What mechanism does glucose employ to cause peripheral neuropathy?

Glucose can lead to peripheral neuropathy primarily through osmotic damage, which occurs due to the conversion of excess glucose into sorbitol. This process is mediated by the enzyme aldose reductase, which catalyzes the reduction of glucose to sorbitol. Sorbitol, being an alcohol sugar, has different osmotic properties compared to glucose.

When there is chronic hyperglycemia, elevated levels of glucose result in increased sorbitol production. Sorbitol is less permeable to nerve membranes, causing it to accumulate within cells, particularly in nerve tissues. This accumulation leads to osmotic and cellular stress, resulting in nerve damage and dysfunction. The increased intracellular sorbitol attracts water, leading to neuronal swelling and ultimately deterioration of nerve function, contributing to peripheral neuropathy.

Understanding this mechanism underscores the importance of managing blood glucose levels in patients with diabetes to prevent complications such as peripheral neuropathy. Other mechanisms listed in the choices, such as direct nerve injury or impairment of blood supply, do not specifically explain the underlying process of osmotic damage that is central to the neuropathy seen in the context of elevated glucose levels.