Chronic, eye-threatening corneal pathology can arise from diabetic corneal neuropathy. Although the exact cause is unknown, it is thought that corneal disease is caused by a decrease in corneal sensitivity and loss of neurotrophic support. There is a lack of data on the connection between nerve damage to the corneal epithelium and nerve loss. In a streptozotocininduced diabetic mouse model, we used three-dimensional imaging in vivo and in situ to investigate changes in nerve morphology and the corneal epithelium. Streptozotocin-treated mice displayed growth retardation and elevated serum glucose levels that were consistent with severe diabetes. After six weeks of disease, the length of the subbasal nerve plexus decreased. Corneal epithelial thinning and a decrease in basal epithelial cell density were linked to the subbasal nerve plexus's disappearance. On the other hand, the age of the animal was linked to the loss of the terminal epithelial nerves [1]. Importantly, this is the first rodent model of type 1 diabetes to exhibit corneal epithelial thinning and a decrease in basal epithelial cell density, both of which have previously been observed in diabetic corneal neuropathy patients. These discoveries demonstrate that in sort 1 diabetes, nerve fiber harm is clear in the sub basal nerve plexus before terminal epithelial nerve misfortune and that neurotrophic support from both the sub basal nerve plexus and terminal epithelial nerves is fundamental for the upkeep of corneal epithelial homeostasis.
