Tunc Sevket Ercan, Delibasi Bulent Tolga, Delibasi Tuncay
Division of Rheumatology, Toronto Western Hospital, University of Toronto, Toronto, Canada.
Long School of Medicine, University of Texas Health Science Center San Antonio, San Antonio, Texas, USA.
Curr Diabetes Rev. 2025 Jun 16. doi: 10.2174/0115733998298686250526041742.
Type 2 diabetes mellitus (T2DM) remains one of the most prevalent chronic metabolic disorders globally, presenting an ongoing challenge in terms of prevention and management. The majority of existing therapeutic strategies focus primarily on glycemic control. However, the role of inflammation in the pathogenesis of the disease is being recognized increasingly, which has brought to light a critical gap in our understanding of diabetes treatment in the context of anti-inflammatory therapeutics. Inflammatory reactions are essential to the development and progression of T2DM. The NLRP3 inflammasome, along with its downstream inflammatory factors, is a key mediator of these responses. Recent data underscore the significance of Interleukin- 1β (IL-1β) in instigating and sustaining inflammation-related organ dysfunction in T2DM. Consequently, factors governing NLRP3 activation and IL-1β expression emerge as potential therapeutic targets. Here, we aim to examine one such therapeutic agent, colchicine, which can potentially manage inflammation associated with T2DM. As an anti-inflammatory medicine, colchicine can inhibit the assembly and activation of the NLRP3 inflammasome via various mechanisms, thereby mitigating inflammation. In this context, the study discusses the mechanisms that link metabolic disorders with the onset of chronic inflammation, evaluates clinical studies and trials that investigate the efficacy and safety of colchicine, as well as discusses its benefits and limitations as an anti-inflammatory therapy in T2DM. The goal is to provide a clear framework for understanding the role of colchicine in the therapeutic landscape of T2DM, potentially leading to novel approaches for managing the disease.
2型糖尿病（T2DM）仍然是全球最普遍的慢性代谢紊乱疾病之一，在预防和管理方面持续带来挑战。现有的大多数治疗策略主要集中在血糖控制上。然而，炎症在该疾病发病机制中的作用越来越受到认可，这揭示了我们在抗炎治疗背景下对糖尿病治疗理解上的一个关键差距。炎症反应对于T2DM的发生和发展至关重要。NLRP3炎性小体及其下游炎症因子是这些反应的关键介质。最近的数据强调了白细胞介素-1β（IL-1β）在引发和维持T2DM中与炎症相关的器官功能障碍方面的重要性。因此，控制NLRP3激活和IL-1β表达的因素成为潜在的治疗靶点。在此，我们旨在研究一种这样的治疗药物——秋水仙碱，它可能有助于控制与T2DM相关的炎症。作为一种抗炎药物，秋水仙碱可通过多种机制抑制NLRP3炎性小体的组装和激活，从而减轻炎症。在此背景下，本研究讨论了将代谢紊乱与慢性炎症发作联系起来的机制，评估了研究秋水仙碱疗效和安全性的临床研究与试验，并讨论了其作为T2DM抗炎治疗的益处和局限性。目标是提供一个清晰的框架，以理解秋水仙碱在T2DM治疗领域中的作用，可能会带来管理该疾病的新方法。
