Polyneuropathy in impaired glucose tolerance: is postprandial hyperglycemia the main culprit? A mini-review

Abstract

There is accumulating evidence for the mutual relationship between peripheral neuropathy and impaired glucose tolerance (IGT). The key factor in the pathogenesis of neuropathy in IGT is postprandial hyperglycemia, which induces increased oxidative stress, endothelial dysfunction, and activation of both protein kinase C and the polyol pathway, leading to impaired neuronal metabolism and DNA damage. Other pathogenic factors include dyslipidemia and the metabolic syndrome. The cornerstone of management is improved glycemic control, although a long sustainable effect has not been documented yet, calling for further supportive trials. Secondary therapeutic targets encompass hypolipidemic and antihypertensive treatment, smoking cessation and weight loss. The increasing awareness of peripheral neuropathy in IGT is expected to improve healthcare provision in subjects with this condition.