Abstract：
BACKGROUND: Type 2 diabetes mellitus (T2DM) is a worldwide socioeconomic burden, and is accompanied by a variety of metabolic disorders, as well as nerve dysfunction referred to as diabetic neuropathy (DN). Despite a tremendous body of research, the pathogenesis of DN remains largely elusive. Currently, two schools of thought exist regarding the pathogenesis of diabetic neuropathy: a) mitochondrial-induced toxicity, and b) microvascular damage. Both mechanisms signify DN as an intractable disease and, as a consequence, therapeutic approaches treat symptoms with limited efficacy and risk of side effects.
OBJECTIVE: Here, we propose that the human body exclusively employs mechanisms of adaptation to protect itself during an adverse event. For this purpose, two control systems are defined, namely the autonomic and the neural control systems. The autonomic control system responds via inflammatory and immune responses, while the neural control system regulates neural signaling, via plastic adaptation. Both systems are proposed to regulate a network of temporal and causative connections which unravel the complex nature of diabetic complications.
RESULTS: A significant result of this approach infers that both systems make DN reversible, thus opening the door to novel therapeutic applications.
OBJECTIVE: Here, we propose that the human body exclusively employs mechanisms of adaptation to protect itself during an adverse event. For this purpose, two control systems are defined, namely the autonomic and the neural control systems. The autonomic control system responds via inflammatory and immune responses, while the neural control system regulates neural signaling, via plastic adaptation. Both systems are proposed to regulate a network of temporal and causative connections which unravel the complex nature of diabetic complications.
RESULTS: A significant result of this approach infers that both systems make DN reversible, thus opening the door to novel therapeutic applications.
摘要：
背景：2型糖尿病（T2DM）是一种世界性的社会经济负担，并伴有各种代谢紊乱，以及称为糖尿病神经病变（DN）的神经功能障碍。尽管有大量的研究，DN的发病机制在很大程度上仍然难以捉摸。目前,关于糖尿病神经病变的发病机制存在两种观点：a）线粒体诱导的毒性，和b)微血管损伤。这两种机制都表明DN是一种顽固性疾病，因此，治疗方法治疗症状的疗效和副作用的风险有限。
目标：这里，我们建议人体在不良事件中专门使用适应机制来保护自己。为此,定义了两个控制系统，即自主和神经控制系统。自主控制系统通过炎症和免疫反应做出反应，而神经控制系统调节神经信号，通过塑料适应。提出了两种系统来调节时间和因果关系的网络，这些网络揭示了糖尿病并发症的复杂性。
结果：这种方法的重要结果推断，两个系统都使DN可逆，从而打开了新的治疗应用的大门。
目标：这里，我们建议人体在不良事件中专门使用适应机制来保护自己。为此,定义了两个控制系统，即自主和神经控制系统。自主控制系统通过炎症和免疫反应做出反应，而神经控制系统调节神经信号，通过塑料适应。提出了两种系统来调节时间和因果关系的网络，这些网络揭示了糖尿病并发症的复杂性。
结果：这种方法的重要结果推断，两个系统都使DN可逆，从而打开了新的治疗应用的大门。
