Metabolic Inflammation and Insulin Resistance in Obesity

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 741

Special Issue Editor


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Guest Editor
Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15260, USA
Interests: metabolism; glucose; T cells; fatty acids metabolism

Special Issue Information

Dear Colleagues,

Obesity remains one of the most urgent public health challenges facing society today, especially in developed countries. Both obesity and its related conditions impose substantial economic and workforce burdens on healthcare systems worldwide. Over recent decades, research has increasingly demonstrated that obesity contributes not only to systemic insulin resistance but also to chronic, low-grade inflammation. This obesity-associated inflammation is thought to be primarily driven by the remodeling and redistribution of adipose tissue. Additionally, the complex interplay between adipose cells and immune cells in this process indicates a multifactorial mechanism that requires further investigation to fully understand the underlying inflammatory pathways.

We are pleased to introduce our Special Issue, “Metabolic Inflammation and Insulin Resistance in Obesity,” which aims to showcase novel research into the molecular mechanisms of obesity-related inflammation—its origins, progression, and potential therapeutic interventions. We encourage submissions that incorporate animal models or clinical studies, as these provide valuable insights with translational relevance. Through this issue, we hope to deepen understanding in this area and help guide future research directions.

While obesity is a major driver of metabolic inflammation, it is important to acknowledge that other factors, such as stress, aging, and gut dysbiosis, also play significant roles. We hope our future Special Issues will provide more opportunities to explore these related areas.

Dr. Bingxian Xie
Guest Editor

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Keywords

  • obesity-linked inflammation
  • insulin resistance
  • adipose tissue

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Published Papers (1 paper)

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Review

30 pages, 1661 KiB  
Review
Gut Hormones and Inflammatory Bowel Disease
by Jonathan Weng and Chunmin C. Lo
Biomolecules 2025, 15(7), 1013; https://doi.org/10.3390/biom15071013 - 14 Jul 2025
Viewed by 347
Abstract
Obesity-driven inflammation disrupts gut barrier integrity and promotes inflammatory bowel disease (IBD). Emerging evidence highlights gut hormones—including glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), and apolipoprotein A4 (APOA4)—as key regulators of metabolism and mucosal immunity. [...] Read more.
Obesity-driven inflammation disrupts gut barrier integrity and promotes inflammatory bowel disease (IBD). Emerging evidence highlights gut hormones—including glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), and apolipoprotein A4 (APOA4)—as key regulators of metabolism and mucosal immunity. This review outlines known mechanisms and explores therapeutic prospects in IBD. GLP-1 improves glycemic control, induces weight loss, and preserves intestinal barrier function, while GLP-2 enhances epithelial repair and reduces pro-inflammatory cytokine expression in animal models of colitis. GIP facilitates lipid clearance, enhances insulin sensitivity, and limits systemic inflammation. PYY and CCK slow gastric emptying, suppress appetite, and attenuate colonic inflammation via neural pathways. APOA4 regulates lipid transport, increases energy expenditure, and exerts antioxidant and anti-inflammatory effects that alleviate experimental colitis. Synergistic interactions—such as GLP-1/PYY co-administration, PYY-stimulated APOA4 production, and APOA4-enhanced CCK activity—suggest that multi-hormone combinations may offer amplified therapeutic benefits. While preclinical data are promising, clinical evidence supporting gut hormone therapies in IBD remains limited. Dual GIP/GLP-1 receptor agonists improve metabolic and inflammatory parameters, but in clinical use, they are associated with gastrointestinal side effects that warrant further investigation. Future research should evaluate combination therapies in preclinical IBD models, elucidate shared neural and receptor-mediated pathways, and define optimal strategies for applying gut hormone synergy in human IBD. These efforts may uncover safer, metabolically tailored treatments for IBD, particularly in patients with coexisting obesity or metabolic dysfunction. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
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