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Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors

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A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 25 December 2026 | Viewed by 4211

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Prof. Dr. Aleksandra Stefanović

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Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, 11000 Belgrade, Serbia
Interests: obesity; pregnancy; lipids; oxidative stress
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Dear Colleagues,

Despite significant progress in addressing major public health issues, obesity remains one of the most pressing global health challenges of the modern era. As a complex disorder, obesity is characterized by numerous altered metabolic processes that promote chronic low-grade inflammation and oxidative stress. Its development involves multiple mechanisms associated with increased risk for various pathological conditions, including insulin resistance, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, cardiovascular diseases, and cancer.

This Special Issue, titled "Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors", aims to explore the complex molecular mechanisms underlying metabolic dysregulation in obesity and their roles in the onset and progression of common obesity-related diseases. We seek to encourage a comprehensive and integrative approach to obesity research.

We welcome original research papers and reviews that offer new insights into altered metabolic pathways, genetic and epigenetic regulation, immunological features, and other molecular factors involved in obesity. A better understanding of these complex molecular mechanisms may help identify potential biomarkers and therapeutic targets for improved risk assessment, prevention, and treatment of obesity-related conditions.

Prof. Dr. Aleksandra Stefanović
Guest Editor

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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.

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Keywords

obesity
inflammation
oxidative stress
obesity-related diseases
adypocitokines

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Published Papers (5 papers)

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Research

24 pages, 13955 KB

Open AccessArticle

Co-Administration of Trans-Resveratrol and L-Carnitine with a High-Fat and High-Carbohydrate Diet Modulates Liver Transcriptome in Obesity-Resistant DBA/2J Mice

by Ivan V. Gmoshinski, Nikita V. Trusov, Vladimir A. Shipelin and Dmitriy B. Nikityuk

Int. J. Mol. Sci. 2026, 27(17), 7808; https://doi.org/10.3390/ijms27177808 - 31 Aug 2026

Viewed by 164

Abstract

This study examined the effects of the trans-resveratrol (Res) and l-carnitine (l-Car) complex (RC) on mice genetically resistant to obesity. Male DBA/2J mice received low (RCl, 25/300 mg/kg BW) or high (RCh, 50/600 mg/kg BW) doses of the RC for 64 days in a control diet (CD) or a high-fat-high-carbohydrate diet (HFCD). Differential expression (DE) of genes in the liver was analyzed using DNA microarrays. HFCD alone altered 471 genes (1.7%) versus CD. In CD-fed mice, RCl and RCh affected 170 (0.6%) and 321 (1.2%) genes, respectively. In HFCD-fed mice, RCl and RCh affected 109 (0.4%) and 223 (0.8%) genes. Opposite DE changes between HFCD and RC + HFCD occurred in immune recognition and fat-storage genes (Ccl24, Fabp7, Cd74, H2-Ab1, Srebf1, etc.). Uniform responses to HFCD and RC + CD were seen in Ppard, Irs-1, Tsku, Cyp26b1, Il1r1, Onecut1, Per1, Nlrd2, Rgs16, Grem2, Klf9, and Lpin1. RC effects were consistent with liver morphology. Key RC-targeted pathways included retinoid metabolism, PPAR signaling, and antigen presentation. In HFCD-fed mice, additional pathways were steroid biosynthesis, oxylipin metabolism, and Jak-STAT signaling. DBA/2J mice may exhibit an innate compensatory response involving PPAR signaling, Srebf1, and Socs2, and the contribution of polymorphisms in these genes merits separate investigation in future studies of obesity resistance. Full article

(This article belongs to the Special Issue Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors)

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16 pages, 1774 KB

Open AccessArticle

High-Fat Diet-Induced Obesity Enhances Small Intestinal Glucose and NaCl Absorption Through Selective Transporter Reprogramming

by Balasubramanian Palaniappan, Niraj Nepal, John Crutchley and Subha Arthur

Int. J. Mol. Sci. 2026, 27(9), 3961; https://doi.org/10.3390/ijms27093961 - 29 Apr 2026

