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有关Ⅰ、Ⅱ型糖尿病神经病变的病因争论集中于代谢和血管因素两个方面。以往曾认为代谢失衡是引起神经病变的原因,目前较倾向是由于长期高血糖的结果,若干遗传因素如机体乙酰化状态可预测病人神经病变的危险性的看法尚未定论。最近,通过胰腺移植成功,血糖水平恢复正常病人,其多发性神经病变的发展就停止,又进一步支持了代谢性病因的假设。虽然多元醇代谢途径神经肌醇与神经机能障碍间关系尚不清楚,但已在人和实验动物两方面都证实多元醇代谢途径可能影响周围神经血
Etiology controversy about type I and type II diabetic neuropathy has focused on both metabolic and vascular factors. Metabolic imbalances have been previously thought to be the cause of neuropathy, and the current trend is due to the long-term consequences of hyperglycemia. The existence of several genetic factors such as the acetylation status of the body predicts the risk of neuropathy in patients is not yet conclusive. Recently, the success of pancreas transplantation, the return of blood glucose levels to normal patients, the development of multiple neuropathies ceased, and further support for the hypothesis of metabolic etiology. Although the relationship between the myo-inositol and neurological dysfunction of the polyol metabolic pathway is not clear, it has been demonstrated in both human and laboratory animals that polyol metabolic pathways may affect peripheral blood