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Biomedicines
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Advanced Research in Metabolic Syndrome (2nd Edition)
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Advanced Research in Metabolic Syndrome (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 2732

Special Issue Editor

Dr. Balazs Varga

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary
Interests: diabetes; hypercholesterolaemia; microcirculation; heart; retina; brain; blood vessels; pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of Biomedicines focuses on advanced research in metabolic syndrome, regardless of whether it is preclinical drug development research on laboratory animals or clinical research carried out with bioactive agents. As metabolic syndrome is highly diverse, affecting many organs (heart, brain, blood vessels, kidney, retina, etc.), and the intertwined diseases of the syndrome, such as obesity, diabetes, dyslipidemia, and hypertension, pose major challenges themselves, advanced therapeutic approaches developed against the syndrome can be of great benefit. Even less obviously related diseases—such as metabolic syndrome-related dementia types, endocrine function disorders, or microbiome changes—may also be of interest to readers. Investigations of the prevention and treatment of macro- and microcirculatory damage associated with the different aforementioned diseases of metabolic syndrome are most welcome, but studies on other well-recognized pathways related to the syndrome, such as oxidative stress, inflammation, and necro-apopto-autophagy, are also welcome.

Dr. Balazs Varga
Guest Editor

Manuscript Submission Information

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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

  • obesity
  • diabetes
  • dyslipidemia
  • hypertension
  • microcirculatory damage
  • ischemia–reperfusion
  • necro-apopto-autophagy
  • laboratory animals
  • bioactive agents

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Published Papers (3 papers)

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Research

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11 pages, 273 KB  
Article
Analysis of Genetic Variants MTHFR C677T, ACE I/D, AT1R A1166C and eNOS 4a/b in the Context of Essential Hypertension Susceptibility
by Remus Nica, Silvia Nica, Luciana Teodora Rotaru, Mihai Toma, Lavinia Mariana Berca, Dănuț Cimponeriu and Roxana Măciucă
Biomedicines 2025, 13(11), 2807; https://doi.org/10.3390/biomedicines13112807 - 18 Nov 2025
Viewed by 423
Abstract
Arterial hypertension (AH) is an important risk factor for cardiovascular diseases, a group of diseases that constitutes the most frequent cause of death worldwide. Most AH patients globally are diagnosed with essential hypertension (EH), since they do not present an identifiable cause for [...] Read more.
Arterial hypertension (AH) is an important risk factor for cardiovascular diseases, a group of diseases that constitutes the most frequent cause of death worldwide. Most AH patients globally are diagnosed with essential hypertension (EH), since they do not present an identifiable cause for high blood pressure (HBP). The aim of this study was to assess the associations between EH and genetic variants MTHFR C677T, ACE I/D, AT1R A1166C and eNOS 4a/b in the adult Caucasian population of Romania. Methods: A case–control study was conducted including 845 EH patients and 845 controls. Clinical, para-clinical and lifestyle data were collected from each patient, as well as blood samples for genotyping the polymorphisms of four candidate genes for EH—MTHFR C677T (rs1801133), ACE I/D (rs4646994), AT1R A1166C (rs5186) and eNOS 4a/b—using PCR-based methods. Results: EH was associated with both genetic and environmental factors. Carriers of ACE DD and MTHFR TT genotypes presented an increased risk for EH (ACE DD: OR = 1.44, p = 0.0007; MTHFR TT: OR = 1.46, p = 0.0007). Lifestyle (smoking, physical activity) aspects were associated with EH. The risk of EH increased when both polymorphisms were associated with smoking (ACE DD: OR = 1.62, p = 0.0005; MTHFR TT: OR = 1.68, p = 0.0004). Conclusions: Our findings indicate that ACE I/D and MTHFR C677T may play a role in EH susceptibility, whereas polymorphisms AT1R A1166C and eNOS 4a/b do not appear to be associated. Furthermore, the interaction between genetic factors (ACE I/D, MTHFR C677T) and lifestyle factors such as smoking suggests an increased risk for developing essential hypertension. Full article
(This article belongs to the Special Issue Advanced Research in Metabolic Syndrome (2nd Edition))
14 pages, 2235 KB  
Article
Comparison of Anti-Obesity Effects of Ginger Extract Alone and Mixed with Long Pepper Extract
by Gunju Song, Hyein Han, Heegu Jin, Jongwon Kim, Hyeongmin Kim, Yi-Seul Seo, Heewon Song and Boo-Yong Lee
Biomedicines 2025, 13(9), 2077; https://doi.org/10.3390/biomedicines13092077 - 26 Aug 2025
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Abstract
Background/Objectives: Obesity is a chronic metabolic disorder characterized by the excessive expansion of adipose tissue and impaired energy homeostasis. Natural products, such as plant extracts, are gaining attention as potential anti-obesity agents. This study aimed to evaluate and compare the anti-obesity effects of [...] Read more.
Background/Objectives: Obesity is a chronic metabolic disorder characterized by the excessive expansion of adipose tissue and impaired energy homeostasis. Natural products, such as plant extracts, are gaining attention as potential anti-obesity agents. This study aimed to evaluate and compare the anti-obesity effects of ginger (Zingiber officinale Roscoe) extract alone and as a mixture with long pepper (Piper longum L.) extract in a mouse model of high-fat diet-induced obesity. Methods: Male ICR mice were fed a high-fat diet to induce obesity and were orally administered ginger extract (60 mg/kg/day) or a 1:1 mixture of ginger and long pepper extracts (30 mg/kg/day each) for 8 weeks. Body weight, fat mass, glucose tolerance, and serum lipid levels were measured. Results: Ginger extract alone significantly reduced body weight gain and visceral and subcutaneous fat accumulation and improved glucose homeostasis and serum lipid profiles compared to the high-fat diet group. These effects were more pronounced than those observed with the mixture group. Ginger extract upregulated lipolytic markers via activation of the protein kinase A (PKA) signaling pathway and increased expression of uncoupling protein 1 (UCP1), indicating browning of white adipose tissue. Conclusions: Ginger extract alone exhibited significant anti-obesity effects compared to the mixture with long pepper extract. These findings suggest that ginger extract may serve as a promising natural agent for the prevention and management of obesity-related metabolic dysfunction. Full article
(This article belongs to the Special Issue Advanced Research in Metabolic Syndrome (2nd Edition))
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Review