Viewed by 761

Abstract

Metabolic dysfunction, a hallmark of diet-induced obesity (DIO), is increasingly attributed to alterations in intestinal nutrient and electrolyte transport. Yet the mechanisms that drive obesity-associated functional alterations of intestinal transporters remain incompletely understood. In this context, the effects of a high-fat diet (HFD) induced obesity on sodium-dependent glucose co-transporter 1 (SGLT1), Na⁺/H⁺ exchanger 3 (NHE3), and Cl⁻/HCO₃⁻ exchangers (DRA/PAT1), the primary glucose, sodium, and chloride absorptive pathways in mice small intestinal villus cells, were investigated. SGLT1 activity significantly increased in intact villus cells and brush border membrane vesicles (BBMV) from HFD-fed mice. Kinetic analysis demonstrated reduced Km without a change in Vmax, indicating enhanced transporter affinity. Notably, SGLT1 mRNA and protein expression, including BBM localization, were unchanged. Basolateral Na⁺/K⁺-ATPase activity was decreased, excluding enhanced Na⁺ gradient generation as the mechanism for SGLT1 stimulation. In contrast, DRA/PAT1 activity was significantly increased in HFD-fed mice, and kinetic studies revealed elevated Vmax without a change in Km, indicating increased transport capacity. DRA/PAT1 mRNA, total protein, and BBM expression were all significantly elevated. NHE3 activity and expression remained unchanged. These findings demonstrate that DIO enhances intestinal glucose absorption by increasing SGLT1 affinity and chloride absorption by upregulating DRA/PAT1 transcription. These transporter-specific alterations may amplify nutrient absorption and contribute to metabolic dysregulation in obesity. Full article

(This article belongs to the Special Issue Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors)

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17 pages, 667 KB

Open AccessArticle

Ferritin and Liver Steatosis in Children: Interactions Between Metabolic Clustering and PNPLA3 Variants

by Mihaela-Andreea Podeanu, Raluca Elena Sandu, Bianca Ștefănița Vintilescu, Claudiu Marinel Ionele, Ion Rogoveanu, Ioana Streață, Carmen Elena Niculescu, Dan Nicolae Florescu, Sergiu-Marian Cazacu, Ștefania Cornelia Andrei, Adina Maria Barbu and Mioara Desdemona Stepan

Int. J. Mol. Sci. 2026, 27(7), 3044; https://doi.org/10.3390/ijms27073044 - 27 Mar 2026

Viewed by 720

Abstract

Metabolic abnormalities are frequently associated with hepatic steatosis and low-grade inflammation, yet the contributions of iron metabolism and genetic susceptibility are not fully understood. We aimed to investigate the relationship between serum ferritin, hepatic steatosis, metabolic risk clustering, and the PNPLA3 rs738409 gene variant in children. A total of 68 children aged 6–14 years underwent anthropometric, biochemical, imaging, and genetic assessment. Hepatic steatosis was present in 72.1% of participants, with fibrosis greater than F1 in 42.6%. Serum ferritin showed a strong correlation with echographic liver steatosis severity (ρ = 0.804, p < 0.001) and a moderate correlation with the number of metabolic risk components (ρ = 0.482, p < 0.001). The highest metabolic burden occurred in children with low iron and elevated ferritin. While PNPLA3 status did not independently predict ferritin levels, carriers had a significantly higher prevalence of hypertension (50.0% vs. 25.0%, p = 0.038) and a non-significant trend toward low HDL-C (65.0% vs. 42.9%, p = 0.070). Ferritin was associated with metabolic clustering and ultrasound-defined hepatic steatosis, acting as a nonspecific marker of combined metabolic and hepatic alterations. PNPLA3 genotype was not independently related to ferritin or fibrosis in early pediatric disease. Given the cross-sectional design and the relatively small sample size, these findings should be interpreted as exploratory and further studies including larger populations and direct inflammatory markers should be conducted. Full article

(This article belongs to the Special Issue Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors)

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17 pages, 695 KB

Open AccessArticle

Abdominal Obesity, Hepatic Steatosis, Oxidative Stress and Diastolic Dysfunction in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease

by Luca Colangeli, Ilaria Milani, Maria Eugenia Parrotta, Susanna Longo, Alessandro Nucera, Massimo Federici, Simonetta Palleschi, Barbara Rossi, Alessandro Mantovani, Saverio Muscoli, Frida Leonetti, Danila Capoccia, Paolo Sbraccia and Valeria Guglielmi

