Impaired corneal nerve markers in type 2 diabetic rats: comparison to models of diet-induced obesity and diet reversal.

BACKGROUND

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.

PURPOSE: The purpose of this study was to contrast the impact of cafeteria-diet-induced obesity model with a cafeteria diet combined with streptozotocin-induced type 2 diabetic model 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.

METHODS

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.

RESULTS

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).

CONCLUSION

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.