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Obesity: From Molecular Mechanisms to Clinical Aspects
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Obesity: From Molecular Mechanisms to Clinical Aspects

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 April 2025) | Viewed by 3559

Special Issue Editor

Prof. Dr. Bunzo Matsuura

E-Mail Website
Guest Editor
Department of Lifestyle-Related Medicine and Endocrinology, Graduate School of Medicine, Ehime University, Shitsukawa 454, Toon, Ehime 791-0295, Japan
Interests: gut hormone; thyroid disease; obesity; diabetes mellitus; nonalcoholic fatty liver disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is a serious global health problem with high mortality and morbidity rates. Food intake, physical activity, adipokines, gut hormones, inflammation, genetics and epigenetics, bariatric surgery, and synthetic agents affect the development and progression of obesity and obesity-related diseases, such as diabetes, metabolic-associated steatotic liver diseases, cardiovascular diseases, and cancers. The reduction in adipose tissue in obese subjects represents an important goal for the prevention and treatment of these chronic diseases. We invite articles that are based on novel ideas for cellular and individual studies, as well as review articles. Pure clinical reports may not be accepted.

Prof. Dr. Bunzo Matsuura
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • food intake
  • physical activity
  • adipose tissue
  • adipokines
  • gut hormones
  • nervous system
  • gut–brain axis
  • bariatric surgery
  • inflammation and immune response
  • genetics and epigenetics

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Published Papers (4 papers)

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Research

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12 pages, 2784 KiB  
Article
Depletion of WWP1 Increases Adrb3 Expression and Lipolysis in White Adipose Tissue of Obese Mice
by Yuka Nozaki, Yuko Ose, Chinatsu Ohmori, Yuhei Mizunoe, Masaki Kobayashi, Akiyoshi Saitoh and Yoshikazu Higami
Int. J. Mol. Sci. 2025, 26(9), 4219; https://doi.org/10.3390/ijms26094219 - 29 Apr 2025
Viewed by 66
Abstract
Obesity is defined as abnormal or excessive accumulation of body fat and contributes to several metabolic disorders. White adipose tissue (WAT) releases energy as free fatty acids and glycerol from triglycerides through a process called lipolysis. People with obesity have impaired catecholamine-stimulated lipolysis, [...] Read more.
Obesity is defined as abnormal or excessive accumulation of body fat and contributes to several metabolic disorders. White adipose tissue (WAT) releases energy as free fatty acids and glycerol from triglycerides through a process called lipolysis. People with obesity have impaired catecholamine-stimulated lipolysis, but comprehensive understanding of this lipolysis is still unclear. We previously showed that expression of WW domain-containing E3 ubiquitin ligase 1 (WWP1), a member of the HECT-type E3 family of ubiquitin ligases, was increased in WAT of obese mice. In this study, we generated Wwp1 knockout (KO) mice to evaluate the effect of WWP1 in WAT of obese mice. The mRNA levels of beta-3 adrenergic receptor (Adrb3), which were decreased with a high-fat diet, were increased by Wwp1 KO in WAT. Moreover, Wwp1 KO mice showed increased phosphorylated hormone-sensitive lipase levels in WAT. In contrast, noradrenaline and its metabolism were not altered in WAT of obese Wwp1 KO mice. These findings indicate that WWP1, which is increased in adipocytes because of obesity, is a candidate for suppressing lipolysis independently of noradrenaline metabolism. We anticipate that inhibition of WWP1 is a promising approach for a new treatment of obesity and type-2 diabetes using Adrb3 agonists. Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
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15 pages, 2078 KiB  
Article
Distinct T Cell Subset Profiles and T-Cell Receptor Signatures in Metabolically Unhealthy Obesity
by Yoona Chung, Ji Yeon Chang, Shindy Soedono, Vivi Julietta, Esther Jin Joo, Soon Hyo Kwon, Sung Il Choi, Yong Jin Kim and Kae Won Cho
Int. J. Mol. Sci. 2025, 26(7), 3372; https://doi.org/10.3390/ijms26073372 - 4 Apr 2025
Viewed by 296
Abstract
Metabolically unhealthy obesity (MUO) is associated with increased inflammation and a higher risk of metabolic disorders compared to metabolically healthy obesity (MHO). T cell dysregulation in blood and adipose tissue may contribute to obesity-induced metabolic dysfunction, yet the characteristics of T cell subset [...] Read more.
Metabolically unhealthy obesity (MUO) is associated with increased inflammation and a higher risk of metabolic disorders compared to metabolically healthy obesity (MHO). T cell dysregulation in blood and adipose tissue may contribute to obesity-induced metabolic dysfunction, yet the characteristics of T cell subset profiles and T-cell receptor (TCR) repertoires in MHO and MUO remain unclear. We analyzed T cell subsets and TCR repertoires in peripheral blood and omental adipose tissue (oAT) from age- and BMI-matched MHO and MUO individuals using flow cytometry and high-throughput TCR sequencing. MUO individuals exhibited a higher proportion of memory CD4+ T cells in both compartments, with an increased frequency of central memory T cells. Circulating CD8+ T cells were increased in MUO, whereas CD8+ T cell subset composition remained unchanged in both blood and oAT. The TCR repertoire in oAT was significantly more restricted than in blood and showed greater skewing in MUO, with selective amplification of specific TRB V genes (TRBV12-4, TRBV18, TRBV7-9) and altered CDR3 length distributions. These findings suggest that distinct CD4+ T cell populations and specific TCR signatures may serve as potential biomarkers for metabolic dysfunction in obesity, providing insights into immune mechanisms underlying the transition from MHO to MUO. Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
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18 pages, 1290 KiB  
Article
Circulating hs-CRP, IL-18, Chemerin, Leptin, and Adiponectin Levels Reflect Cardiometabolic Dysfunction in Adults with Excess Weight
by Óscar Javier Lara-Guzmán, Ángela María Arango-González, Rafael Álvarez-Quintero, Juan S. Escobar, Katalina Muñoz-Durango and Jelver Alexander Sierra
Int. J. Mol. Sci. 2025, 26(3), 1176; https://doi.org/10.3390/ijms26031176 - 29 Jan 2025
Cited by 1 | Viewed by 742
Abstract
Up to 30% of individuals with obesity may exhibit normal insulin sensitivity, a favorable lipid profile, and no signs of hypertension. This prompts the exploration of factors distinguishing cardiometabolically healthy individuals from those developing complications. This cross-sectional study included 116 individuals categorized into [...] Read more.
Up to 30% of individuals with obesity may exhibit normal insulin sensitivity, a favorable lipid profile, and no signs of hypertension. This prompts the exploration of factors distinguishing cardiometabolically healthy individuals from those developing complications. This cross-sectional study included 116 individuals categorized into four groups by combining abdominal obesity and cardiometabolic health statuses. We compared circulating adipokines and gut microbiota composition between these groups. Individuals with abdominal obesity had higher levels of hs-CRP, TNF-α, MCP-1, IL-18, chemerin, and leptin, and a less favorable gut microbiota composition, including higher levels of potentially harmful bacteria (CAG-Pathogen) and lower levels of beneficial bacteria (CAG-Ruminococcaceae and CAG-Akkermansia), compared to those with adequate waist circumference. Those with obesity but cardiometabolically healthy displayed similar adipokine levels and microbiota composition to those with adequate waist. In contrast, individuals with abdominal obesity cardiometabolically abnormal exhibited significantly higher levels of hs-CRP, IL-18, chemerin, and leptin, and lower levels of adiponectin and CAG-Ruminococcaceae compared to those with abdominal obesity cardiometabolically healthy and adequate waist. Additionally, they differed in hs-CRP and adiponectin/leptin ratio from individuals with obesity cardiometabolically healthy. These findings suggest that altered adipokine profiles and gut microbiota may contribute to the development or persistence of cardiometabolic complications in obesity. Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
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Review

