Unhealthy dietary habits are key risk factors for type 2 diabetes, a prevalent metabolic disease with significant health implications. Diabetic peripheral neuropathy is a common complication of type 2 diabetes that causes sensory and motor impairment. The purpose of this study was to contrast the impact of an obesogenic, cafeteria-diet-induced obesity with a cafeteria diet combined with streptozotocin-induced type 2 diabetes on measures of corneal neuropathy in rats. Additionally, this study explored the effects of diet reversal and the correlation between corneal nerve parameters and metabolic factors. After consuming the cafeteria diet for 13 weeks, the corneas of rats were dissected, corneal nerves were stained with β III tubulin antibody, visualized by confocal microscopy, and analysed using Image J. Corneal nerve fibre length and density were significantly reduced in cafeteria diet-induced obese ( p = .002) and type 2 diabetic rats ( p = .015). However, there was no difference in corneal nerve tortuosity among the normal, cafeteria-fed, type 2 diabetic, and cafeteria-diet reversal groups. After 8 weeks of diet reversal, corneal nerve fiber length and density did not differ significantly between control and diet reversal groups (NC vs. Caf-R; p > .05). Corneal nerve damage occurred in obese rats in the absence of hyperglycemia. Overall, results support the utility of monitoring corneal nerve integrity as a diagnostic marker of neuropathy before the onset of diabetes. The data also suggests that diet reversal may be an effective therapeutic strategy for maintaining corneal nerve health. • High-fat, high-sugar diet + STZ feeding induced a type 2-like diabetes in rats. • Type 2 diabetes was associated with reduced corneal nerve length and density. • Corneal nerves served as sensitive biomarkers of early neuropathic change. • Diet reversal mitigated metabolic dysfunction and ocular nerve damage.
Khan et al. (Wed,) studied this question.