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Biomedicines
Special Issues
Adiposity, Inflammation, and Metabolic Regulation: Molecular Mechanisms and Therapeutic Strategies
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Adiposity, Inflammation, and Metabolic Regulation: Molecular Mechanisms and Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 2741

Special Issue Editor

Dr. Qianfen Wan

E-Mail Website
Guest Editor
Naomi Berrie Diabetes Center, Columbia University, New York, NY 10032, USA
Interests: metabolism; obesity; diabetes; cancer

Special Issue Information

Dear Colleagues,

Obesity, a global epidemic characterized by excessive adipose tissue accumulation, poses a substantial burden on public health. Associated with a myriad of metabolic disorders, including insulin resistance with associated hyperinsulinemia, type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease, obesity is a complex condition influenced by genetic, environmental, and behavioral factors.

Emerging evidence highlights the pivotal role of adipose tissue inflammation in the pathogenesis of obesity and its metabolic complications. Hypertrophic adipocytes, infiltrated immune cells, and the release of pro-inflammatory adipokines contribute to a chronic low-grade inflammatory state that impairs insulin sensitivity, disrupts lipid metabolism, and promotes systemic inflammation. Despite these advancements, the precise mechanisms underlying adipose tissue expansion, its metabolic consequences, and the development of obesity-related comorbidities remain incompletely understood.

While recent therapeutic interventions, such as GLP-1 receptor agonists, have demonstrated efficacy in weight management and metabolic improvement, the underlying mechanisms of action, particularly at the level of adipose tissue, require further exploration. A deeper understanding of adipose tissue biology, inflammation, and its interaction with systemic metabolism is crucial for developing targeted and effective therapeutic strategies.

To advance our knowledge in this critical area, this Special Issue invites original research and review articles that explore the following (but are not limited to them):

  • The interrelationships between obesity and insulin resistance/hyperinsulinemia.
  • The cellular and molecular mechanisms governing adipocyte differentiation, function, and dysfunction.
  • The role of inflammation in adipose tissue, including the involvement of immune cells and inflammatory signaling pathways.
  • The complex interplay between adipose tissue, systemic metabolism, and the development of obesity-related complications.
  • Novel therapeutic approaches targeting adipose tissue biology and inflammation for the prevention and treatment of obesity.

We encourage submissions that contribute to a comprehensive understanding of obesity pathogenesis and inform the development of innovative treatment strategies.

We look forward to receiving your contributions.

Dr. Qianfen Wan
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.

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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

  • adipose tissue
  • inflammation
  • obesity and its metabolic complications
  • obesity pathogenesis

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Published Papers (3 papers)

