Cross-regulation between adipose tissue innervation and metaflammation: a potential therapeutic target for obesity

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity, marked by adipose tissue dysfunction and systemic metaflammation, poses a major global health burden. Emerging evidence underscores a critical interplay between neural regulation and immune-metabolic crosstalk in obesity pathogenesis. This review highlights the dynamic roles of sympathetic and sensory nerves in lipid metabolism, as well as metaflammation involving macrophage polarization, inflammatory cytokine cascades, and mitochondrial dysfunction. In obesity, decreased sympathetic nerve density and impaired adrenergic receptor signaling compromise lipolysis and thermogenesis, while sensory neuropeptides worsen metabolic dysregulation through immune cell interactions. Adipose tissue macrophages adopt pro-inflammatory phenotypes, releasing cytokines that inhibit insulin signaling - forming pathological crown-like structures. Mitochondrial dysfunction, characterized by excessive fission and reduced fusion, disrupts energy homeostasis and increases oxidative stress. Therapeutic approaches targeting neuropeptide signaling, inflammasome activation, and mitochondrial dynamics show promise in restoring metabolic balance. The neuro-immune-metabolic axis thus represents a novel therapeutic frontier for obesity, supporting integrated strategies targeting neural, inflammatory, and mitochondrial pathways.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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