Introduction
Diabesity—the intersection of obesity and type 2 diabetes—is typically described as a metabolic disorder. However, growing evidence now shows that immune imbalance, particularly involving mast cells, plays a significant role in driving the chronic inflammation underlying metabolic dysfunction.
Mast Cells as Drivers of Metabolic Inflammation
Research shows that mast cells accumulate in expanding adipose tissue, especially visceral fat. Once activated, they release mediators such as histamine, IL-6, TNF-α, prostaglandins, tryptase, and chymase. These signals contribute to:
- Chronic low-grade inflammation
- Adipose tissue fibrosis
- Insulin resistance
- Dysregulated energy metabolism
Mast Cell Mediators That Influence Metabolism
Mast cell mediators influence metabolic function in several ways:
Histamine
Affects glucose uptake, lipid metabolism, and appetite regulation.
Prostaglandin D₂ and Leukotrienes
Modulate adipogenesis and mitochondrial function.
Tryptase and Chymase
Drive extracellular matrix remodeling and amplify inflammation.
Clinical Implications
Understanding the immunometabolic effects of mast cells opens new pathways for improved evaluation and treatment. Potential biomarkers for clinical testing include:
- Histamine
- Prostaglandin D₂ metabolites
- Tryptase
- Leukotriene metabolites
Clinically, mast-cell stabilization or mediator-targeted therapy may complement metabolic treatment strategies.
Conclusion
Mast cells are emerging as key mediators connecting inflammation, obesity, and impaired glucose metabolism. Incorporating mast-cell-related biomarkers into diabesity evaluations may help clinicians identify inflammatory contributors earlier and guide more targeted interventions.
References
Afrin, L. B., et al. (2013). Diagnosis of mast cell activation syndrome. Diagnosis.
Hoh, S. Y., Pierroz, D., & Bornstein, S. R. (2018). Mast cells in chronic low-grade inflammation within adipose tissue. Obesity Reviews, 19(12), 1493–1507. https://doi.org/10.1111/obr.12746
King, R., & Ajjan, R. (2013). Inflammation, diabesity and cardiovascular disease. Diabesity in Practice, 2, 29–35.