Department of Pharmacology and Therapeutics, University of Florida, College of Medicine Gainesville, FL, USA.
Front Endocrinol (Lausanne). 2012 Dec 21;3:170. doi: 10.3389/fendo.2012.00170. eCollection 2012.
Diabetes and hyperglycemia create a proinflammatory microenvironment that progresses to microvascular complications such as nephropathy, retinopathy, and neuropathy. Diet-induced insulin resistance is a potential initiator of this change in type 2 diabetes which can increase adipokines and generate a chronic low-grade inflammatory state. Advanced glycation end-products and its receptor, glycation end-products AGE receptor axis, reactive oxygen species, and hypoxia can also interact to worsen complications. Numerous efforts have gained way to understanding the mechanisms of these modulators and attenuation of the inflammatory response, however, effective treatments have still not emerged. The complexity of inflammatory signaling may suggest a need for multi-targeted therapy. This review presents recent findings aimed at new treatment strategies.
糖尿病和高血糖会导致促炎微环境的形成，从而引发微血管并发症，如肾病、视网膜病变和神经病变。饮食引起的胰岛素抵抗是 2 型糖尿病发生这种变化的潜在启动因素，它会增加脂肪因子并产生慢性低度炎症状态。晚期糖基化终产物及其受体、糖基化终产物 AGE 受体轴、活性氧和缺氧也会相互作用，使并发症恶化。人们已经做出了许多努力来了解这些调节剂的机制以及炎症反应的衰减，但仍然没有出现有效的治疗方法。炎症信号的复杂性可能表明需要采用多靶点治疗。本文综述了旨在探索新的治疗策略的最新研究结果。
