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Mechanisms and Pathophysiology of Obesity
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Mechanisms and Pathophysiology of Obesity

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 August 2025) | Viewed by 2370

Special Issue Editor

Dr. Padmamalini Baskaran

E-Mail Website
Guest Editor
College of Pharmacy, Howard University, Washington, DC 20059, USA
Interests: TRPV1; capsaicin; obesity; insulin resistance; metabolic dysfunction-associated steatotic liver disease

Special Issue Information

Dear Colleagues,

Obesity is a chronic, relapsing condition characterized by excess body fat. It occurs when the balance is lost between energy intake vs. expenditure. Obesity is caused by many factors, including genetics, viruses, environment, physical activity and diet, insulin resistance, inflammation, gut microbiome, medications, circadian rhythms, psychological distress and stress, pollution, parental body mass index, maternal smoking, etc. Hormones, growth factors, and organs and tissues regulate the progression of obesity. The molecular mechanisms and pathophysiology of obesity involve a complex interplay of various factors.

There are serious health consequences due to obesity. Excessive fat accumulation not only disrupts the normal function of adipose tissue but also places a burden on organs such as the heart and liver, elevating the risk of multiple chronic diseases. Therefore, research is important to understand the unexplored mechanisms and develop effective interventions to improve health outcomes and digital tools to monitor and provide real-time feedback to help patients.

Dr. Padmamalini Baskaran
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 100 words) can be sent to the Editorial Office for announcement on this website.

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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 2200 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

  • understanding genetic factors for obesity at the molecular level
  • understanding environmental factors for obesity at the molecular level
  • contribution of insulin resistance to obesity and ways to combat
  • circadian misalignment–molecular level understanding of its contribution to obesity and ways to mitigate it
  • effective and individualized obesity treatment strategies for stress
  • molecular understanding of the influence of parental obesity on childhood overweight
  • molecular mechanisms of maternal smoking on childhood obesity
  • therapeutic interventions for obesity through recombinant hormones
  • role of gut hormones in the treatment of obesity
  • development of new digital tools for weight management interventions

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Published Papers (3 papers)

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Research

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18 pages, 2745 KB  
Article
Obesity-Induced MASLD Is Reversed by Capsaicin via Hepatic TRPV1 Activation
by Padmamalini Baskaran, Ryan Christensen, Kimberley D. Bruce and Robert H. Eckel
Curr. Issues Mol. Biol. 2025, 47(8), 618; https://doi.org/10.3390/cimb47080618 - 4 Aug 2025
Viewed by 891
Abstract
Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive liver disorder associated with metabolic risk factors such as obesity, type 2 diabetes, and cardiovascular disease. If left untreated, the accumulation of excess hepatic fat can lead to inflammation, fibrosis, cirrhosis, [...] Read more.
Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive liver disorder associated with metabolic risk factors such as obesity, type 2 diabetes, and cardiovascular disease. If left untreated, the accumulation of excess hepatic fat can lead to inflammation, fibrosis, cirrhosis, hepatocellular carcinoma, and ultimately liver failure. Capsaicin (CAP), the primary pungent compound in chili peppers, has previously been shown to prevent weight gain in high-fat diet (HFD)-induced obesity models. In this study, we investigated the potential of dietary CAP to prevent HFD-induced MASLD. Methods: C57BL/6 mice were fed an HFD (60% kcal from fat) with or without 0.01% CAP supplementation for 26 weeks. We evaluated CAP’s effects on hepatic fat accumulation, inflammation, and mitochondrial function to determine its role in preventing MASLD. Results: CAP acts as a potent and selective agonist of the transient receptor potential vanilloid 1 (TRPV1) channel. We confirmed TRPV1 expression in the liver and demonstrated that CAP activates hepatic TRPV1, thereby preventing steatosis, improving insulin sensitivity, reducing inflammation, and enhancing fatty acid oxidation. These beneficial effects were observed in wild-type but not in TRPV1 knockout mice. Mechanistically, CAP-induced TRPV1 activation promotes calcium influx and activates AMPK, which leads to SIRT1-dependent upregulation of PPARα and PGC-1α, enhancing mitochondrial biogenesis and lipid metabolism. Conclusions: Our findings suggest that dietary CAP prevents MASLD through TRPV1 activation. TRPV1 signaling represents a promising therapeutic target for the prevention and management of MASLD in individuals with metabolic disorders. Full article
(This article belongs to the Special Issue Mechanisms and Pathophysiology of Obesity)
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Review

