Experimental eye research · 2026
Impaired corneal nerve markers in type 2 diabetic rats: comparison to models of diet-induced obesity and diet reversal.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Khan Samea, Hossain Md Jakir, Markoulli Maria, Willcox Mark, Kendig Michael D, Morris Margaret J
Аннотация
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.
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.