Adipose tissue dysfunction disrupts metabolic homeostasis: mechanisms linking fat dysregulation to disease

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)

Background Metabolic disease incidence continues rising globally. Adipose tissue dysfunction serves as a crucial pathophysiological mediator. We evaluate molecular mechanisms linking adipose dysfunction to metabolic dysregulation. Methods We systematically reviewed literature on adipose biology, stress mechanisms, inflammation, and metabolic networks. Analysis prioritized methodologically robust studies from the past decade. Results Adipose dysfunction disrupts metabolic homeostasis through complex molecular networks. Stressed adipocytes exhibit mitochondrial impairment and endoplasmic reticulum (ER) stress. These changes alter inflammatory mediators and adipokine secretion. Brown and beige adipose regulate energy balance via uncoupling protein 1 (UCP1)-mediated thermogenesis. Key transcriptional regulators, PGC-1α and PR domain containing 16 (PRDM16), control thermogenic adipocyte development. Cellular senescence contributes significantly to age-related adipose dysfunction through inflammatory secretory phenotypes. Brown fat also secretes specialized factors influencing whole-body metabolism, emphasizing adipose tissue's endocrine function. Conclusion Adipose dysfunction represents a critical nexus in metabolic disease pathogenesis. Cellular stress, inflammation, and metabolic dysregulation converge at this point. Novel therapies targeting thermogenic activation and cellular s

Evidence level

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

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