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Life sciences · Journal article
Frontiers in Endocrinology · September 25, 2026
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Obesity-related asthma (OBA) is a clinically important asthma phenotype characterized by poor disease control, increased exacerbation risk, and frequent corticosteroid insensitivity. Although obesity-related mechanical loading contributes to respiratory symptoms, it does not fully explain the inflammatory, functional, and structural features of this phenotype. This review examines adipokine dysregulation, particularly leptin excess and adiponectin insufficiency, as a biologically plausible axis linking systemic metabolic dysfunction to airway-relevant pathology. Epidemiological, animal, and airway-cellular evidence supports adipokine involvement of variable strength in three interconnected domains, including immune amplification through context-dependent macrophage and NLRP3 inflammasome activation, airway hyperresponsiveness (AHR) through inflammatory, neural bronchomotor, and airway smooth muscle (ASM) pathways, and remodeling through epithelial repair failure, ASM proliferation, peribronchial adipose tissue (PBAT) and airway-associated adipose tissue (AAAT) adipose-airway crosstalk, fibroblast activation, and extracellular matrix (ECM) deposition. A spatial-temporal model is proposed in which systemic endocrine adipokine signals may be complemented by local adipose-airway paracrine effects, while persistent metabolic inflammation may shift disease expression from a potentially reversible inflammatory and hyperresponsive state toward remodeling-predominant pathology. Clinically, adipokines are best viewed as candidate stratification markers integrated with metabolic, inflammatory, functional, and structural readouts, and metabolic interventions should be interpreted as phenotype-directed interventions with potential disease-modifying relevance and biomarker endpoints. The translational value of this framework lies in guiding airway-focused validation, longitudinal phenotyping, and mechanistic intervention trials that can distinguish weight-loss effects from direct metabolic-inflammatory airway modulation.