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Obesity: From Molecular Mechanisms to Clinical Aspects

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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
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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

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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 (1 paper)

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Review

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
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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