Catana Oana Maria, Nemes Alexandra Floriana, Cioboata Ramona, Toma Claudia Lucia, Mitroi Denisa Maria, Calarasu Cristina, Streba Costin Teodor
Doctoral School, University of Medicine and Pharmacy, 200349 Craiova, Romania.
Neonatology Department, Memorial Life Hospital Bucharest, 010719 Bucharest, Romania.
J Clin Med. 2025 Apr 10;14(8):2611. doi: 10.3390/jcm14082611.
Chronic obstructive pulmonary disease (COPD) is a progressive and debilitating condition characterized by airflow limitations and systemic inflammation. The interaction between the metabolic and inflammatory pathways plays a key role in disease progression, with leptin and insulin emerging as pivotal metabolic regulators. Leptin, an adipokine that regulates energy homeostasis, and insulin, the primary regulator of glucose metabolism, are both altered in COPD patients. This narrative review provides an in-depth examination of the roles of leptin and insulin in COPD pathogenesis, focusing on the molecular mechanisms through which these metabolic regulators interact with inflammatory pathways and how their dysregulation contributes to a spectrum of extrapulmonary manifestations. These disturbances not only exacerbate COPD symptoms but also increase the risk of comorbidities such as metabolic syndrome, diabetes, cardiovascular disease, or muscle wasting. By exploring the underlying mechanisms of leptin and insulin dysregulation in COPD, this review underscores the significance of the metabolic-inflammatory axis, suggesting that restoring metabolic balance through leptin and insulin modulation could offer novel therapeutic strategies for improving clinical outcomes.
慢性阻塞性肺疾病（COPD）是一种进行性、使人衰弱的疾病，其特征为气流受限和全身炎症。代谢途径与炎症途径之间的相互作用在疾病进展中起关键作用，瘦素和胰岛素已成为关键的代谢调节因子。瘦素是一种调节能量稳态的脂肪因子，而胰岛素是葡萄糖代谢的主要调节因子，二者在COPD患者中均发生改变。本叙述性综述深入探讨了瘦素和胰岛素在COPD发病机制中的作用，重点关注这些代谢调节因子与炎症途径相互作用的分子机制，以及它们的失调如何导致一系列肺外表现。这些紊乱不仅会加重COPD症状，还会增加代谢综合征、糖尿病、心血管疾病或肌肉萎缩等合并症的风险。通过探索COPD中瘦素和胰岛素失调的潜在机制，本综述强调了代谢-炎症轴的重要性，表明通过调节瘦素和胰岛素来恢复代谢平衡可能为改善临床结局提供新的治疗策略。