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29 pages, 1131 KB  
Review
Bisphenol F and Steatotic Liver Disease: Resolving the PXR Paradox Through Stress Pathway Mechanisms
by Enwar Abdalkarim AbdalHussin, Zariyantey Abd Hamid, Muhd Hanis Md Idris, Maizatul Hasyima Omar and Izatus Shima Taib
Biomedicines 2026, 14(1), 30; https://doi.org/10.3390/biomedicines14010030 - 22 Dec 2025
Abstract
Steatotic liver disease (SLD) represents a major global health burden, with environmental toxicants emerging as critical contributors alongside metabolic dysfunction. Bisphenol F (BPF), an increasingly prevalent replacement for bisphenol A, is widely detected in human biological samples and environment, yet its hepatotoxic mechanisms [...] Read more.
Steatotic liver disease (SLD) represents a major global health burden, with environmental toxicants emerging as critical contributors alongside metabolic dysfunction. Bisphenol F (BPF), an increasingly prevalent replacement for bisphenol A, is widely detected in human biological samples and environment, yet its hepatotoxic mechanisms remain incompletely characterized. This review synthesizes current evidence on BPF-induced SLD, with a particular focus on resolving the “pregnane X receptor (PXR) paradox”, the mismatch between BPF’s weak direct activation of PXR and the PXR-like metabolic effects observed in vivo. Comprehensive analysis of mechanistic pathways reveals that BPF-induced SLD develops predominantly through PXR-independent mechanisms involving oxidative stress, endoplasmic reticulum dysfunction, Drp1-mediated mitochondrial fission, NLRP3/NF-κB-driven inflammation, dysregulated post-translational modifications, and epigenetic remodelling. These converging pathways collectively disrupt hepatic lipid metabolism, promote triglyceride accumulation, and establish a self-perpetuating cycle of metabolic dysfunction. Notably, weak indirect PXR modulation via oxidative stress represents a secondary, non-causal mechanism unsupported by functional validation. This framework distinguishes toxicant-induced steatosis from metabolic dysfunction-associated steatotic liver disease while highlighting critical evidence gaps—particularly the absence of causal PXR validation studies and human epidemiological data. Therapeutic opportunities exist at validated convergence points including mitochondrial dynamics (Drp1), inflammatory signalling (NLRP3/NF-κB), and energy metabolism (AMPK-mTOR), though combination strategies targeting multiple pathways will likely be required for durable disease reversal. These findings necessitate the expansion of regulatory screening paradigms to incorporate cellular stress pathway biomarkers alongside traditional nuclear receptor endpoints, ensuring comprehensive hepatotoxic risk assessment of emerging BPA substitutes. Full article
(This article belongs to the Special Issue Advanced Research in Metabolic Syndrome (2nd Edition))
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