Review uncovers key pathological mechanisms and therapeutic strategies in diabetes mellitus, highlighting the necessity of early intervention to prevent progressive nerve damage.
AbstractDiabetic neuropathy (DN) is a significant microvascular complication observed in both type 1 andtype 2 diabetes mellitus. It is distinguished by progressive injury to peripheral nerves, which occurs due toprolonged high blood sugar, disrupted metabolic processes, and impaired blood supply. This review deliversan in-depth overview of the biological mechanisms contributing to DN, such as oxidative stress, activation ofthe polyol pathway, and the accumulation of advanced glycation end-products.Global studies reveal that nearly half of individuals with long-standing diabetes eventually developsome degree of neuropathy. Clinical presentations may include distal symmetric polyneuropathy, autonomicdysfunction, or focal forms of nerve damage. Diagnosis requires careful clinical assessment supported byelectrophysiological testing and advanced tools like corneal confocal microscopy. The risk of developing DNrises with factors such as disease duration, unstable glucose levels, hypertension, abnormal lipid profiles, andsmoking.Management primarily involves strict glucose regulation, disease-modifying therapies such as alpha-lipoicacid, and pain-relieving agents like duloxetine or pregabalin. Novel therapies aimed at nerve repair andreducing inflammation are currently under investigation.
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D. Swarnalatha, Vanarasi Kalyani, Chinttanoori Varsha, Gundala Anu and Ravilla Varshini Sree (2026) studied this question.
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