Int. J. Mol. Sci. 2026, 27(4), 1968; https://doi.org/10.3390/ijms27041968 - 18 Feb 2026

Cited by 1 | Viewed by 1078

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a key contributor to the development of heart failure with preserved ejection fraction in individuals with obesity. This study aimed to investigate whether MASLD and diastolic dysfunction are independently associated with abdominal obesity through shared metabolic and oxidative mechanisms. We conducted a cross-sectional study in a tertiary university hospital including patients aged ≥ 50 years with obesity and MASLD. Clinical, anthropometric, biochemical, and oxidative stress parameters were collected, and hepatic steatosis and fibrosis were assessed using vibration-controlled transient elastography (FibroScan^®). Patients were stratified according to the presence or absence of echocardiographic diastolic dysfunction. A total of 73 patients was included in the analysis and 27.4% had diastolic dysfunction. Patients with diastolic dysfunction were older and had higher body weight, body mass index (BMI) and waist circumference. Markers of hepatic steatosis, including fatty liver index (FLI) and controlled attenuation parameter (CAP), were higher in patients with diastolic dysfunction, whereas fibrosis measures were not. CAP was independently associated with diastolic dysfunction after adjustment for age and sex, but this association was lost after further adjustment for waist circumference, suggesting a mediating role of central adiposity. Plasma glutathione was inversely associated with FLI, but oxidative stress markers were not associated with diastolic dysfunction or steatosis severity. In conclusion, in patients ≥ 50 years with MASLD and obesity, diastolic dysfunction was common and closely related to abdominal obesity, highlighting MASLD as a multisystem condition with early cardiac involvement. Full article

(This article belongs to the Special Issue Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors)

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13 pages, 1707 KB

Open AccessArticle

Effects of Two Moderate-Intensity Aerobic Exercise Prescriptions on Inflammatory Cytokines and Oxidative Stress Biomarkers in Obese Hispanic Females

by Kyung-Shin Park, Paola Canales Gonzalez, Miguel Nieto and Brett S. Nickerson

Int. J. Mol. Sci. 2026, 27(4), 1834; https://doi.org/10.3390/ijms27041834 - 14 Feb 2026

Cited by 1 | Viewed by 697

Abstract

This study examined effects of two moderate-intensity aerobic exercise prescriptions on inflammatory cytokines and oxidative stress biomarkers in middle-aged obese Hispanic females. Fifty-four subjects were randomly assigned to a lower-moderate intensity group (55% VO₂max, LT, n = 18), an upper-moderate intensity group (70% VO₂max, HT, n = 19), or a non-exercise control group (CON, n = 17). Blood samples collected before and after a 12-week intervention were analyzed for tumor necrosis factor-alpha (TNF-α), adiponectin, C-reactive protein (CRP), total antioxidant status (TAS), and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Body fat percentage (%BF) and visceral adipose tissue (VAT) were assessed using dual-energy X-ray absorptiometry. TNF-α significantly decreased in both LT (p = 0.004) and HT (p < 0.001). Significant increases in adiponectin (p = 0.001) and reductions in CRP (p < 0.001) were observed within the HT, whereas these changes were not significant within the LT. TAS significantly increased in both exercise groups (p < 0.001), and 8-OHdG significantly decreased in the HT (p < 0.001) and LT (p = 0.002). Both LT and HT demonstrated significant reductions in %BF (p < 0.001) and VAT (p < 0.05), with no significant changes in CON. Results indicate that moderate-intensity aerobic exercise improves inflammatory and oxidative stress profiles when total exercise volume is matched, regardless of differences in exercise intensity within the moderate range. Although post-intervention differences between groups were not statistically significant, the observation that CRP, adiponectin, and 8-OHdG changed significantly only within HT suggests that exercise intensity may influence biomarker responsiveness and warrants further investigation. Full article

(This article belongs to the Special Issue Advances in Obesity Research: Metabolic Pathways and Pathophysiological Factors)

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