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Research

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15 pages, 2829 KiB  
Article
Converted Macrophage Polarization and Expression of COL6α3—Early Predictors of Remodeling Processes in Adipose Tissue of Male Children
by Robert Mujkić, Darija Šnajder Mujkić, Karla Rožac, Anita Matić, Tanja Kovač Lukić, Dalibor Divković and Kristina Selthofer-Relatić
Biomedicines 2025, 13(4), 935; https://doi.org/10.3390/biomedicines13040935 - 10 Apr 2025
Viewed by 357
Abstract
Background/Objectives: Overweight and obesity in early childhood is a serious public health problem as in most cases it persists into adulthood and significantly affects the quality of life. The aim of this study was to investigate the mechanisms that trigger extracellular matrix (ECM) [...] Read more.
Background/Objectives: Overweight and obesity in early childhood is a serious public health problem as in most cases it persists into adulthood and significantly affects the quality of life. The aim of this study was to investigate the mechanisms that trigger extracellular matrix (ECM) remodeling in the subcutaneous (SAT) and visceral (VAT) adipose tissue of male children in relation to their body weight. Methods: During elective abdominal surgery, SAT and VAT were acquired from 75 male subjects undergoing hernia repair (inguinal herniorrhaphy by Ferguson) or orchidopexy. Based on their Z-score, subjects were separated into two groups. The morphometry of both adipose tissue compartments was assessed after hematoxylin and eosin histological staining, immunohistochemistry to quantify CD163+ cells and the number of crown-like structures (CLSs), and real-time polymerase chain reaction to assess the relative gene expression for collagen VI subtype alpha 3 (COL6α3). Results: Obese and overweight individuals were found to have higher numbers of CD163+ cells, greater numbers of CLSs in VAT and SAT, and a higher expression of COL6α3 in both compartments. Conclusions: Obesity in childhood may lead to increased COL6α3 gene expression and promote the activation of macrophage polarization, compromise the structural integrity of the ECM, and thus influence the development of inflammatory processes. Full article
(This article belongs to the Special Issue Adiposity, Inflammation, and Metabolic Regulation: Molecular Mechanisms and Therapeutic Strategies)
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15 pages, 5376 KiB  
Article
Butyrate Prevents Obesity Accompanied by HDAC9-Mediated Browning of White Adipose Tissue
by Jing Yang, Guoli Li, Shan Wang, Mingqian He, Sijing Dong, Ting Wang, Binyin Shi, Patrick C. N. Rensen and Yanan Wang
Biomedicines 2025, 13(2), 260; https://doi.org/10.3390/biomedicines13020260 - 21 Jan 2025
Viewed by 1717
Abstract
Background/Objectives: Mounting evidence indicates that the short-chain fatty acid butyrate protects against obesity and associated comorbidities, partially through the induction of adipose tissue thermogenesis. However, the effects of butyrate on white adipose tissue (WAT) browning and its molecular mechanism are still elusive. The [...] Read more.
Background/Objectives: Mounting evidence indicates that the short-chain fatty acid butyrate protects against obesity and associated comorbidities, partially through the induction of adipose tissue thermogenesis. However, the effects of butyrate on white adipose tissue (WAT) browning and its molecular mechanism are still elusive. The objective of this study was to investigate butyrate-induced thermogenesis in white adipose tissue and its underlying mechanism. Methods: We studied the effects of butyrate on diet-induced obesity in the humanized APOE*3-Leiden.CETP transgenic mouse model and explored factors related to white adipose browning. Specifically, mice were challenged with a high-fat diet supplemented with butyrate. Adiposity was measured to assess obesity development. Energy metabolism was detected using an indirect calorimetry system. RNA-seq analysis was conducted to analyze the transcription landscape of WAT and responsible targets. Furthermore, the revealed molecular mechanism was verified in vitro. Results: Butyrate alleviated high-fat diet-induced obesity and promoted energy expenditure accompanied by brown adipose tissue activation and WAT browning. Mechanistically, RNA-seq analysis revealed that butyrate downregulated HDAC9 in WAT. Additionally, butyrate decreased HDAC9 while increasing thermogenesis in vitro. Inhibition of HDAC9 with TMP269 promoted thermogenic gene expression, mimicking the effects of butyrate. Conclusions: Butyrate protects against diet-induced obesity accompanied by decreasing the expression of HDAC9 in white adipose tissue and inducing browning. This study reveals a new mechanism whereby butyrate activates adaptive thermogenesis and provides new insights for the development of weight-loss drugs targeting adipose HDAC9. Full article
(This article belongs to the Special Issue Adiposity, Inflammation, and Metabolic Regulation: Molecular Mechanisms and Therapeutic Strategies)
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Review

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16 pages, 1922 KiB  
Review
Obesity and Asthma in Children—Coexistence or Pathophysiological Connections?
by Clarissa Mazzotta and László Barkai
Biomedicines 2025, 13(5), 1114; https://doi.org/10.3390/biomedicines13051114 - 4 May 2025
Viewed by 182
Abstract
The aim of this narrative review is to explore possible connections that might lead to both obesity and asthma; it will explain factors and mechanisms involved in disease pathogenesis, focusing particularly on diet and nutrients, the microbiome, inflammatory and metabolic dysregulation, lung function, [...] Read more.
The aim of this narrative review is to explore possible connections that might lead to both obesity and asthma; it will explain factors and mechanisms involved in disease pathogenesis, focusing particularly on diet and nutrients, the microbiome, inflammatory and metabolic dysregulation, lung function, the genetics/genomics of obese asthma, risk of exacerbation, atopy, and response to treatment. It highlights the role that obesity plays as a risk factor for and disease modifier of asthma, understanding the evidence supporting lifestyle changes in influencing disease progression. Pathophysiological mechanisms in obesity-related asthma have influences on the course of disease pathology. Due to these factors, the child with obese asthma needs a specific therapeutic approach taking into account the common unresponsiveness to bronchodilators, increased requirements for controller medications, poorer steroid effectiveness, and better response to leukotriene receptor (LTR) inhibitors. Therapeutic strategies centered on prevention are suggested and the development of resources to assist families with weight loss strategies and lifestyle changes is shown to be useful for effective weight control and optimal asthma management. Obese children with asthma generally should receive interventions that encourage daily physical activity, weight loss, and normalization of nutrient levels, and monitoring of common obesity-related sequelae should be considered by healthcare providers managing obese children with difficult to control asthma. Recognizing and identifying an asthmatic patient is not always easy and a detailed medical history of the patient, with particular attention paid to their presenting and past symptoms, and a complete physical examination play pivotal and fundamental roles in determining the final diagnosis. Full article
(This article belongs to the Special Issue Adiposity, Inflammation, and Metabolic Regulation: Molecular Mechanisms and Therapeutic Strategies)
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