Olivares-Vicente Mariló, Herranz-López María
Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Miguel Hernández University (UMH), 03202 Elche, Spain.
Int J Mol Sci. 2025 Sep 2;26(17):8544. doi: 10.3390/ijms26178544.
Adipose tissue functions not only as a lipid storage depot but also as an active endocrine organ that regulates key physiological processes. In obesity, oxidative stress disrupts the molecular pathways for adipose tissue homeostasis, triggering chronic inflammation, tissue dysfunction, and metabolic disorders. This review explores the mechanisms by which lipid storage drives adipose tissue expansion, highlighting the detrimental effects of hypertrophy in promoting oxidative stress, inflammation, and insulin resistance. These processes can ultimately contribute to metabolic pathologies such as cardiovascular diseases and type 2 diabetes. We also discuss how lipid composition influences these pathways, acting as signaling molecules that activate inflammatory and oxidative stress-related signaling cascades. Additionally, we compile evidence from studies on individuals with obesity, identifying lipids, oxidative stress markers, and inflammatory mediators as potential biomarkers of metabolic dysfunction. Finally, we assess the therapeutic potential of antioxidants in mitigating the metabolic effects of obesity, focusing on their mechanisms of actions. By integrating these insights, this review aims to clarify the complex relationship between oxidative stress, lipid metabolism, and inflammation, and highlight the role of antioxidant molecules in addressing adipose tissue dysfunction in obesity.
脂肪组织不仅作为脂质储存库发挥作用，还作为调节关键生理过程的活跃内分泌器官。在肥胖症中，氧化应激会破坏脂肪组织稳态的分子途径，引发慢性炎症、组织功能障碍和代谢紊乱。本综述探讨了脂质储存驱动脂肪组织扩张的机制，强调了肥大在促进氧化应激、炎症和胰岛素抵抗方面的有害影响。这些过程最终可能导致心血管疾病和2型糖尿病等代谢性疾病。我们还讨论了脂质组成如何影响这些途径，作为激活炎症和氧化应激相关信号级联的信号分子。此外，我们汇总了对肥胖个体的研究证据，确定脂质、氧化应激标志物和炎症介质为代谢功能障碍的潜在生物标志物。最后，我们评估了抗氧化剂在减轻肥胖症代谢影响方面的治疗潜力，重点关注其作用机制。通过整合这些见解，本综述旨在阐明氧化应激、脂质代谢和炎症之间的复杂关系，并突出抗氧化分子在解决肥胖症中脂肪组织功能障碍方面的作用。
