Targeting adipose remodeling: Synergistic mechanisms of drugs and adipose-derived stem cells in obese type 2 diabetes mellitus.

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)

Type 2 diabetes mellitus, particularly when accompanied by obesity, has become a major global public health burden. Visceral adipose tissue accumulation contributes to insulin resistance, lipotoxicity, and chronic inflammation, thereby accelerating metabolic deterioration. Although pharmacological agents such as pioglitazone and metformin are effective in modulating fat distribution and improving metabolic parameters, their roles in adipose tissue remodeling remain insufficiently elucidated. Recent advances in regenerative medicine have highlighted the therapeutic potential of adipose-derived stem cells, owing to their differentiation capacity, anti-inflammatory secretory profile, and involvement in metabolic homeostasis. This review summarized current pharmacological and stem cell-based strategies targeting adipose tissue dysfunction in patients with obesity and type 2 diabetes mellitus with a particular focus on the mechanistic roles of adipokines, mitochondrial dysfunction, and extracellular matrix remodeling in visceral adipose tissue. It further discussed the potential synergistic benefits of adipose-derived stem cell-based combination interventions. Finally, the review envisioned future directions for integrating molecularly targeted drugs with cell therapies in the personalized management of metabolic disorders.

Evidence level

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

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