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22 pages, 1102 KiB  
Review
The Evolving Role of Neutrophils and Neutrophil Extracellular Traps (NETs) in Obesity and Related Diseases: Recent Insights and Advances
by Serena Altamura, Francesca Lombardi, Paola Palumbo, Benedetta Cinque, Claudio Ferri, Rita Del Pinto and Davide Pietropaoli
Int. J. Mol. Sci. 2024, 25(24), 13633; https://doi.org/10.3390/ijms252413633 - 20 Dec 2024
Viewed by 1560
Abstract
Obesity is a chronic, multifactorial disease characterized by persistent low-grade tissue and systemic inflammation. Fat accumulation in adipose tissue (AT) leads to stress and dysfunctional adipocytes, along with the infiltration of immune cells, which initiates and sustains inflammation. Neutrophils are the first immune [...] Read more.
Obesity is a chronic, multifactorial disease characterized by persistent low-grade tissue and systemic inflammation. Fat accumulation in adipose tissue (AT) leads to stress and dysfunctional adipocytes, along with the infiltration of immune cells, which initiates and sustains inflammation. Neutrophils are the first immune cells to infiltrate AT during high-fat diet (HFD)-induced obesity. Emerging evidence suggests that the formation and release of neutrophil extracellular traps (NETs) play a significant role in the progression of obesity and related diseases. Additionally, obesity is associated with an imbalance in gut microbiota and increased intestinal barrier permeability, resulting in the translocation of live bacteria, bacterial deoxyribonucleic acid (DNA), lipopolysaccharides (LPS), and pro-inflammatory cytokines into the bloodstream and AT, thereby contributing to metabolic inflammation. Recent research has also shown that short-chain fatty acids (SCFAs), produced by gut microbiota, can influence various functions of neutrophils, including their activation, migration, and the generation of inflammatory mediators. This review comprehensively summarizes recent advancements in understanding the role of neutrophils and NET formation in the pathophysiology of obesity and related disorders while also focusing on updated potential therapeutic approaches targeting NETs based on studies conducted in humans and animal models. Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
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