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21 pages, 3927 KB  
Review
Mechanisms Linking Obesity with Non-Alcoholic Fatty Liver Disease (NAFLD) and Cardiovascular Diseases (CVDs)—The Role of Oxidative Stress
by Fani-Niki Varra, Michail Varras, Viktoria-Konstantina Varra and Panagiotis Theodosis-Nobelos
Curr. Issues Mol. Biol. 2025, 47(9), 766; https://doi.org/10.3390/cimb47090766 - 16 Sep 2025
Viewed by 52
Abstract
Obesity concerns a wide range of the population, tending to become a major factor for diseases’ progression and fatality rate increases, with implications concerning the cardiovascular system’s deterioration. Obesity is closely linked with metabolic derangements concerning lipid storage and circulation, and the cellular [...] Read more.
Obesity concerns a wide range of the population, tending to become a major factor for diseases’ progression and fatality rate increases, with implications concerning the cardiovascular system’s deterioration. Obesity is closely linked with metabolic derangements concerning lipid storage and circulation, and the cellular metabolism affecting most of the internal organs, especially liver and cellular function. In this current study, an analysis of the linking mechanisms between obesity, lipid deterioration, liver, and lipid tissue homeostasis will be performed, with special attention to the pathophysiological characteristics of these detrimental effects on the NAFLD (non-alcoholic fatty liver disease) and the cellular function of the endothelial blood cells, with special reference to the additional burdening of obesity on the autonomous nervous system signaling, and the resulting hypertension. Despite the very complex and pluripotent pathogenic mechanisms with which obesity is intervening in these processes, it could be safely deduced that metabolic and lipid transport manipulation could serve as a crucial factor towards the cellular and tissue function improvement, as the interlinkages in the mechanisms, although highly analyzed, have not been completely deciphered until now. Full article
(This article belongs to the Special Issue Mechanisms and Pathophysiology of Obesity)
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13 pages, 1448 KB  
Review
A Review of Syndromic Forms of Obesity: Genetic Etiology, Clinical Features, and Molecular Diagnosis
by Anam Farzand, Mohd Adzim Khalil Rohin, Sana Javaid Awan, Zubair Sharif, Adnan Yaseen and Abdul Momin Rizwan Ahmad
Curr. Issues Mol. Biol. 2025, 47(9), 718; https://doi.org/10.3390/cimb47090718 - 3 Sep 2025
Viewed by 732
Abstract
Background: Syndromic forms of obesity are uncommon, complicated illnesses that include early-onset obesity along with other clinical characteristics such as organ-specific abnormalities, dysmorphic symptoms, and intellectual incapacity. These syndromes frequently have a strong genetic foundation, involving copy number variations, monogenic mutations, and chromosomal [...] Read more.
Background: Syndromic forms of obesity are uncommon, complicated illnesses that include early-onset obesity along with other clinical characteristics such as organ-specific abnormalities, dysmorphic symptoms, and intellectual incapacity. These syndromes frequently have a strong genetic foundation, involving copy number variations, monogenic mutations, and chromosomal abnormalities. Methods: Using terms like “syndromic obesity,” “genetic diagnosis,” and “monogenic obesity,” a comprehensive literature search was conducted to find articles published between 2000 and 2025 in PubMed, Scopus, and Web of Science. Peer-reviewed research addressing the clinical, molecular, or genetic aspects of syndromic obesity were among the inclusion criteria. Conference abstracts, non-English publications, and research without genetic validation were among the exclusion criteria. The whole genetic, clinical, diagnostic, and therapeutic domains were thematically synthesized to create a thorough, fact-based story. Research using chromosomal microarray analysis (CMA), whole-exome sequencing (WES), next-generation sequencing (NGS), and new long-read sequencing platforms was highlighted. Results: Despite the fact that molecular diagnostics, especially NGS and CMA, have made tremendous progress in identifying pathogenic variants, between 30 and 40 percent of instances of syndromic obesity are still genetically unexplained. One significant issue is the variation in phenotype across people with the same mutation, which suggests the impact of environmental modifiers and epigenetic variables. In addition, differences in access to genetic testing, particularly in areas with limited resources, can make it difficult to diagnose patients in a timely manner. Additionally, recent research emphasizes the possible contribution of gene–environment interactions, gut microbiota, and multi-omic integration to modifying disease expression. Conclusions: Syndromic obesity is still poorly understood in a variety of groups despite significant advancements in technology. Multi-layered genomic investigations, functional genomic integration, and standardized diagnostic frameworks are necessary to close existing gaps. The development of tailored treatment plans, such as gene editing and focused pharmaceutical therapies as well as fair access to cutting-edge diagnostics are essential to improving outcomes for people with syndromic obesity. Full article
(This article belongs to the Special Issue Mechanisms and Pathophysiology of Obesity)
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