—particularly GLP-1 and dual GLP-1/GIP receptor agonists—on metabolic pathways associated with epicardial fat that are implicated in obesity-induced cardiomyopathy. Further clinical trials are required to clarify the impact of these therapies on the course and prognosis of heart failure, as well as on the epidemiology and societal burden of the disease. Full article
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21 pages, 333 KiB  
Review
Incorporating Postbiotics into Intervention for Managing Obesity
by Emília Hijová, Izabela Bertková and Jana Štofilová
Int. J. Mol. Sci. 2025, 26(11), 5362; https://doi.org/10.3390/ijms26115362 - 3 Jun 2025
Viewed by 1057
Abstract
Obesity is reaching global epidemic proportions worldwide, posing a significant burden on individual health and society. Altered gut microbiota is considered a key factor in the pathogenesis of many diseases, producing metabolites that contribute to the health-beneficial properties of postbiotics. Postbiotics, bioactive microbial [...] Read more.
Obesity is reaching global epidemic proportions worldwide, posing a significant burden on individual health and society. Altered gut microbiota is considered a key factor in the pathogenesis of many diseases, producing metabolites that contribute to the health-beneficial properties of postbiotics. Postbiotics, bioactive microbial components derived from probiotics, are emerging as a valuable strategy in modern medicine and a promising alternative for managing obesity without the need for live bacteria. This work provides a comprehensive overview of the potential health benefits of postbiotics, particularly in relation to obesity, which represents an important health challenge. Despite the encouraging insights into the health benefits of postbiotics, we highlight the need for further research to clarify the mechanisms and the specific roles of different postbiotic components. Integrating postbiotics into health interventions has the potential to enhance preventive care and significantly improve health outcomes in at-risk populations. Full article
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